Functional connections between two brain regions are the strongest indicator that pathologic, accumulated tau will spread from one to another.
Under diabetic conditions, SERP1 binds secretase subunit, cranking up cleavage of APP but not Notch. The finding offers a mechanistic link between diabetes and Alzheimer’s.
The cells are primed to attack. Their targets include Epstein-Barr virus peptides.
In nonhuman primates, three classes of LRRK2 kinase inhibitor cause microscopic changes in lung morphology, but they are reversible and do not impair breathing. Parkinson’s programs remain on track.
Two studies reveal new aspects of the neurovascular physiology that regulate the flow of oxygenated blood into the brain’s arterioles and capillaries in response to neuronal stimulation.
A large, cross-sectional study finds that RO-948 PET discriminates AD dementia from other disorders more accurately than do CSF biomarkers or MRI.
Harvard or MIT? The microbiomes of mice raised in different facilities dictated their response to C9 deficiency, including whether they died young. Do gut microbes influence ALS?
Built to cross the blood-brain barrier, the vehicle delivers therapeutic antibodies, enzymes, and potentially small molecules such as oligonucleotides.
Many Alzheimer’s trials had minimal dosing interruptions, but recruitment stopped for a time. Others trials fared worse, with some scrapped altogether. One administered study drug in an ambulance.
The first ever cryoEM structures of Aβ fibrils extracted from AD tissue look quite different than prior structures of fibrils generated in vitro. For starters, they are right-hand twisted, not left-hand.
Sex-specific polygenic hazard scores predict pathology and cognitive decline.
In vicinity of plaques, astrocytes and glia change gene expression in concert.
Analysis of a chimeric mouse shows that the cells express the same genes they do in the human brain, survey their environment, and respond to injuries and amyloid.
Much of the neuron loss in rTg4510 mice comes from accidental disruptions in mouse genes rather than expression of mutant tau. Pathology spreads quickly in human tau knock-ins.
Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.