In vicinity of plaques, astrocytes and glia change gene expression in concert.
The protein forms cohesive rafts along microtubules, protecting them from digestion and regulating movement of molecular motors.
Eliminating microglia in a mouse model of amyloidosis nearly abolished parenchymal plaques, but led to a huge buildup of amyloid in cerebral blood vessels.
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.
In induced human microglia, the E4 allele profoundly affected their health and cellular responses, while familial Alzheimer’s mutations had little effect.
Analysis of a chimeric mouse shows that the cells express the same genes they do in the human brain, survey their environment, and respond to injuries and amyloid.
Much of the neuron loss in rTg4510 mice comes from accidental disruptions in mouse genes rather than expression of mutant tau. Pathology spreads quickly in human tau knock-ins.
In healthy, older adults specific EEG patterns correlated with plaque and tangle burdens.
A meta-analysis of 47 studies suggests CSF NfL is particularly elevated in a select few, suggesting it could help in differential diagnosis.
Fully automated immunoassay could offer cost-effective screening for AD.
In a large observational study, men given androgen-deprivation therapy to combat prostate cancer had a higher chance of being diagnosed with Alzheimer’s or dementia within eight years.
In carriers of a PD-causing mutation, PET scans showed serotonin transporter loss before motor symptoms set in.
USC has agreed to compensate UCSD $50 million for poaching Aisen, his staff, and ADCS.
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.