Nearly Two Years After FDA Approval, Relyvrio Bombs Phase 3 for ALS
All endpoints were missed. Company to consider withdrawing the drug, as discussed during FDA Advisory Committee meeting.
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All endpoints were missed. Company to consider withdrawing the drug, as discussed during FDA Advisory Committee meeting.
In snoozing mice, silencing neurons dampened ion waves in the interstitial fluid and slowed the flow of solutes. Activating neurons powered CSF flow through the brain.
In a multiple sclerosis model, activated microglia reverse electron transport (RET) in their mitochondria, creating oxidative stress. Blocking RET eased pathology.
One variant promotes expression of TMEM106b in a subset of excitatory neurons, reducing their numbers. Another boosts ApoE4 in microglia.
In a small dose-finding study, Roche’s new brain-shuttle-based anti-amyloid antibody mopped up nearly all plaques in three months, without triggering edema.
Last summer saw a first: the traditional approval of a disease-modifying Alzheimer's therapy. Solid progress on biomarkers, and a flourishing of basic research, made for a good year.
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.
£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.
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.