New Ways to Target TREM2 Beg the Question: Up or Down?
Lowering TREM2 via antisense oligos cleared plaques in mice, while antibody fragments reduced shedding of sTREM2. Best therapeutic strategy? Still hazy.
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Lowering TREM2 via antisense oligos cleared plaques in mice, while antibody fragments reduced shedding of sTREM2. Best therapeutic strategy? Still hazy.
These changeable cells can revive plasticity in the adult brain, match themselves to GABA synapses, and strip away healthy synaptic spines in reaction to stress. What do they do in depression, PTSD?
Senescent astrocytes spew HMGB1, a harbinger of cell death. Blocking this release prevented cell senescence, reduced neurofibrillary tangles, and improved memory in mice.
At AAIC, leading Alzheimer’s clinicians plug gaps in the FDA label. They urge exclusion of people with cerebrovascular risk, and an MRI monitoring bonanza. Meanwhile, clinical rollout starts slow, with major hospitals declining to administer.
Data from a Phase 2 trial also suggested that when amyloid dropped in treated brain, plasma p-tau217 followed suit. Using a CAMD progression model, Lilly claims the biomarker responses correlated with slower decline.
Initial results from the first trial of an antisense oligonucleotide against tau in Alzheimer’s are in. BIIB080 appears safe and curbed total tau and phospho-tau 181 levels in the CSF. Clinical outcomes were not assessed.
Biogen sponsors an observational study on the drug’s effects; no word yet on the FDA-required Phase 4 trial. Meanwhile, researchers suggest other ways to test efficacy.
In the wake of the controversial thumbs-up for Aduhelm, the U.S. federal government is probing not only aducanumab’s price and approval history, but also the FDA’s accelerated approval pathway in general.
In an open-label Phase 2 study, fluid biomarkers suggested the anti-sortilin antibody restored lysosomal function and reduced neuroinflammation in people with symptomatic FTD. Tantalizingly, participants worsened less than historical controls.
Found in one Swedish family, this mutation speeds up plaque deposition by way of two different mechanisms, leading to disease onset as young as age 40.
AD risk scores based on gene expression in microglia associate with having amyloid plaques, and a microglial genomic atlas displays how variants influence gene expression. Polygenic variation in neurons sways cognition.
Among old people with high total tau levels in plasma, cognition slid far less in those who are active than in their inactive peers. Could blood tests motivate at-risk people to exercise?
Decades before tangles become rampant, the biomarker p-tau231 rises in both CSF and plasma. More surprising: neuroinflammation markers do, too.
Topline results from a Phase 2 trial of semorinemab suggest the therapeutic antibody may have eased the cognitive downturn in people with mild to moderate Alzheimer’s disease.
Aβ oligomers rev up glutamate release, depressing synapses for the long term. This instigates the pathological phosphorylation of tau.
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