In ADNI, blood marker exposes ongoing neurodegeneration across disease stages.
Long recognized in dendrites, scientists now report that substantial synaptic proteome remodeling happens on the axonal side, too.
A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
Exposing AD mice to multisensory gamma therapy induced 40-Hz waves in their brains, plus effects on amyloid, tau, microglia, blood vessels, and cognitive function.
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.
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?
Amyloid plaques in postmortem human cortex correlated with the proportion of microglia that were activated, not with microglial numbers. Tau pathology and cognitive decline come later.
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.
An electron microscopy study reveals a jumbled mess of membrane chunks and malfunctioning organelles, bound together by phosphorylated or truncated α-synuclein.
By loosening their chromatin straitjackets, and reining in their RNA watchdogs, tau unleashes transposable elements into the genome.
The microfluidic device could test the vascular contributions to neurodegenerative disease and bioavailability of drugs for the brain.
A new PET tracer belies previous results from animal models and postmortem studies. Caveat emptor for trials of HDAC inhibitors?
Translatome profiling suggests ApoE drives a microglial gene-expression signature found in aging, Aβ amyloidosis, and tauopathy.
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.