Internal Medicine News

A work group convened by the Alzheimer’s Association has released revised biology-based criteria for the diagnosis and staging of Alzheimer’s disease, including a new biomarker classification system that incorporates fluid and imaging biomarkers as well as an updated disease staging system. 

“Plasma markers are here now, and it’s very important to incorporate them into the criteria for diagnosis,” said senior author Maria C. Carrillo, PhD, Alzheimer’s Association chief science officer and medical affairs lead. 

The revised criteria are the first updates since 2018.

“Defining diseases biologically, rather than based on syndromic presentation, has long been standard in many areas of medicine — including cancer, heart disease, and diabetes — and is becoming a unifying concept common to all neurodegenerative diseases,” lead author Clifford Jack Jr, MD, with Mayo Clinic, Rochester, Minnesota, said in a news release from the Alzheimer’s Association. 

“These updates to the diagnostic criteria are needed now because we know more about the underlying biology of Alzheimer’s and we are able to measure those changes,” Dr. Jack added. 

The 2024 revised criteria for diagnosis and staging of Alzheimer’s disease were published online in Alzheimer’s & Dementia. 
 

Core Biomarkers Defined

The revised criteria define Alzheimer’s disease as a biologic process that begins with the appearance of Alzheimer’s disease neuropathologic change (ADNPC) in the absence of symptoms. Progression of the neuropathologic burden leads to the later appearance and progression of clinical symptoms.

The work group organized Alzheimer’s disease biomarkers into three broad categories: (1) core biomarkers of ADNPC, (2) nonspecific biomarkers that are important in Alzheimer’s disease but are also involved in other brain diseases, and (3) biomarkers of diseases or conditions that commonly coexist with Alzheimer’s disease.

Core Alzheimer’s biomarkers are subdivided into Core 1 and Core 2. 

Core 1 biomarkers become abnormal early in the disease course and directly measure either amyloid plaques or phosphorylated tau (p-tau). They include amyloid PET; cerebrospinal fluid (CSF) amyloid beta 42/40 ratio, CSF p-tau181/amyloid beta 42 ratio, and CSF total (t)-tau/amyloid beta 42 ratio; and “accurate” plasma biomarkers, such as p-tau217. 

“An abnormal Core 1 biomarker result is sufficient to establish a diagnosis of Alzheimer’s disease and to inform clinical decision making [sic] throughout the disease continuum,” the work group wrote. 

Core 2 biomarkers become abnormal later in the disease process and are more closely linked with the onset of symptoms. Core 2 biomarkers include tau PET and certain soluble tau fragments associated with tau proteinopathy (eg, MTBR-tau243) but also pT205 and nonphosphorylated mid-region tau fragments. 

Core 2 biomarkers, when combined with Core 1, may be used to stage biologic disease severity; abnormal Core 2 biomarkers “increase confidence that Alzheimer’s disease is contributing to symptoms,” the work group noted. 

The revised criteria give clinicians “the flexibility to use plasma or PET scans or CSF,” Dr. Carrillo said. “They will have several tools that they can choose from and offer this variety of tools to their patients. We need different tools for different individuals. There will be differences in coverage and access to these diagnostics.” 

The revised criteria also include an integrated biologic and clinical staging scheme that acknowledges the fact that common co-pathologies, cognitive reserve, and resistance may modify relationships between clinical and biologic Alzheimer’s disease stages. 
 

Formal Guidelines to Come 

The work group noted that currently, the clinical use of Alzheimer’s disease biomarkers is intended for the evaluation of symptomatic patients, not cognitively unimpaired individuals.

Disease-targeted therapies have not yet been approved for cognitively unimpaired individuals. For this reason, the work group currently recommends against diagnostic testing in cognitively unimpaired individuals outside the context of observational or therapeutic research studies. 

This recommendation would change in the future if disease-targeted therapies that are currently being evaluated in trials demonstrate a benefit in preventing cognitive decline and are approved for use in preclinical Alzheimer’s disease, they wrote. 

They emphasize that the revised criteria are not intended to provide step-by-step clinical practice guidelines for clinicians. Rather, they provide general principles to inform diagnosis and staging of Alzheimer’s disease that reflect current science.

“This is just the beginning,” said Dr. Carrillo. “This is a gathering of the evidence to date and putting it in one place so we can have a consensus and actually a way to test it and make it better as we add new science.”

This also serves as a “springboard” for the Alzheimer’s Association to create formal clinical guidelines. “That will come, hopefully, over the next 12 months. We’ll be working on it, and we hope to have that in 2025,” Dr. Carrillo said. 

The revised criteria also emphasize the role of the clinician. 

“The biologically based diagnosis of Alzheimer’s disease is meant to assist, rather than supplant, the clinical evaluation of individuals with cognitive impairment,” the work group wrote in a related commentary published online in Nature Medicine. 

Recent diagnostics and therapeutic developments “herald a virtuous cycle in which improvements in diagnostic methods enable more sophisticated treatment approaches, which in turn steer advances in diagnostic methods,” they continued. “An unchanging principle, however, is that effective treatment will always rely on the ability to diagnose and stage the biology driving the disease process.”

Funding for this research was provided by the National Institutes of Health, Alexander family professorship, GHR Foundation, Alzheimer’s Association, Veterans Administration, Life Molecular Imaging, Michael J. Fox Foundation for Parkinson’s Research, Avid Radiopharmaceuticals, Eli Lilly, Gates Foundation, Biogen, C2N Diagnostics, Eisai, Fujirebio, GE Healthcare, Roche, National Institute on Aging, Roche/Genentech, BrightFocus Foundation, Hoffmann-La Roche, Novo Nordisk, Toyama, National MS Society, Alzheimer Drug Discovery Foundation, and others. A complete list of donors and disclosures is included in the original article.

 A version of this article appeared on Medscape.com.

A work group convened by the Alzheimer’s Association has released revised biology-based criteria for the diagnosis and staging of Alzheimer’s disease, including a new biomarker classification system that incorporates fluid and imaging biomarkers as well as an updated disease staging system. 

“Plasma markers are here now, and it’s very important to incorporate them into the criteria for diagnosis,” said senior author Maria C. Carrillo, PhD, Alzheimer’s Association chief science officer and medical affairs lead. 

The revised criteria are the first updates since 2018.

“Defining diseases biologically, rather than based on syndromic presentation, has long been standard in many areas of medicine — including cancer, heart disease, and diabetes — and is becoming a unifying concept common to all neurodegenerative diseases,” lead author Clifford Jack Jr, MD, with Mayo Clinic, Rochester, Minnesota, said in a news release from the Alzheimer’s Association. 

“These updates to the diagnostic criteria are needed now because we know more about the underlying biology of Alzheimer’s and we are able to measure those changes,” Dr. Jack added. 

The 2024 revised criteria for diagnosis and staging of Alzheimer’s disease were published online in Alzheimer’s & Dementia. 
 

Core Biomarkers Defined

The revised criteria define Alzheimer’s disease as a biologic process that begins with the appearance of Alzheimer’s disease neuropathologic change (ADNPC) in the absence of symptoms. Progression of the neuropathologic burden leads to the later appearance and progression of clinical symptoms.

The work group organized Alzheimer’s disease biomarkers into three broad categories: (1) core biomarkers of ADNPC, (2) nonspecific biomarkers that are important in Alzheimer’s disease but are also involved in other brain diseases, and (3) biomarkers of diseases or conditions that commonly coexist with Alzheimer’s disease.

