In London, researchers claimed that a monomer is the minimal structure required for tau strains. On the other hand, the sky seems the limit for the number of Aβ strains that form in an individual brain.
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 prevalence of chronic traumatic encephalopathy supports a link between multiple concussions and this degenerative tauopathy, though the sample is self-selected.
Armed with what they consider comprehensive data sets from the DIAN initiative, researchers are beginning a quest to settle an old question that may become key to drug approvals for late-onset AD.
NAPA's latest collective exercise was a conference to update the field on progress in the past three years and advise the NIH on how to spend the next round of funds.
White-matter hyperintensities, astrocyte damage, hypoperfusion, and amyloid angiopathy draw scrutiny as factors in the complex relationship between cerebrovascular and neurodegenerative processes in dementia.
At CTAD, former FDA neurology leader Rusty Katz urged Alzheimer’s trialists to stop fussing over disease progression. He recommended going after a large effect, regardless of whether it can garner a label of disease modification. That, he says, may mean combination trials.