From Menarche to Menopause: Shorter Span Linked to Higher Risk of Dementia
Women who started menstruation after the age of 16, and/or entered menopause before 47, had higher rates of dementia later in life.
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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.
In ADNI, blood marker exposes ongoing neurodegeneration across disease stages.
An electron microscopy study reveals a jumbled mess of membrane chunks and malfunctioning organelles, bound together by phosphorylated or truncated α-synuclein.
Long recognized in dendrites, scientists now report that substantial synaptic proteome remodeling happens on the axonal side, too.
The locus incertus fine-tunes hippocampus neural activity to control memory formation in stressful situations. Could a new understanding of these circuits shed light on memory loss in Alzheimer’s?
A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
Serial amyloid and tau scans in cognitively healthy people indicate that the speed at which a person’s tau accumulates best predicts his or her future cognitive decline.
Aβ deposits make distal neurons vulnerable to insults, including from local Aβ, says imaging study. The combination hastens cognitive decline.
New strains have amyloid, neurodegeneration, and neuroinflammation, all against a background of natural genetic variation.
New evidence suggests the dimers impede clearance of glutamate from synapses, contributing to the hyperexcitability seen early in Alzheimer’s disease.
The phenotype of ApoE4 astrocytes and microglia resembles that of these cells in Alzheimer’s brain. Could defects in lipid metabolism and the extracellular matrix bring on the disease?
The microfluidic device could test the vascular contributions to neurodegenerative disease and bioavailability of drugs for the brain.
By yanking a nuclear protein out of its pore, phosphorylated tau makes nuclei leaky, disrupting the strictly controlled passage of proteins and setting tau up for aggregation.