Different polymorphisms in MS4A genes up- or downregulate levels of TREM2, modulating levels of the shed ectodomain in the cerebrospinal fluid and AD risk.
Among former National Football League players who died with CTE, tau tangles, crumbling white matter, and arteriolosclerosis independently contributed to dementia.
At AAIC, researchers touted phospho-tau species, especially p217 and p181. They tick up in CSF as an early response to amyloid accumulation.
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?
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
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.
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
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.
Loss of ataxin-1 intensifies BACE1 expression, Alzheimer’s pathogenesis. Is that how ataxin GWAS variants increase AD risk?
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?
Passive monitoring of old people in their everyday lives is starting to generate new indicators for cognitive impairment.
New genes linked to early and late-onset AD offer up mechanistic insight, potential targets for treatment.
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In patient-derived neurons, tau mutations scupper lysosomes and SORLA shunts APP through different types of endosomes.