Core Alzheimer’s biomarkers are subdivided into Core 1 and Core 2. 

Core 1 biomarkers become abnormal early in the disease course and directly measure either amyloid plaques or phosphorylated tau (p-tau). They include amyloid PET; cerebrospinal fluid (CSF) amyloid beta 42/40 ratio, CSF p-tau181/amyloid beta 42 ratio, and CSF total (t)-tau/amyloid beta 42 ratio; and “accurate” plasma biomarkers, such as p-tau217. 

“An abnormal Core 1 biomarker result is sufficient to establish a diagnosis of Alzheimer’s disease and to inform clinical decision making [sic] throughout the disease continuum,” the work group wrote. 

Core 2 biomarkers become abnormal later in the disease process and are more closely linked with the onset of symptoms. Core 2 biomarkers include tau PET and certain soluble tau fragments associated with tau proteinopathy (eg, MTBR-tau243) but also pT205 and nonphosphorylated mid-region tau fragments. 

Core 2 biomarkers, when combined with Core 1, may be used to stage biologic disease severity; abnormal Core 2 biomarkers “increase confidence that Alzheimer’s disease is contributing to symptoms,” the work group noted. 

The revised criteria give clinicians “the flexibility to use plasma or PET scans or CSF,” Dr. Carrillo said. “They will have several tools that they can choose from and offer this variety of tools to their patients. We need different tools for different individuals. There will be differences in coverage and access to these diagnostics.” 

The revised criteria also include an integrated biologic and clinical staging scheme that acknowledges the fact that common co-pathologies, cognitive reserve, and resistance may modify relationships between clinical and biologic Alzheimer’s disease stages. 
 

Formal Guidelines to Come 

The work group noted that currently, the clinical use of Alzheimer’s disease biomarkers is intended for the evaluation of symptomatic patients, not cognitively unimpaired individuals.

Disease-targeted therapies have not yet been approved for cognitively unimpaired individuals. For this reason, the work group currently recommends against diagnostic testing in cognitively unimpaired individuals outside the context of observational or therapeutic research studies. 

This recommendation would change in the future if disease-targeted therapies that are currently being evaluated in trials demonstrate a benefit in preventing cognitive decline and are approved for use in preclinical Alzheimer’s disease, they wrote. 

They emphasize that the revised criteria are not intended to provide step-by-step clinical practice guidelines for clinicians. Rather, they provide general principles to inform diagnosis and staging of Alzheimer’s disease that reflect current science.

“This is just the beginning,” said Dr. Carrillo. “This is a gathering of the evidence to date and putting it in one place so we can have a consensus and actually a way to test it and make it better as we add new science.”

This also serves as a “springboard” for the Alzheimer’s Association to create formal clinical guidelines. “That will come, hopefully, over the next 12 months. We’ll be working on it, and we hope to have that in 2025,” Dr. Carrillo said. 

The revised criteria also emphasize the role of the clinician. 

“The biologically based diagnosis of Alzheimer’s disease is meant to assist, rather than supplant, the clinical evaluation of individuals with cognitive impairment,” the work group wrote in a related commentary published online in Nature Medicine. 

Recent diagnostics and therapeutic developments “herald a virtuous cycle in which improvements in diagnostic methods enable more sophisticated treatment approaches, which in turn steer advances in diagnostic methods,” they continued. “An unchanging principle, however, is that effective treatment will always rely on the ability to diagnose and stage the biology driving the disease process.”

Funding for this research was provided by the National Institutes of Health, Alexander family professorship, GHR Foundation, Alzheimer’s Association, Veterans Administration, Life Molecular Imaging, Michael J. Fox Foundation for Parkinson’s Research, Avid Radiopharmaceuticals, Eli Lilly, Gates Foundation, Biogen, C2N Diagnostics, Eisai, Fujirebio, GE Healthcare, Roche, National Institute on Aging, Roche/Genentech, BrightFocus Foundation, Hoffmann-La Roche, Novo Nordisk, Toyama, National MS Society, Alzheimer Drug Discovery Foundation, and others. A complete list of donors and disclosures is included in the original article.

 A version of this article appeared on Medscape.com.

A work group convened by the Alzheimer’s Association has released revised biology-based criteria for the diagnosis and staging of Alzheimer’s disease, including a new biomarker classification system that incorporates fluid and imaging biomarkers as well as an updated disease staging system. 

“Plasma markers are here now, and it’s very important to incorporate them into the criteria for diagnosis,” said senior author Maria C. Carrillo, PhD, Alzheimer’s Association chief science officer and medical affairs lead. 

The revised criteria are the first updates since 2018.

“Defining diseases biologically, rather than based on syndromic presentation, has long been standard in many areas of medicine — including cancer, heart disease, and diabetes — and is becoming a unifying concept common to all neurodegenerative diseases,” lead author Clifford Jack Jr, MD, with Mayo Clinic, Rochester, Minnesota, said in a news release from the Alzheimer’s Association. 

“These updates to the diagnostic criteria are needed now because we know more about the underlying biology of Alzheimer’s and we are able to measure those changes,” Dr. Jack added. 

The 2024 revised criteria for diagnosis and staging of Alzheimer’s disease were published online in Alzheimer’s & Dementia. 
 

Core Biomarkers Defined

The revised criteria define Alzheimer’s disease as a biologic process that begins with the appearance of Alzheimer’s disease neuropathologic change (ADNPC) in the absence of symptoms. Progression of the neuropathologic burden leads to the later appearance and progression of clinical symptoms.

The work group organized Alzheimer’s disease biomarkers into three broad categories: (1) core biomarkers of ADNPC, (2) nonspecific biomarkers that are important in Alzheimer’s disease but are also involved in other brain diseases, and (3) biomarkers of diseases or conditions that commonly coexist with Alzheimer’s disease.

Core Alzheimer’s biomarkers are subdivided into Core 1 and Core 2. 

Core 1 biomarkers become abnormal early in the disease course and directly measure either amyloid plaques or phosphorylated tau (p-tau). They include amyloid PET; cerebrospinal fluid (CSF) amyloid beta 42/40 ratio, CSF p-tau181/amyloid beta 42 ratio, and CSF total (t)-tau/amyloid beta 42 ratio; and “accurate” plasma biomarkers, such as p-tau217. 

“An abnormal Core 1 biomarker result is sufficient to establish a diagnosis of Alzheimer’s disease and to inform clinical decision making [sic] throughout the disease continuum,” the work group wrote. 

Core 2 biomarkers become abnormal later in the disease process and are more closely linked with the onset of symptoms. Core 2 biomarkers include tau PET and certain soluble tau fragments associated with tau proteinopathy (eg, MTBR-tau243) but also pT205 and nonphosphorylated mid-region tau fragments. 

Core 2 biomarkers, when combined with Core 1, may be used to stage biologic disease severity; abnormal Core 2 biomarkers “increase confidence that Alzheimer’s disease is contributing to symptoms,” the work group noted. 

The revised criteria give clinicians “the flexibility to use plasma or PET scans or CSF,” Dr. Carrillo said. “They will have several tools that they can choose from and offer this variety of tools to their patients. We need different tools for different individuals. There will be differences in coverage and access to these diagnostics.” 

The revised criteria also include an integrated biologic and clinical staging scheme that acknowledges the fact that common co-pathologies, cognitive reserve, and resistance may modify relationships between clinical and biologic Alzheimer’s disease stages. 
 

