Skin Deep: Punch Biopsies Detect Synucleinopathies
In a small sample set, phosphorylated α-synuclein was detected in the dermis of four such disorders.
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In a small sample set, phosphorylated α-synuclein was detected in the dermis of four such disorders.
Researchers at AD/PD showcased progress in modeling these conditions, detecting CAA, and potentially mitigating microhemorrhages.
One variant promotes expression of TMEM106b in a subset of excitatory neurons, reducing their numbers. Another boosts ApoE4 in microglia.
Cerebrospinal fluid rides the pulses of cerebral arteries to enter the brain and spread into cortical tissue. This supports the existence of a human glymphatic system.
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.
Based on exploratory endpoints and post hoc analyses, TauRx claims HMTM benefits a subgroup of participants with MCI. Trialists are unconvinced.
In peripheral macrophages and microglia, the receptor disrupts glucose metabolism. TREM1-deficient amyloidosis mice also had healthier neurons, better memories.
In a multiple sclerosis model, activated microglia reverse electron transport (RET) in their mitochondria, creating oxidative stress. Blocking RET eased pathology.
Fast Plaque Clearance with Little ARIA? So Teases Trontinemab at AD/PD 2024 TauRx Parses Subgroups to Make the Case for Methylene Blue Derivative, Again Therapeutic Contenders Target Hard-to-Reach Pockets of Tau Mouse Models and Markers for Cerebral Amylo
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.
In APOE4/4 microglia, Aβ triggers an uptick of a triglyceride synthesis enzyme. The cells then accumulate lipid droplets and release something neurotoxic.
Lamivudine slightly improved markers of astrogliosis and amyloid pathology. The drug suppresses activity of retrotransposons that are under-methylated in AD.
All endpoints were missed. Company to consider withdrawing the drug, as discussed during FDA Advisory Committee meeting.
Modeling physiological dipeptide repeat expression and partial loss of normal C9ORF72 protein, new knock-in mice show a TGF-β1-driven collagen response in their spinal neurons.
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.
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