While a Fly Sleeps, Its Glia Burn Neuronal Lipids to Refresh the Brain
In awake fruit flies, neurons pass toxic lipids to glia for storage. When the flies sleep, glia metabolize the fat to reset for a new day.
47 RESULTS
Sort By:
In awake fruit flies, neurons pass toxic lipids to glia for storage. When the flies sleep, glia metabolize the fat to reset for a new day.
A single-nuclei RNA-Seq study found more autophagy and chaperone gene expression in familial AD brain, more intense microglial activation in sporadic.
Mitochondrial activation waned in brain cells a year before mice developed plaques. Inhibiting the kinase GSK3β partially restored the organelles.
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.
All endpoints were missed. Company to consider withdrawing the drug, as discussed during FDA Advisory Committee meeting.
ApoE2 reported as raising risk for progressive supranuclear palsy, a rare tauopathy.
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.
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.
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.
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.
One variant promotes expression of TMEM106b in a subset of excitatory neurons, reducing their numbers. Another boosts ApoE4 in microglia.
In peripheral macrophages and microglia, the receptor disrupts glucose metabolism. TREM1-deficient amyloidosis mice also had healthier neurons, better memories.
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.