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.
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?
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
At this year’s AAIC, no sooner had scientists reported that phospho-tau in the CSF might reflect early responses to amyloid, than they reported parallel data for phospho-tau in blood.
At AAIC, researchers touted phospho-tau species, especially p217 and p181. They tick up in CSF as an early response to amyloid accumulation.
Using a collection of isogenic iPSC-derived neurons harboring different familial AD mutations, researchers found that, across the board, the mutations meddled with endosomes via elevated β-CTF.
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?
Different polymorphisms in MS4A genes up- or downregulate levels of TREM2, modulating levels of the shed ectodomain in the cerebrospinal fluid and AD risk.
New genes linked to early and late-onset AD offer up mechanistic insight, potential targets for treatment.