Formal Guidelines to Come 

The work group noted that currently, the clinical use of Alzheimer’s disease biomarkers is intended for the evaluation of symptomatic patients, not cognitively unimpaired individuals.

Disease-targeted therapies have not yet been approved for cognitively unimpaired individuals. For this reason, the work group currently recommends against diagnostic testing in cognitively unimpaired individuals outside the context of observational or therapeutic research studies. 

This recommendation would change in the future if disease-targeted therapies that are currently being evaluated in trials demonstrate a benefit in preventing cognitive decline and are approved for use in preclinical Alzheimer’s disease, they wrote. 

They emphasize that the revised criteria are not intended to provide step-by-step clinical practice guidelines for clinicians. Rather, they provide general principles to inform diagnosis and staging of Alzheimer’s disease that reflect current science.

“This is just the beginning,” said Dr. Carrillo. “This is a gathering of the evidence to date and putting it in one place so we can have a consensus and actually a way to test it and make it better as we add new science.”

This also serves as a “springboard” for the Alzheimer’s Association to create formal clinical guidelines. “That will come, hopefully, over the next 12 months. We’ll be working on it, and we hope to have that in 2025,” Dr. Carrillo said. 

The revised criteria also emphasize the role of the clinician. 

“The biologically based diagnosis of Alzheimer’s disease is meant to assist, rather than supplant, the clinical evaluation of individuals with cognitive impairment,” the work group wrote in a related commentary published online in Nature Medicine. 

Recent diagnostics and therapeutic developments “herald a virtuous cycle in which improvements in diagnostic methods enable more sophisticated treatment approaches, which in turn steer advances in diagnostic methods,” they continued. “An unchanging principle, however, is that effective treatment will always rely on the ability to diagnose and stage the biology driving the disease process.”

Funding for this research was provided by the National Institutes of Health, Alexander family professorship, GHR Foundation, Alzheimer’s Association, Veterans Administration, Life Molecular Imaging, Michael J. Fox Foundation for Parkinson’s Research, Avid Radiopharmaceuticals, Eli Lilly, Gates Foundation, Biogen, C2N Diagnostics, Eisai, Fujirebio, GE Healthcare, Roche, National Institute on Aging, Roche/Genentech, BrightFocus Foundation, Hoffmann-La Roche, Novo Nordisk, Toyama, National MS Society, Alzheimer Drug Discovery Foundation, and others. A complete list of donors and disclosures is included in the original article.

 A version of this article appeared on Medscape.com.

A tool routinely used to evaluate concussion in college athletes fails to accurately diagnose the condition in many cases, a new study showed.

Investigators found that almost half of athletes diagnosed with a concussion tested normally on the Sports Concussion Assessment Tool 5 (SCAT5), the recommended tool for measuring cognitive skills in concussion evaluations. The most accurate measure of concussion was symptoms reported by the athletes.

“If you don’t do well on the cognitive exam, it suggests you have a concussion. But many people who are concussed do fine on the exam,” lead author Kimberly Harmon, MD, professor of family medicine and section head of sports medicine at the University of Washington School of Medicine, Seattle, said in a news release.

The study was published online in JAMA Network Open.

Introduced in 2004, the SCAT was created to standardize the collection of information clinicians use to diagnose concussion, including evaluation of symptoms, orientation, and balance. It also uses a 10-word list to assess immediate memory and delayed recall.

Dr. Harmon’s own experiences as a team physician led her to wonder about the accuracy of the cognitive screening portion of the SCAT. She saw that “some people were concussed, and they did well on the recall test. Some people weren’t concussed, and they didn’t do well. So I thought we should study it,” she said.

Investigators compared 92 National Collegiate Athletic Association (NCAA) Division 1 athletes who had sustained a concussion between 2020 and 2022 and had a concussion evaluation within 48 hours to 92 matched nonconcussed teammates (overall cohort, 52% men). Most concussions occurred in those who played football, followed by volleyball.

All athletes had previously completed NCAA-required baseline concussion screenings. Participants completed the SCAT5 screening test within 2 weeks of the incident concussion.

No significant differences were found between the baseline scores of athletes with and without concussion. Moreover, responses on the word recall section of the SCAT5 held little predictive value for concussion.

Nearly half (45%) of athletes with concussion performed at or even above their baseline cognitive report, which the authors said highlights the limitations of the cognitive components of SCAT5.

The most accurate predictor of concussion was participants’ responses to questions about their symptoms.

“If you get hit in the head and go to the sideline and say, ‘I have a headache, I’m dizzy, I don’t feel right,’ I can say with pretty good assurance that you have a concussion,” Dr. Harmon continued. “I don’t need to do any testing.”

Unfortunately, the problem is “that some athletes don’t want to come out. They don’t report their symptoms or may not recognize their symptoms. So then you need an objective, accurate test to tell you whether you can safely put the athlete back on the field. We don’t have that right now.”

The study did not control for concussion history, and the all–Division 1 cohort means the findings may not be generalizable to other athletes.

Nevertheless, investigators said the study “affirms that reported symptoms are the most sensitive indicator of concussion, and there are limitations to the objective cognitive testing included in the SCAT.” They concluded that concussion “remains a clinical diagnosis that should be based on a thorough review of signs, symptoms, and clinical findings.”

This study was funded in part by donations from University of Washington alumni Jack and Luellen Cherneski and the Chisholm Foundation. Dr. Harmon reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

A tool routinely used to evaluate concussion in college athletes fails to accurately diagnose the condition in many cases, a new study showed.

Investigators found that almost half of athletes diagnosed with a concussion tested normally on the Sports Concussion Assessment Tool 5 (SCAT5), the recommended tool for measuring cognitive skills in concussion evaluations. The most accurate measure of concussion was symptoms reported by the athletes.

“If you don’t do well on the cognitive exam, it suggests you have a concussion. But many people who are concussed do fine on the exam,” lead author Kimberly Harmon, MD, professor of family medicine and section head of sports medicine at the University of Washington School of Medicine, Seattle, said in a news release.

The study was published online in JAMA Network Open.

Introduced in 2004, the SCAT was created to standardize the collection of information clinicians use to diagnose concussion, including evaluation of symptoms, orientation, and balance. It also uses a 10-word list to assess immediate memory and delayed recall.

Dr. Harmon’s own experiences as a team physician led her to wonder about the accuracy of the cognitive screening portion of the SCAT. She saw that “some people were concussed, and they did well on the recall test. Some people weren’t concussed, and they didn’t do well. So I thought we should study it,” she said.

Investigators compared 92 National Collegiate Athletic Association (NCAA) Division 1 athletes who had sustained a concussion between 2020 and 2022 and had a concussion evaluation within 48 hours to 92 matched nonconcussed teammates (overall cohort, 52% men). Most concussions occurred in those who played football, followed by volleyball.

All athletes had previously completed NCAA-required baseline concussion screenings. Participants completed the SCAT5 screening test within 2 weeks of the incident concussion.

No significant differences were found between the baseline scores of athletes with and without concussion. Moreover, responses on the word recall section of the SCAT5 held little predictive value for concussion.

Nearly half (45%) of athletes with concussion performed at or even above their baseline cognitive report, which the authors said highlights the limitations of the cognitive components of SCAT5.

The most accurate predictor of concussion was participants’ responses to questions about their symptoms.

“If you get hit in the head and go to the sideline and say, ‘I have a headache, I’m dizzy, I don’t feel right,’ I can say with pretty good assurance that you have a concussion,” Dr. Harmon continued. “I don’t need to do any testing.”

