Newly Identified Microglia Contain Lipid Droplets, Harm Brain
These cells accumulate in old mouse and human hippocampi, as well as in a mouse model of neurodegenerative disease.
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These cells accumulate in old mouse and human hippocampi, as well as in a mouse model of neurodegenerative disease.
In vicinity of plaques, astrocytes and glia change gene expression in concert.
Hypertension in people as young as the mid-30s can predict late-life cerebrovascular disease and brain shrinkage. Intensive reduction of blood pressure can prevent the damage, but not when given in late life.
In a tauopathy model, knocking out C3 spared synapses and neurons. In an amyloidosis model, deleting C3 preserved dendritic spines, but exacerbated plaque growth.
Older people who lived healthy lifestyles had a third lower risk of dementia than their unhealthy peers, but only if their genetic risk for the disease was low.
Loss of ataxin-1 intensifies BACE1 expression, Alzheimer’s pathogenesis. Is that how ataxin GWAS variants increase AD risk?
Smartphones and gamified apps move cognitive testing from the lab into the real world. But keeping people engaged remains a problem. Is passive monitoring the answer?
Passive monitoring of old people in their everyday lives is starting to generate new indicators for cognitive impairment.
The protein forms cohesive rafts along microtubules, protecting them from digestion and regulating movement of molecular motors.
The pattern varied from person to person, depending on the site of injury, in contrast to the stereotyped distribution of tau tangles seen in Alzheimer’s disease.
The organelles express unique sets of proteins depending on their environment. Astrocyte mitochondria process lipids better than those in neurons.
New data strengthen the idea that a healthy locus coeruleus keeps memory sharp into old age.
The Phase 2 study missed its primary endpoint. While fewer developed dementia in the treatment group, the effect was not statistically significant. People on drug had less brain atrophy than those on placebo.
Biogen and Eisai announced the discontinuation of the Phase 3 program. Elenbecestat was the only remaining BACE inhibitor being tested for AD.
In induced human microglia, the E4 allele profoundly affected their health and cellular responses, while familial Alzheimer’s mutations had little effect.
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