To Block Tau’s Proteopathic Spread, Antibody Must Attack its Mid-Region
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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The epitope that a therapeutic tau antibody targets determines whether it prevents seeding in cellular assays, raising questions about first-generation antibody trials.
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.
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.
An antagonist to this receptor was trounced in Phase 3 trial.
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.
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.
An infrared spectral signature of amyloid β-sheets predicted AD conversion years before diagnosis.
Researchers at AAT-AD/PD discussed investigational PD treatments that aim to modify disease by hitting genetic risk factors.
In animal models, a PD risk gene revs up the immune system to fight infections, while probiotic bacteria slow α-synuclein aggregation.
Massive meta-analysis finds no link with AD or PD.
At AAT-AD/PD, scientists said an α-synuclein PET tracer is headed into trials. And marmosets model PD behaviors better than rodents. (Spoiler alert: They kick their partners while they sleep.)
Thirty-five reviews cover two decades of Alzheimer’s research.
The drug had no effect on any clinical measure, while there were side effects such as rashes, insomnia, and thoughts of suicide.
Biogen showed results from clinical trials of anti-Aβ and anti-α-synuclein antibodies at the American Academy of Neurology annual meeting.
Aggregates that form inside, or just pass through, oligodendrocytes take on the properties of the virulent strain that gives rise to multiple system atrophy.