Unfortunately, the problem is “that some athletes don’t want to come out. They don’t report their symptoms or may not recognize their symptoms. So then you need an objective, accurate test to tell you whether you can safely put the athlete back on the field. We don’t have that right now.”

The study did not control for concussion history, and the all–Division 1 cohort means the findings may not be generalizable to other athletes.

Nevertheless, investigators said the study “affirms that reported symptoms are the most sensitive indicator of concussion, and there are limitations to the objective cognitive testing included in the SCAT.” They concluded that concussion “remains a clinical diagnosis that should be based on a thorough review of signs, symptoms, and clinical findings.”

This study was funded in part by donations from University of Washington alumni Jack and Luellen Cherneski and the Chisholm Foundation. Dr. Harmon reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

A tool routinely used to evaluate concussion in college athletes fails to accurately diagnose the condition in many cases, a new study showed.

Investigators found that almost half of athletes diagnosed with a concussion tested normally on the Sports Concussion Assessment Tool 5 (SCAT5), the recommended tool for measuring cognitive skills in concussion evaluations. The most accurate measure of concussion was symptoms reported by the athletes.

“If you don’t do well on the cognitive exam, it suggests you have a concussion. But many people who are concussed do fine on the exam,” lead author Kimberly Harmon, MD, professor of family medicine and section head of sports medicine at the University of Washington School of Medicine, Seattle, said in a news release.

The study was published online in JAMA Network Open.

Introduced in 2004, the SCAT was created to standardize the collection of information clinicians use to diagnose concussion, including evaluation of symptoms, orientation, and balance. It also uses a 10-word list to assess immediate memory and delayed recall.

Dr. Harmon’s own experiences as a team physician led her to wonder about the accuracy of the cognitive screening portion of the SCAT. She saw that “some people were concussed, and they did well on the recall test. Some people weren’t concussed, and they didn’t do well. So I thought we should study it,” she said.

Investigators compared 92 National Collegiate Athletic Association (NCAA) Division 1 athletes who had sustained a concussion between 2020 and 2022 and had a concussion evaluation within 48 hours to 92 matched nonconcussed teammates (overall cohort, 52% men). Most concussions occurred in those who played football, followed by volleyball.

All athletes had previously completed NCAA-required baseline concussion screenings. Participants completed the SCAT5 screening test within 2 weeks of the incident concussion.

No significant differences were found between the baseline scores of athletes with and without concussion. Moreover, responses on the word recall section of the SCAT5 held little predictive value for concussion.

Nearly half (45%) of athletes with concussion performed at or even above their baseline cognitive report, which the authors said highlights the limitations of the cognitive components of SCAT5.

The most accurate predictor of concussion was participants’ responses to questions about their symptoms.

“If you get hit in the head and go to the sideline and say, ‘I have a headache, I’m dizzy, I don’t feel right,’ I can say with pretty good assurance that you have a concussion,” Dr. Harmon continued. “I don’t need to do any testing.”

Unfortunately, the problem is “that some athletes don’t want to come out. They don’t report their symptoms or may not recognize their symptoms. So then you need an objective, accurate test to tell you whether you can safely put the athlete back on the field. We don’t have that right now.”

The study did not control for concussion history, and the all–Division 1 cohort means the findings may not be generalizable to other athletes.

Nevertheless, investigators said the study “affirms that reported symptoms are the most sensitive indicator of concussion, and there are limitations to the objective cognitive testing included in the SCAT.” They concluded that concussion “remains a clinical diagnosis that should be based on a thorough review of signs, symptoms, and clinical findings.”

This study was funded in part by donations from University of Washington alumni Jack and Luellen Cherneski and the Chisholm Foundation. Dr. Harmon reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

TOPLINE:

A study found that patients who die by suicide within a year after discharge from inpatient mental health care are less likely to have primary care consultation in the first 2 weeks, highlighting a gap during the high-risk transition period.

METHODOLOGY:

• Researchers used a nested case-control study design, analyzing the records of 613 people who died by suicide within a year of being discharged from an inpatient psychiatric facility in England between 2001 and 2019.
• Of these, 93 (15.4%) died within 2 weeks of discharge.
• Each patient was matched with up to 20 control individuals who were discharged at a similar time but were living.
• Researchers evaluated primary care consultations after discharge.

TAKEAWAY:

• People who died by suicide within a year were less likely to have had a primary care consultation within 2 weeks of discharge (adjusted odds ratio [aOR], 0.61; P = .01).
• Those who died by suicide had higher odds for a consultation in the week preceding their death (aOR, 1.71; P < .001) and the prescription of three or more psychotropic medications (aOR, 1.73; P < .001).
• Evidence of discharge communication between the facility and primary care clinician was infrequent, highlighting a gap in continuity of care.
• Approximately 40% of people who died within 2 weeks of discharge had a documented visit with a primary care clinician during that period.

IN PRACTICE:

“Primary care clinicians have opportunities to intervene and should prioritize patients experiencing transition from inpatient care,” the authors wrote.

SOURCE:

The study was led by Rebecca Musgrove, PhD, of the Centre for Mental Health and Safety at The University of Manchester in England, and published online on June 12 in BJGP Open.

LIMITATIONS:

The study’s reliance on individuals registered with the Clinical Practice Research Datalink may have caused some suicide cases to be excluded, limiting generalizability. Lack of linked up-to-date mental health records may have led to the omission of significant post-discharge care data. Incomplete discharge documentation may undercount informational continuity, affecting multivariable analysis.

DISCLOSURES:

The study was supported by the National Institute of Health and Care Research. Some authors declared serving as members of advisory groups and receiving grants and personal fees from various sources.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

A study found that patients who die by suicide within a year after discharge from inpatient mental health care are less likely to have primary care consultation in the first 2 weeks, highlighting a gap during the high-risk transition period.

METHODOLOGY:

• Researchers used a nested case-control study design, analyzing the records of 613 people who died by suicide within a year of being discharged from an inpatient psychiatric facility in England between 2001 and 2019.
• Of these, 93 (15.4%) died within 2 weeks of discharge.
• Each patient was matched with up to 20 control individuals who were discharged at a similar time but were living.
• Researchers evaluated primary care consultations after discharge.

TAKEAWAY:

• People who died by suicide within a year were less likely to have had a primary care consultation within 2 weeks of discharge (adjusted odds ratio [aOR], 0.61; P = .01).
• Those who died by suicide had higher odds for a consultation in the week preceding their death (aOR, 1.71; P < .001) and the prescription of three or more psychotropic medications (aOR, 1.73; P < .001).
• Evidence of discharge communication between the facility and primary care clinician was infrequent, highlighting a gap in continuity of care.
• Approximately 40% of people who died within 2 weeks of discharge had a documented visit with a primary care clinician during that period.

IN PRACTICE:

“Primary care clinicians have opportunities to intervene and should prioritize patients experiencing transition from inpatient care,” the authors wrote.

SOURCE:

The study was led by Rebecca Musgrove, PhD, of the Centre for Mental Health and Safety at The University of Manchester in England, and published online on June 12 in BJGP Open.

LIMITATIONS:

The study’s reliance on individuals registered with the Clinical Practice Research Datalink may have caused some suicide cases to be excluded, limiting generalizability. Lack of linked up-to-date mental health records may have led to the omission of significant post-discharge care data. Incomplete discharge documentation may undercount informational continuity, affecting multivariable analysis.

