Two New p-Tau217 Blood Tests Join a Crowded Field
C2N’s PrecivityAD2 and ALZpath Inc.’s p-tau217 immunoassay identify people with AD with good accuracy.
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.
Regulated intramembrane proteolysis is the game, and γ-secretase is the name. After decades of research led to failed γ-secretase inhibitor programs, research on this prolific protease quietened. Now comes renewed interest from several fronts. Scientists debate what controls the sequential chipping of small peptides from the C-terminal of the Aβ sequence. The answer could inform the development of γ-secretase modulators, one of which is en route to Phase 2. And far beyond APP, scientists have found a new way to out γ-secretase substrates, identifying 59 new ones in microglia alone. This γ-secretase proteome appears to regulate cell state decisions, and without the protease, microglia react abnormally to amyloid plaques.
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