In patient-derived neurons, tau mutations scupper lysosomes and SORLA shunts APP through different types of endosomes.
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.
Passive monitoring of old people in their everyday lives is starting to generate new indicators for cognitive impairment.
Smartphones and gamified apps move cognitive testing from the lab into the real world. But keeping people engaged remains a problem. Is passive monitoring the answer?
Loss of ataxin-1 intensifies BACE1 expression, Alzheimer’s pathogenesis. Is that how ataxin GWAS variants increase AD risk?
Longitudinal ADNI data tie higher sTREM2 in CSF to slower cognitive decline, reinforcing the idea that TREM2 activity protects the brain from AD pathology.
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.
In a tauopathy model, knocking out C3 spared synapses and neurons. In an amyloidosis model, deleting C3 preserved dendritic spines, but exacerbated plaque growth.
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.
In vicinity of plaques, astrocytes and glia change gene expression in concert.
These cells accumulate in old mouse and human hippocampi, as well as in a mouse model of neurodegenerative disease.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.