DISCLOSURES:

The study was supported by the National Institute of Health and Care Research. Some authors declared serving as members of advisory groups and receiving grants and personal fees from various sources.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

A study found that patients who die by suicide within a year after discharge from inpatient mental health care are less likely to have primary care consultation in the first 2 weeks, highlighting a gap during the high-risk transition period.

METHODOLOGY:

• Researchers used a nested case-control study design, analyzing the records of 613 people who died by suicide within a year of being discharged from an inpatient psychiatric facility in England between 2001 and 2019.
• Of these, 93 (15.4%) died within 2 weeks of discharge.
• Each patient was matched with up to 20 control individuals who were discharged at a similar time but were living.
• Researchers evaluated primary care consultations after discharge.

TAKEAWAY:

• People who died by suicide within a year were less likely to have had a primary care consultation within 2 weeks of discharge (adjusted odds ratio [aOR], 0.61; P = .01).
• Those who died by suicide had higher odds for a consultation in the week preceding their death (aOR, 1.71; P < .001) and the prescription of three or more psychotropic medications (aOR, 1.73; P < .001).
• Evidence of discharge communication between the facility and primary care clinician was infrequent, highlighting a gap in continuity of care.
• Approximately 40% of people who died within 2 weeks of discharge had a documented visit with a primary care clinician during that period.

IN PRACTICE:

“Primary care clinicians have opportunities to intervene and should prioritize patients experiencing transition from inpatient care,” the authors wrote.

SOURCE:

The study was led by Rebecca Musgrove, PhD, of the Centre for Mental Health and Safety at The University of Manchester in England, and published online on June 12 in BJGP Open.

LIMITATIONS:

The study’s reliance on individuals registered with the Clinical Practice Research Datalink may have caused some suicide cases to be excluded, limiting generalizability. Lack of linked up-to-date mental health records may have led to the omission of significant post-discharge care data. Incomplete discharge documentation may undercount informational continuity, affecting multivariable analysis.

DISCLOSURES:

The study was supported by the National Institute of Health and Care Research. Some authors declared serving as members of advisory groups and receiving grants and personal fees from various sources.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

The Food and Drug Administration (FDA) has issued new draft guidance that does not require additional switching studies for biosimilars seeking interchangeability. These studies were previously recommended to demonstrate that switching between the biosimilar and its reference product showed no greater risk than using the reference product alone.

“The recommendations in today’s draft guidance, when finalized, will provide clarity and transparency about the FDA’s thinking and align the review and approval process with existing and emerging science,” said Sarah Yim, MD, director of the FDA’s Office of Therapeutic Biologics and Biosimilars in a statement on June 20. “We have gained valuable experience reviewing both biosimilar and interchangeable biosimilar medications over the past 10 years. Both biosimilars and interchangeable biosimilars meet the same high standard of biosimilarity for FDA approval and both are as safe and effective as the reference product.”

An interchangeable status allows a biosimilar product to be swapped with the reference product without involvement from the prescribing provider, depending on state law.

While switching studies were not required under previous FDA guidance, the 2019 document did state that the agency “expects that applications generally will include data from a switching study or studies in one or more appropriate conditions of use.”

However, of the 13 biosimilars that received interchangeability status, 9 did not include switching study data.

“Experience has shown that, for the products approved as biosimilars to date, the risk in terms of safety or diminished efficacy is insignificant following single or multiple switches between a reference product and a biosimilar product,” the FDA stated. The agency’s investigators also conducted a systematic review of switching studies, which found no differences in risk for death, serious adverse events, and treatment discontinuations in participants switched between biosimilars and reference products and those that remained on reference products.

“Additionally, today’s analytical tools can accurately evaluate the structure and effects [of] biologic products, both in the lab (in vitro) and in living organisms (in vivo) with more precision and sensitivity than switching studies,” the agency noted.

The FDA is now calling for commentary on these draft recommendations to be submitted by Aug. 20, 2024.

A version of this article first appeared on Medscape.com.

The Food and Drug Administration (FDA) has issued new draft guidance that does not require additional switching studies for biosimilars seeking interchangeability. These studies were previously recommended to demonstrate that switching between the biosimilar and its reference product showed no greater risk than using the reference product alone.

“The recommendations in today’s draft guidance, when finalized, will provide clarity and transparency about the FDA’s thinking and align the review and approval process with existing and emerging science,” said Sarah Yim, MD, director of the FDA’s Office of Therapeutic Biologics and Biosimilars in a statement on June 20. “We have gained valuable experience reviewing both biosimilar and interchangeable biosimilar medications over the past 10 years. Both biosimilars and interchangeable biosimilars meet the same high standard of biosimilarity for FDA approval and both are as safe and effective as the reference product.”

An interchangeable status allows a biosimilar product to be swapped with the reference product without involvement from the prescribing provider, depending on state law.

While switching studies were not required under previous FDA guidance, the 2019 document did state that the agency “expects that applications generally will include data from a switching study or studies in one or more appropriate conditions of use.”

However, of the 13 biosimilars that received interchangeability status, 9 did not include switching study data.

“Experience has shown that, for the products approved as biosimilars to date, the risk in terms of safety or diminished efficacy is insignificant following single or multiple switches between a reference product and a biosimilar product,” the FDA stated. The agency’s investigators also conducted a systematic review of switching studies, which found no differences in risk for death, serious adverse events, and treatment discontinuations in participants switched between biosimilars and reference products and those that remained on reference products.

“Additionally, today’s analytical tools can accurately evaluate the structure and effects [of] biologic products, both in the lab (in vitro) and in living organisms (in vivo) with more precision and sensitivity than switching studies,” the agency noted.

The FDA is now calling for commentary on these draft recommendations to be submitted by Aug. 20, 2024.

A version of this article first appeared on Medscape.com.

The Food and Drug Administration (FDA) has issued new draft guidance that does not require additional switching studies for biosimilars seeking interchangeability. These studies were previously recommended to demonstrate that switching between the biosimilar and its reference product showed no greater risk than using the reference product alone.

“The recommendations in today’s draft guidance, when finalized, will provide clarity and transparency about the FDA’s thinking and align the review and approval process with existing and emerging science,” said Sarah Yim, MD, director of the FDA’s Office of Therapeutic Biologics and Biosimilars in a statement on June 20. “We have gained valuable experience reviewing both biosimilar and interchangeable biosimilar medications over the past 10 years. Both biosimilars and interchangeable biosimilars meet the same high standard of biosimilarity for FDA approval and both are as safe and effective as the reference product.”

An interchangeable status allows a biosimilar product to be swapped with the reference product without involvement from the prescribing provider, depending on state law.

While switching studies were not required under previous FDA guidance, the 2019 document did state that the agency “expects that applications generally will include data from a switching study or studies in one or more appropriate conditions of use.”

However, of the 13 biosimilars that received interchangeability status, 9 did not include switching study data.

“Experience has shown that, for the products approved as biosimilars to date, the risk in terms of safety or diminished efficacy is insignificant following single or multiple switches between a reference product and a biosimilar product,” the FDA stated. The agency’s investigators also conducted a systematic review of switching studies, which found no differences in risk for death, serious adverse events, and treatment discontinuations in participants switched between biosimilars and reference products and those that remained on reference products.

“Additionally, today’s analytical tools can accurately evaluate the structure and effects [of] biologic products, both in the lab (in vitro) and in living organisms (in vivo) with more precision and sensitivity than switching studies,” the agency noted.

The FDA is now calling for commentary on these draft recommendations to be submitted by Aug. 20, 2024.

