Robert Balaban opened the discussion by observing that heart disease and AD research share certain characteristics, including a weak familial linkage, poor penetrance of some of the known risk factors, and a poor understanding of the interplay between environmental and behavioral factors with gene-gene interactions.
Tim Clark began by laying out recommendations about the information infrastructure required if many groups want to be able to do collective experimentation, to share data, and to exploit automated pattern recognition in that shared data.
Brain extracts from AD patients, but not their cerebrospinal fluid, contain exceedingly potent Aβ seeds that survive formaldehyde treatment. The findings further implicate Aβ in prion-like pathology.
Neural circuits in the hippocampus defy current views about its structure and function.
Data suggest Aβ-dependent and –independent pathways combine forces to compromise cognition in otherwise healthy people.
In narrower claim, the drug is said to promote ApoE lipidation only in brain regions with extensive amyloid in mice carrying human ApoE4.
Starved for a protein that regulates lipids, neurons suffer and Aβ production soars, according to a new study.
Researchers have partnered with Google-funded Calico Life Sciences to develop a molecule that protects neurons in a variety of conditions.
Protein oligomers may be to blame in TDP-43 proteinopathies, as in other neurodegenerative conditions.
Older people who complain of memory problems are more likely to become measurably impaired and to have Alzheimer’s pathology in the brain, especially if they smoke or carry an ApoE4 allele.
MGH meeting traces arc of scientific discoveries from 1980s to today’s cutting edge.
Getting a close-up view of nicastrin, scientists find more evidence that this γ-secretase subunit snags substrates for presenilin.
People who lose their sense of smell have triple the odds of dying within five years. Some speculate neurodegenerative disease is involved.
In mouse models, removing this growth factor only from immune cells worsened pathology and memory.
Two studies claim that α-synuclein multimers have a physiological role as wranglers of synaptic vesicles. They come to different conclusions on the finer points, but could they fit into one grand model?
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