A chemist at the University of Cambridge, Dobson developed equations that described the kinetics of protein aggregation in diseases such as 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.
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.
These cells accumulate in old mouse and human hippocampi, as well as in a mouse model of neurodegenerative disease.
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.
In vicinity of plaques, astrocytes and glia change gene expression in concert.
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.
What’s with all those head-to-head comparison studies of academic and commercial biomarker tests? Could we not just pick one that works, and be done?
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.