A version of this article first appeared on Medscape.com.

Baricitinib may be the superior choice to tumor necrosis factor (TNF) inhibitors in patients with rheumatoid arthritis (RA) for whom conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) have failed, according to a new study.

After 12 weeks, patients taking baricitinib achieved a 50% improvement in RA symptoms according to American College of Rheumatology response criteria (ACR50) at twice the rate as in patients assigned to receive TNF inhibitors. In addition, 75% of the baricitinib group achieved a 28-joint Disease Activity Score with C-reactive protein under 2.6, compared with less than half of patients taking TNF inhibitors.
 

Putting Safety Into the Equation

However, safety concerns also need to be considered when prescribing medication, noted Andrew Wang, MD, PhD, a rheumatologist at Yale School of Medicine in New Haven, Connecticut. He was not involved with the study, called PERFECTRA.

“This category of drugs — JAK-STAT [inhibitors] — are much newer than TNF inhibitors, CTLAs, B-cell depleters, and the other tools we have,” he said, “with relatively less real-world experience and potential downsides in the future.”

drorotulibudisethowofrorupivegotodesetatagutotuleswucaspikitibameludewodrapravugaroclojocopretawraprethutotabrudrekasabrewiphiphiche

Study Details

In the study, researchers enrolled 199 patients with active RA for which previous use of at least one csDMARD had failed and randomly assigned 97 patients to receive baricitinib and the remainder to receive a TNF inhibitor: 64% started on adalimumab, 33% started on etanercept, and the rest used golimumab or infliximab.

For all patients, the suggested treatment allocation was provided via randomization lists, but physicians and patients ultimately decided treatment via shared decision-making.

Patients were diagnosed less than 5 years ago, had received no previous treatment with biologics or targeted synthetic DMARDs, and had no contraindications for TNF inhibitors or baricitinib. Researchers recruited patients from September 2019 through February 2022 across 15 health centers in the Netherlands and Belgium. The study was funded by Eli Lilly, which manufactures baricitinib, although the study was investigator initiated.

Patients were on average aged 55 years, and about two thirds were women. The average disease duration was 2 years.

At 12 weeks, 42% of the baricitinib group achieved ACR50, compared with 20% of the TNF inhibitor group. All patient-reported outcome measures showed improvement over the study period, favoring baricitinib. More patients receiving baricitinib remained on the medication overall than patients on a TNF inhibitor: At 48 weeks, 70% of patients receiving a TNF inhibitor and 80% of patients receiving baricitinib had continued taking their assigned treatment.

These results are not surprising, Wang noted, as “JAK inhibitors hit many arms of immune signaling, whereas TNF blockers just hit TNF.” However, there is a trade-off between potent, effective drugs and toxicity, he added.

“I would not be as bullish on starting baricitinib in a patient off the bat, in the same way that nobody would want to keep patients on glucocorticoids [any longer than is] minimally necessary.”

While the study was not powered to compare safety between the two drugs, there were no adverse events during the study that had not been previously reported.

“Prescribers have to be aware that cardiovascular and malignant [serious adverse events] are more frequently reported” with JAK inhibitors than with TNF inhibitors, the authors wrote. “Obviously, this has to be considered carefully in risk-benefit discussions with any individual patient.”

Dr. Wang noted that, in general, he and his colleagues would not start with a JAK inhibitor first except for special circumstances: For example, if a patient will not use an injectable medication, or for some reason, it’s impractical for the patient’s lifestyle to use medication that requires constant refrigeration.

“I think the take-home message here is these are, in general, lifelong diseases, and so a rheumatologist and their patients have to develop good relationships to monitor whether or not we’re hitting the sweet spot of keeping disease under control” while also avoiding overmedication and toxicity, he said.

One potential solution, which Dr. Wang has also done in his clinical practice, is to initiate a JAK inhibitor in patients who need it but then switch to a different modality after achieving disease control.

“You can imagine a scenario where you get them to a very low [Disease Activity Score] with baricitinib, for example, and then you switch them to a TNF inhibitor,” he said. “I can imagine that there would be ways that you could get the best of both worlds.”

PERFECTRA was financially supported by an unrestricted grant from Eli Lilly. The authors reported financial relationships with AbbVie, Eli Lilly, Galapagos, and Janssen-Cilag. Dr. Wang serves on NGM Bio’s science advisory board, consults for TCG Labs-Soleil and Seranova Bio, and has received funding from AstraZeneca.

A version of this article first appeared on Medscape.com.

Baricitinib may be the superior choice to tumor necrosis factor (TNF) inhibitors in patients with rheumatoid arthritis (RA) for whom conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) have failed, according to a new study.

After 12 weeks, patients taking baricitinib achieved a 50% improvement in RA symptoms according to American College of Rheumatology response criteria (ACR50) at twice the rate as in patients assigned to receive TNF inhibitors. In addition, 75% of the baricitinib group achieved a 28-joint Disease Activity Score with C-reactive protein under 2.6, compared with less than half of patients taking TNF inhibitors.
 

Putting Safety Into the Equation

However, safety concerns also need to be considered when prescribing medication, noted Andrew Wang, MD, PhD, a rheumatologist at Yale School of Medicine in New Haven, Connecticut. He was not involved with the study, called PERFECTRA.

“This category of drugs — JAK-STAT [inhibitors] — are much newer than TNF inhibitors, CTLAs, B-cell depleters, and the other tools we have,” he said, “with relatively less real-world experience and potential downsides in the future.”

drorotulibudisethowofrorupivegotodesetatagutotuleswucaspikitibameludewodrapravugaroclojocopretawraprethutotabrudrekasabrewiphiphiche

Study Details

In the study, researchers enrolled 199 patients with active RA for which previous use of at least one csDMARD had failed and randomly assigned 97 patients to receive baricitinib and the remainder to receive a TNF inhibitor: 64% started on adalimumab, 33% started on etanercept, and the rest used golimumab or infliximab.

For all patients, the suggested treatment allocation was provided via randomization lists, but physicians and patients ultimately decided treatment via shared decision-making.

Patients were diagnosed less than 5 years ago, had received no previous treatment with biologics or targeted synthetic DMARDs, and had no contraindications for TNF inhibitors or baricitinib. Researchers recruited patients from September 2019 through February 2022 across 15 health centers in the Netherlands and Belgium. The study was funded by Eli Lilly, which manufactures baricitinib, although the study was investigator initiated.

Patients were on average aged 55 years, and about two thirds were women. The average disease duration was 2 years.

At 12 weeks, 42% of the baricitinib group achieved ACR50, compared with 20% of the TNF inhibitor group. All patient-reported outcome measures showed improvement over the study period, favoring baricitinib. More patients receiving baricitinib remained on the medication overall than patients on a TNF inhibitor: At 48 weeks, 70% of patients receiving a TNF inhibitor and 80% of patients receiving baricitinib had continued taking their assigned treatment.

These results are not surprising, Wang noted, as “JAK inhibitors hit many arms of immune signaling, whereas TNF blockers just hit TNF.” However, there is a trade-off between potent, effective drugs and toxicity, he added.

“I would not be as bullish on starting baricitinib in a patient off the bat, in the same way that nobody would want to keep patients on glucocorticoids [any longer than is] minimally necessary.”

While the study was not powered to compare safety between the two drugs, there were no adverse events during the study that had not been previously reported.

