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.
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.
Biogen and Eisai announced the discontinuation of the Phase 3 program. Elenbecestat was the only remaining BACE inhibitor being tested for AD.
Cataloguing enhancer-promoter interactions in the four major cell types of the brain, researchers found that Alzheimer’s risk variants predominantly appeared in microglial enhancers.
Specific patterns of expression defined distinct subtypes of neurons, astrocytes, oligodendrocytes, and microglia in this early affected brain region.
Prior research has focused on microglia interacting with synapses. New data show they also deal directly with the neuronal cell body. Like little conference rooms, specialized junctions host this communication.
At CTAD, researchers discussed possible paths forward. One option: exploring whether low doses prevent plaque accumulation while avoiding the cognitive side effects.
In Alzheimer’s brain, granulovacuolar bodies in neurons harbor activated necrosomes. They correlate with tau pathology and neuron loss, raising new questions about how neurons die in this disease.
In a conditional mouse knockout, lack of neuronal BIN1 slowed excitatory signaling, leading to spatial memory problems. Could this play a role in Alzheimer’s?
Longitudinal ADNI data tie higher sTREM2 in CSF to slower cognitive decline, reinforcing the idea that TREM2 activity protects the brain from AD pathology.
The same endothelial cell response is found in various models of brain disease.
Functional variants of AD GWAS hits found in enhancers of myeloid genes.
Women who started menstruation after the age of 16, and/or entered menopause before 47, had higher rates of dementia later in life.
The Phase 3 trial ended early when prodromal AD patients on the BACE1 inhibitor declined faster than those on placebo.
Flortaucipir in former NFL players cropped up in regions known to be affected by chronic traumatic encephalopathy, but uptake was low compared with AD. Whether this reflects low tau deposition or poor tracer binding remain to be seen.