In the dura, these lymphocytes release interleukin 17, activating perivascular macrophages. They curb cerebral blood flow, and mice become forgetful.
Cryo-EM reveals a common conformational progenitor for tau filaments found in Alzheimer’s disease and chronic traumatic encephalopathy.
Each associates with distinct AD risk variants, brain atrophy, and disease severity.
C2N’s PrecivityAD2 and ALZpath Inc.’s p-tau217 immunoassay identify people with AD with good accuracy.
For a diagnostic test, specificity and sensitivity fall a little shy. Using two cut points might solve the problem.
Adding palmitate makes an estrogen receptor linger at the synapse, curbing α-synuclein aggregation, motor deficits, and faulty memory. In mice.
This clarification comes after geriatricians argued that diagnosing AD in people without symptoms is premature, and the NIH pulled its name.
Faulty lipid metabolism is being blamed for supercharging tau phosphorylation. Restoring lipid efflux protects the mouse brain.
Signaling within microglia requires dozens of substrates of γ-secretase. Without the enzyme, the cells barely react to plaques in mice.
Smartphone- and web-based cognitive tasks detected amyloid positivity, early Alzheimer’s, better than in-person tests. Some are being used in clinical trials.
In amyloid immunotherapy trials to date, abolishing plaque leads to better outcomes months later. Cognitive benefits lag behind amyloid removal.
In a Phase 1 trial of Roche’s RG6289, both plasma and CSF Aβ37 climbed, while Aβ42 fell.
At high concentrations, Aβ42 gums up the protease’s active site. A new theory explains how γ-secretase modulators work. One is en route to Phase 2.
The largest genome-wide association study for PSP tied six risk loci to the tauopathy, including one new locus near the complement C4A gene.
Roche’s “brain shuttle” antibody, trontinemab, cleared plaque in Phase 1 with little ARIA, highlighting that bypassing vascular amyloid could be the key.
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