Are T Cells to Blame for Cognitive Impairment Caused by Hypertension?
In the dura, these lymphocytes release interleukin 17, activating perivascular macrophages. They curb cerebral blood flow, and mice become forgetful.
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In the dura, these lymphocytes release interleukin 17, activating perivascular macrophages. They curb cerebral blood flow, and mice become forgetful.
Proteins in human blood flag organ-specific accelerated aging and disease risk. For cognition, 49 proteins better predicted decline then did plasma p-tau 181.
The software could improve prognosis, speed referrals, for people with MCI, the developer claims.
A large, unbiased study found 125 proteins in the CSF that tick up or down in early familial AD. A set of nine identified FAD mutation carriers better than did Aβ and tau.
A new immunoassay detects N-terminal fragments of tau. They predict tangle accumulation, cortical atrophy, and cognitive decline.
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.
Mitochondrial activation waned in brain cells a year before mice developed plaques. Inhibiting the kinase GSK3β partially restored the organelles.
Two different model systems catalogued cell states: DAM-like, antigen-presenting, cytokine-, and interferon-based. More work is needed to pin down function.
Tauopathy cranks up lipid synthesis in neurons, which slip the fats to microglia. Blocking AMP kinase greases this process.
A new study challenges this idea, finding that in mice, clearance of an injected dye slowed during sleep and anesthesia.
When carrying a pathogenic tau variant, microglia were bad at phagocytosis, barely made TREM2, and spat out neurotoxic proteins.
Aβ oligomers rev up glutamate release, depressing synapses for the long term. This instigates the pathological phosphorylation of tau.
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.
The enzyme cleaves off three amino acids at a time with a twist of the substrate, and a helping hand from a β-strand.
The FDA turned down Eli Lilly’s application based on insufficient safety data, with fewer than 100 people on the drug for one year.
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