A third trial continues in the United States
The fragment occurs naturally and rises after BACE inhibition, adding another layer of complexity to inhibitor therapy.
In two trials, moderate exercise or supplements of omega-3 fatty acids and antioxidants failed to alter the course of cognitive decline in older adults.
Three studies report that the C9ORF72 expansion prevents RNAs and proteins from shuttling properly between nucleus and cytosol.
A new report paints a stark picture of the coming wave of dementia cases and their staggering cost if prevention or treatment fails to stem the tide.
Scanning for amyloid plaques in the brain may help clinicians diagnose and manage patients with a questionable diagnosis of Alzheimer’s.
The largest trial yet of ApoE4 carriers is pioneering new protocols with increasing use of technology to reach thousands of potential participants and disclose risk information.
Prevention trials are testing new protocols for telling potential participants about their heightened risk for dementia, and exploring the psychological effect of such disclosures.
A leading experimental strategy for combating Alzheimer’s suppresses production of amyloid-β, but new data complicates the science behind this approach. Researchers have now identified an alternative, eta(η)-secretase cleavage of amyloid precursor protein. It generates longer, more abundant peptides than Aβ40/42. One η fragment suppresses synaptic plasticity. Levels of this species rise after β-secretase inhibition, raising the question of whether BACE inhibitor treatment could trade one toxic fragment for another. The jury is out on what the new APP cleavage means, if anything, for BACE inhibitor trials.
Hexanucleotide repeats in the C9ORF72 gene cause amyotrophic lateral sclerosis and frontotemporal dementia—but how? Three research groups now offer the same answer: The mutation disrupts RNAs exiting the nucleus, and proteins trying to get in. Different manifestations of the repeats may be responsible for the traffic jam. Some findings indicated the repeat-laden transcript are to blame, while others point the finger at polydipeptides translated from those RNAs. Experts agreed the real answer may be a bit of both.
To participate in secondary prevention trials, people must learn that they are at heightened risk for Alzheimer’s disease, either because they are accumulating brain amyloid, or because they carry an ApoE4 allele. How will people handle this knowledge, and how should clinicians communicate it to minimize psychological ill effects? At AAIC, speakers outlined how the A4 trial and Alzheimer Prevention Initiative’s ApoE4 study are going about disclosure, and discussed their challenges. Preliminary data indicate that most trial participants take the news in stride, perhaps paving the way for an era in which AD risk disclosure will become part of standard medical practice. Read Alzforum’s coverage.
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