“Prescribers have to be aware that cardiovascular and malignant [serious adverse events] are more frequently reported” with JAK inhibitors than with TNF inhibitors, the authors wrote. “Obviously, this has to be considered carefully in risk-benefit discussions with any individual patient.”

Dr. Wang noted that, in general, he and his colleagues would not start with a JAK inhibitor first except for special circumstances: For example, if a patient will not use an injectable medication, or for some reason, it’s impractical for the patient’s lifestyle to use medication that requires constant refrigeration.

“I think the take-home message here is these are, in general, lifelong diseases, and so a rheumatologist and their patients have to develop good relationships to monitor whether or not we’re hitting the sweet spot of keeping disease under control” while also avoiding overmedication and toxicity, he said.

One potential solution, which Dr. Wang has also done in his clinical practice, is to initiate a JAK inhibitor in patients who need it but then switch to a different modality after achieving disease control.

“You can imagine a scenario where you get them to a very low [Disease Activity Score] with baricitinib, for example, and then you switch them to a TNF inhibitor,” he said. “I can imagine that there would be ways that you could get the best of both worlds.”

PERFECTRA was financially supported by an unrestricted grant from Eli Lilly. The authors reported financial relationships with AbbVie, Eli Lilly, Galapagos, and Janssen-Cilag. Dr. Wang serves on NGM Bio’s science advisory board, consults for TCG Labs-Soleil and Seranova Bio, and has received funding from AstraZeneca.

A version of this article first appeared on Medscape.com.

Baricitinib may be the superior choice to tumor necrosis factor (TNF) inhibitors in patients with rheumatoid arthritis (RA) for whom conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) have failed, according to a new study.

After 12 weeks, patients taking baricitinib achieved a 50% improvement in RA symptoms according to American College of Rheumatology response criteria (ACR50) at twice the rate as in patients assigned to receive TNF inhibitors. In addition, 75% of the baricitinib group achieved a 28-joint Disease Activity Score with C-reactive protein under 2.6, compared with less than half of patients taking TNF inhibitors.
 

Putting Safety Into the Equation

However, safety concerns also need to be considered when prescribing medication, noted Andrew Wang, MD, PhD, a rheumatologist at Yale School of Medicine in New Haven, Connecticut. He was not involved with the study, called PERFECTRA.

“This category of drugs — JAK-STAT [inhibitors] — are much newer than TNF inhibitors, CTLAs, B-cell depleters, and the other tools we have,” he said, “with relatively less real-world experience and potential downsides in the future.”

drorotulibudisethowofrorupivegotodesetatagutotuleswucaspikitibameludewodrapravugaroclojocopretawraprethutotabrudrekasabrewiphiphiche

Study Details

In the study, researchers enrolled 199 patients with active RA for which previous use of at least one csDMARD had failed and randomly assigned 97 patients to receive baricitinib and the remainder to receive a TNF inhibitor: 64% started on adalimumab, 33% started on etanercept, and the rest used golimumab or infliximab.

For all patients, the suggested treatment allocation was provided via randomization lists, but physicians and patients ultimately decided treatment via shared decision-making.

Patients were diagnosed less than 5 years ago, had received no previous treatment with biologics or targeted synthetic DMARDs, and had no contraindications for TNF inhibitors or baricitinib. Researchers recruited patients from September 2019 through February 2022 across 15 health centers in the Netherlands and Belgium. The study was funded by Eli Lilly, which manufactures baricitinib, although the study was investigator initiated.

Patients were on average aged 55 years, and about two thirds were women. The average disease duration was 2 years.

At 12 weeks, 42% of the baricitinib group achieved ACR50, compared with 20% of the TNF inhibitor group. All patient-reported outcome measures showed improvement over the study period, favoring baricitinib. More patients receiving baricitinib remained on the medication overall than patients on a TNF inhibitor: At 48 weeks, 70% of patients receiving a TNF inhibitor and 80% of patients receiving baricitinib had continued taking their assigned treatment.

These results are not surprising, Wang noted, as “JAK inhibitors hit many arms of immune signaling, whereas TNF blockers just hit TNF.” However, there is a trade-off between potent, effective drugs and toxicity, he added.

“I would not be as bullish on starting baricitinib in a patient off the bat, in the same way that nobody would want to keep patients on glucocorticoids [any longer than is] minimally necessary.”

While the study was not powered to compare safety between the two drugs, there were no adverse events during the study that had not been previously reported.

“Prescribers have to be aware that cardiovascular and malignant [serious adverse events] are more frequently reported” with JAK inhibitors than with TNF inhibitors, the authors wrote. “Obviously, this has to be considered carefully in risk-benefit discussions with any individual patient.”

Dr. Wang noted that, in general, he and his colleagues would not start with a JAK inhibitor first except for special circumstances: For example, if a patient will not use an injectable medication, or for some reason, it’s impractical for the patient’s lifestyle to use medication that requires constant refrigeration.

“I think the take-home message here is these are, in general, lifelong diseases, and so a rheumatologist and their patients have to develop good relationships to monitor whether or not we’re hitting the sweet spot of keeping disease under control” while also avoiding overmedication and toxicity, he said.

One potential solution, which Dr. Wang has also done in his clinical practice, is to initiate a JAK inhibitor in patients who need it but then switch to a different modality after achieving disease control.

“You can imagine a scenario where you get them to a very low [Disease Activity Score] with baricitinib, for example, and then you switch them to a TNF inhibitor,” he said. “I can imagine that there would be ways that you could get the best of both worlds.”

PERFECTRA was financially supported by an unrestricted grant from Eli Lilly. The authors reported financial relationships with AbbVie, Eli Lilly, Galapagos, and Janssen-Cilag. Dr. Wang serves on NGM Bio’s science advisory board, consults for TCG Labs-Soleil and Seranova Bio, and has received funding from AstraZeneca.

A version of this article first appeared on Medscape.com.

Certain medications that are used to treat benign prostatic hyperplasia (BPH) are associated with a reduced risk for dementia with Lewy bodies (DLB), the second most common neurodegenerative type of dementia after Alzheimer’s disease.

Investigators found older men taking alpha-1 blockers terazosin, doxazosin, or alfuzosin (Tz/Dz/Az) were 40% less likely to develop DLB than those taking tamsulosin and 37% less likely than men taking the 5-alpha reductase inhibitors (5ARI) finasteride and dutasteride.

“These results are exciting because right now there are no drugs to prevent or treat dementia with Lewy bodies,” study investigator Jacob E. Simmering, PhD, of the University of Iowa in Iowa City, said in a press release. “If we can determine that an existing drug can offer protection against this debilitating disease, that has the potential to greatly reduce its effects.”

The findings were published online in Neurology.
 

Increasing ATP Neuroprotective?

In recent years, investigators have speculated that improving metabolic activity in the brain may reduce the risk for Parkinson’s disease (PD). 

In previous studies, the use of Tz/Dz/Az resulted in the activation of phosphoglycerate kinase-1 (PKG1), which increases the availability of adenosine triphosphate (ATP).

There have been case reports of PD being linked to mutations affecting PGK1. Researchers speculate that increased ATP availability in neurons resulting from the activation of PKG1 allows cells to better adapt to aging and synuclein aggregation.

To investigate whether glycolysis-enhancing drugs might be neuroprotective in those with DLB, investigators conducted a retrospective cohort study using a commercial health insurance claims database and a Medicare supplemental health claims database to follow a sample of men aged > 40 years taking Tz, Dz, or Az (n = 126,313), tamsulosin (n = 437,035), or a 5ARI (n = 80,158) for BPH.

