Alzheimer's research to watch for at AAN

Alzheimer's disease sessions and lectures at this year's American Academy of Neurology annual meeting continue the theme of early detection of symptoms and intervention for modifiable risk factors that have become ever more relevant to ongoing research and treatment efforts.

• Genetics, imaging, and other biomarkers allow us to identify those individuals at the greatest risk, while prevention trials and disease modifying agents have gone from dream to reality. Among the best sessions for these should be Tuesday's Hot Topics plenary session lecture by Alison Goate, D.Phil., titled "Rare and Common Genetic Risk Factors for Alzheimer’s Disease," and the oral abstract session "Amyloid Imaging in the Prediction of and Diagnosis of Alzheimer's Disease," both on March 19. There’s also the Integrated Neuroscience Session, "Alzheimer's Biomarkers in Clinical Practice," on March 18.

• Trials of monoclonal antibodies, such as solanezumab and bapineuzumab, continue to show enough of an effect to keep our interest on amyloid-modifying therapies, but clinical outcomes remain disappointing and again echo the theme that earlier intervention may be needed. These can be found in the March 20 oral abstract session "Aging and Dementia: Epidemiology and Clinical Science," and the March 22 Clinical Trials plenary presentation by Dr. Ann Hake on solanezumab.

• New studies continue to provide evidence in support of "mom's recipe for good health,", i.e., sleep, exercise, and a good diet, and we can only hope that preventing or delaying dementia will add further impetus to the public to comply with these habits.

• At the Hot Topics plenary, Dr. John Trojanowski’s study on spreading tau fibrils in a transgenic mouse model of Alzheimer’s-like tauopathy should be absorbing. We have suspected this sort of tau fibril transmission in amyotrophic lateral sclerosis, of course (their presence in upper and lower motor neurons hardly seems like a coincidence), but it has been more difficult to prove in anatomically more complex areas like the hippocampus. His study contributes importantly to other research suggesting that a degenerative disease starts in a specific area and spreads from there (just as the stages of pathology have always implied).

Alzheimer's disease sessions and lectures at this year's American Academy of Neurology annual meeting continue the theme of early detection of symptoms and intervention for modifiable risk factors that have become ever more relevant to ongoing research and treatment efforts.

• Genetics, imaging, and other biomarkers allow us to identify those individuals at the greatest risk, while prevention trials and disease modifying agents have gone from dream to reality. Among the best sessions for these should be Tuesday's Hot Topics plenary session lecture by Alison Goate, D.Phil., titled "Rare and Common Genetic Risk Factors for Alzheimer’s Disease," and the oral abstract session "Amyloid Imaging in the Prediction of and Diagnosis of Alzheimer's Disease," both on March 19. There’s also the Integrated Neuroscience Session, "Alzheimer's Biomarkers in Clinical Practice," on March 18.

• Trials of monoclonal antibodies, such as solanezumab and bapineuzumab, continue to show enough of an effect to keep our interest on amyloid-modifying therapies, but clinical outcomes remain disappointing and again echo the theme that earlier intervention may be needed. These can be found in the March 20 oral abstract session "Aging and Dementia: Epidemiology and Clinical Science," and the March 22 Clinical Trials plenary presentation by Dr. Ann Hake on solanezumab.

• New studies continue to provide evidence in support of "mom's recipe for good health,", i.e., sleep, exercise, and a good diet, and we can only hope that preventing or delaying dementia will add further impetus to the public to comply with these habits.

• At the Hot Topics plenary, Dr. John Trojanowski’s study on spreading tau fibrils in a transgenic mouse model of Alzheimer’s-like tauopathy should be absorbing. We have suspected this sort of tau fibril transmission in amyotrophic lateral sclerosis, of course (their presence in upper and lower motor neurons hardly seems like a coincidence), but it has been more difficult to prove in anatomically more complex areas like the hippocampus. His study contributes importantly to other research suggesting that a degenerative disease starts in a specific area and spreads from there (just as the stages of pathology have always implied).

Alzheimer's disease sessions and lectures at this year's American Academy of Neurology annual meeting continue the theme of early detection of symptoms and intervention for modifiable risk factors that have become ever more relevant to ongoing research and treatment efforts.

• Genetics, imaging, and other biomarkers allow us to identify those individuals at the greatest risk, while prevention trials and disease modifying agents have gone from dream to reality. Among the best sessions for these should be Tuesday's Hot Topics plenary session lecture by Alison Goate, D.Phil., titled "Rare and Common Genetic Risk Factors for Alzheimer’s Disease," and the oral abstract session "Amyloid Imaging in the Prediction of and Diagnosis of Alzheimer's Disease," both on March 19. There’s also the Integrated Neuroscience Session, "Alzheimer's Biomarkers in Clinical Practice," on March 18.

• Trials of monoclonal antibodies, such as solanezumab and bapineuzumab, continue to show enough of an effect to keep our interest on amyloid-modifying therapies, but clinical outcomes remain disappointing and again echo the theme that earlier intervention may be needed. These can be found in the March 20 oral abstract session "Aging and Dementia: Epidemiology and Clinical Science," and the March 22 Clinical Trials plenary presentation by Dr. Ann Hake on solanezumab.

• New studies continue to provide evidence in support of "mom's recipe for good health,", i.e., sleep, exercise, and a good diet, and we can only hope that preventing or delaying dementia will add further impetus to the public to comply with these habits.

• At the Hot Topics plenary, Dr. John Trojanowski’s study on spreading tau fibrils in a transgenic mouse model of Alzheimer’s-like tauopathy should be absorbing. We have suspected this sort of tau fibril transmission in amyotrophic lateral sclerosis, of course (their presence in upper and lower motor neurons hardly seems like a coincidence), but it has been more difficult to prove in anatomically more complex areas like the hippocampus. His study contributes importantly to other research suggesting that a degenerative disease starts in a specific area and spreads from there (just as the stages of pathology have always implied).