Systemic inflammation can alter the epigenome of microglia, dictating whether the cells clean up Aβ pathology, or exacerbate it.
Massive meta-analysis finds no link with AD or PD.
Volunteers kept awake all night retained more florbetaben in their hippocampi and thalami in morning-after PET scan.
In animal models, a PD risk gene revs up the immune system to fight infections, while probiotic bacteria slow α-synuclein aggregation.
Researchers at AAT-AD/PD discussed investigational PD treatments that aim to modify disease by hitting genetic risk factors.
For the first time, NIA-AA proposal bases diagnosis in living people solely on biomarkers for plaques and tangles.
An infrared spectral signature of amyloid β-sheets predicted AD conversion years before diagnosis.
A study reported that new neurons continue to sprout from the human hippocampus well into the golden years, while another claims they all but disappear after childhood.
A widely popularized finding of shrinking dementia rates is entirely due to less vascular dementia, and is in fact concealing a rise in AD and PD, according to a provocative talk at AAT-AD/PD.
Maybe it’s not hyperexcitability, after all. Correlating electrical activity with muscle strength, scientists conclude that motor neurons become hypoexcitable just before degenerating.
An antagonist to this receptor was trounced in Phase 3 trial.
At AAT-AD/PD, scientists showed that correlated amyloid patches are an even earlier marker than brain-wide positivity, while others puzzled over why tau signals are lower in older people.
Low complexity and globular domains can promote LLPS, and phosphorylation hampers both.
A comparison of these large data sets shows that while the two forms of Alzheimer’s disease have separate triggers, they follow the same course and are much more similar than different.
The epitope that a therapeutic tau antibody targets determines whether it prevents seeding in cellular assays, raising questions about first-generation antibody trials.
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