Sit Less, Move More to Induce Irisin and Stave Off Dementia
In people over 60, sitting for 12 hours per day increased dementia risk. An exercise-induced hormone, irisin, protects via astrocytes, at least in vitro.
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In people over 60, sitting for 12 hours per day increased dementia risk. An exercise-induced hormone, irisin, protects via astrocytes, at least in vitro.
C2N’s PrecivityAD2 and ALZpath Inc.’s p-tau217 immunoassay identify people with AD with good accuracy.
Lilly’s Phase 3 antibody remternetug resembles donanemab, but without pesky antidrug antibodies; Prothena’s Phase 1 PRX012 may need fewer injections.
ALZpath’s assay detected an annual rise in plasma phospho-tau217 in amyloid-positive people, with the steepest increase in those who also have tangles.
Scientists around the globe are studying how best to deploy Alzheimer's plasma tests in the real world. Their focus: primary care.
A Rand report concludes that using blood-based biomarkers and cognitive tests in primary care would halve wait times for new disease-modifying therapies.
With newly available fluid biomarkers that detect α-synuclein pathology in the brain, researchers articulate ways to classify the disease based on its biology.
In more than 52,000 cognitively healthy people, elevated plasma GFAP or NfL more than doubled the risk the person would develop dementia over the next 14 years.
Layer 1 interneurons vanish. Layer 2/3 excitatory neurons become hyperactive, then fade. Microglia change state. Astrocytes react. No symptoms yet. Is this preclinical Alzheimer's?
£50 million in funding will expand trial access, increase recruitment, streamline study processes, and train staff over the next five years.
Methylated CAG-repeat RNAs and 14-3-3θ promote TDP-43 aggregation.
At trials conference, multiple amyloid immunotherapy programs reported greatest cognitive benefits for people whose tau tangle deposition has only just begun.
Lamivudine slightly improved markers of astrogliosis and amyloid pathology. The drug suppresses activity of retrotransposons that are under-methylated in AD.
In APOE4/4 microglia, Aβ triggers an uptick of a triglyceride synthesis enzyme. The cells then accumulate lipid droplets and release something neurotoxic.
O-GlcNAcase inhibitors and a vaccine head to Phase 2. New antibody strategies co-opt the proteasome to clear intracellular and extracellular tau in preclinical models.