Tamsulosin and 5ARI medications do not activate PKG1, so investigators used them as comparators to Tz/Dz/Az. Participants were followed from the medication initiation date until the end of enrollment in the claims databases.

After following claimants for an average of 3 years, 195 participants developed DLB who were taking Tz, Dz, or Az, a rate of 5.21 cases per 10,000 people per year.

During the follow-up period, 1286 participants taking tamsulosin developed DLB, a rate of 10.8 per 10,000 people per year, and among those taking 5ARIs, 193 cases of DLB were reported, a rate of 7.8 per 10,000 people per year.

After matching the groups by age and other health conditions that may explain differences in rates of DLB, men taking Tz/Dz/Az had a 60% lower risk than those taking tamsulosin (P < .001) and a 37% lower risk for developing DLB than those taking the 5ARI medications (P = .012).

“This emerging evidence of a protective association across a spectrum of diseases suggests a broad neuroprotective effect for Tz/Dz/Az, consistent with our hypothesized mechanism that activation of PGK1 increases brain ATP and mitigates neurodegeneration,” the authors wrote.

Study limitations include excluding women from the study, so the findings cannot be generalized to women. Claims analyses were limited to administrative data that could have been incorrect, and the analyses did not include medication dosages.

No study funding or author disclosures were reported.

A version of this article first appeared on Medscape.com.

Certain medications that are used to treat benign prostatic hyperplasia (BPH) are associated with a reduced risk for dementia with Lewy bodies (DLB), the second most common neurodegenerative type of dementia after Alzheimer’s disease.

Investigators found older men taking alpha-1 blockers terazosin, doxazosin, or alfuzosin (Tz/Dz/Az) were 40% less likely to develop DLB than those taking tamsulosin and 37% less likely than men taking the 5-alpha reductase inhibitors (5ARI) finasteride and dutasteride.

“These results are exciting because right now there are no drugs to prevent or treat dementia with Lewy bodies,” study investigator Jacob E. Simmering, PhD, of the University of Iowa in Iowa City, said in a press release. “If we can determine that an existing drug can offer protection against this debilitating disease, that has the potential to greatly reduce its effects.”

The findings were published online in Neurology.
 

Increasing ATP Neuroprotective?

In recent years, investigators have speculated that improving metabolic activity in the brain may reduce the risk for Parkinson’s disease (PD). 

In previous studies, the use of Tz/Dz/Az resulted in the activation of phosphoglycerate kinase-1 (PKG1), which increases the availability of adenosine triphosphate (ATP).

There have been case reports of PD being linked to mutations affecting PGK1. Researchers speculate that increased ATP availability in neurons resulting from the activation of PKG1 allows cells to better adapt to aging and synuclein aggregation.

To investigate whether glycolysis-enhancing drugs might be neuroprotective in those with DLB, investigators conducted a retrospective cohort study using a commercial health insurance claims database and a Medicare supplemental health claims database to follow a sample of men aged > 40 years taking Tz, Dz, or Az (n = 126,313), tamsulosin (n = 437,035), or a 5ARI (n = 80,158) for BPH.

Tamsulosin and 5ARI medications do not activate PKG1, so investigators used them as comparators to Tz/Dz/Az. Participants were followed from the medication initiation date until the end of enrollment in the claims databases.

After following claimants for an average of 3 years, 195 participants developed DLB who were taking Tz, Dz, or Az, a rate of 5.21 cases per 10,000 people per year.

During the follow-up period, 1286 participants taking tamsulosin developed DLB, a rate of 10.8 per 10,000 people per year, and among those taking 5ARIs, 193 cases of DLB were reported, a rate of 7.8 per 10,000 people per year.

After matching the groups by age and other health conditions that may explain differences in rates of DLB, men taking Tz/Dz/Az had a 60% lower risk than those taking tamsulosin (P < .001) and a 37% lower risk for developing DLB than those taking the 5ARI medications (P = .012).

“This emerging evidence of a protective association across a spectrum of diseases suggests a broad neuroprotective effect for Tz/Dz/Az, consistent with our hypothesized mechanism that activation of PGK1 increases brain ATP and mitigates neurodegeneration,” the authors wrote.

Study limitations include excluding women from the study, so the findings cannot be generalized to women. Claims analyses were limited to administrative data that could have been incorrect, and the analyses did not include medication dosages.

No study funding or author disclosures were reported.

A version of this article first appeared on Medscape.com.

Certain medications that are used to treat benign prostatic hyperplasia (BPH) are associated with a reduced risk for dementia with Lewy bodies (DLB), the second most common neurodegenerative type of dementia after Alzheimer’s disease.

Investigators found older men taking alpha-1 blockers terazosin, doxazosin, or alfuzosin (Tz/Dz/Az) were 40% less likely to develop DLB than those taking tamsulosin and 37% less likely than men taking the 5-alpha reductase inhibitors (5ARI) finasteride and dutasteride.

“These results are exciting because right now there are no drugs to prevent or treat dementia with Lewy bodies,” study investigator Jacob E. Simmering, PhD, of the University of Iowa in Iowa City, said in a press release. “If we can determine that an existing drug can offer protection against this debilitating disease, that has the potential to greatly reduce its effects.”

The findings were published online in Neurology.
 

Increasing ATP Neuroprotective?

In recent years, investigators have speculated that improving metabolic activity in the brain may reduce the risk for Parkinson’s disease (PD). 

In previous studies, the use of Tz/Dz/Az resulted in the activation of phosphoglycerate kinase-1 (PKG1), which increases the availability of adenosine triphosphate (ATP).

There have been case reports of PD being linked to mutations affecting PGK1. Researchers speculate that increased ATP availability in neurons resulting from the activation of PKG1 allows cells to better adapt to aging and synuclein aggregation.

To investigate whether glycolysis-enhancing drugs might be neuroprotective in those with DLB, investigators conducted a retrospective cohort study using a commercial health insurance claims database and a Medicare supplemental health claims database to follow a sample of men aged > 40 years taking Tz, Dz, or Az (n = 126,313), tamsulosin (n = 437,035), or a 5ARI (n = 80,158) for BPH.

Tamsulosin and 5ARI medications do not activate PKG1, so investigators used them as comparators to Tz/Dz/Az. Participants were followed from the medication initiation date until the end of enrollment in the claims databases.

After following claimants for an average of 3 years, 195 participants developed DLB who were taking Tz, Dz, or Az, a rate of 5.21 cases per 10,000 people per year.

During the follow-up period, 1286 participants taking tamsulosin developed DLB, a rate of 10.8 per 10,000 people per year, and among those taking 5ARIs, 193 cases of DLB were reported, a rate of 7.8 per 10,000 people per year.

After matching the groups by age and other health conditions that may explain differences in rates of DLB, men taking Tz/Dz/Az had a 60% lower risk than those taking tamsulosin (P < .001) and a 37% lower risk for developing DLB than those taking the 5ARI medications (P = .012).

“This emerging evidence of a protective association across a spectrum of diseases suggests a broad neuroprotective effect for Tz/Dz/Az, consistent with our hypothesized mechanism that activation of PGK1 increases brain ATP and mitigates neurodegeneration,” the authors wrote.

Study limitations include excluding women from the study, so the findings cannot be generalized to women. Claims analyses were limited to administrative data that could have been incorrect, and the analyses did not include medication dosages.

No study funding or author disclosures were reported.

A version of this article first appeared on Medscape.com.