Raw Deal: Lose Ataxin, Gain BACE
Loss of ataxin-1 intensifies BACE1 expression, Alzheimer’s pathogenesis. Is that how ataxin GWAS variants increase AD risk?
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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.
The Phase 2 study missed its primary endpoint. While fewer developed dementia in the treatment group, the effect was not statistically significant. People on drug had less brain atrophy than those on placebo.
The study halted early when the primary endpoint was met, but an unusual trial design and lack of detailed data leave questions unanswered.
In neurons derived from FTD patients, morphological changes at the base of the axon render them hyperexcitable.
$73 million to transform big data into open-access targets and drugs for testing in clinical trials.
Negative findings for AVP-786 belie positive findings from a separate Phase 3 trial announced earlier this year.
The protein helps internalize neuronal interleukin receptors. It also promotes microglial phagocytosis. Does its absence worsen neuroinflammation and Aβ burden?
Using chemical cross-linkers to map contacts among amino acids, structural biologists predict that soluble tau is, in fact, a compact globule containing β-sheets poised to snap into a pathological formation.
Can genetics please parse the confusing spectrum of frontotemporal dementias? Whole genome sequences make a start.
Large IDEAS data set establishes that PET scans are valuable in clinical practice. Other studies suggest CSF biomarker ratios perform nearly as well.
New genes linked to early and late-onset AD offer up mechanistic insight, potential targets for treatment.
Recent conferences revealed that tau is most toxic in oligomeric form, that tau oligomers propagate throughout the brain, and that tau oligomers might harm synapses from within or via astrocytes.
The DIAN Trials Unit is nearing the end of its first two secondary prevention trials. It has begun a cognitive run-in period for its next trial, of a tau-based drug, and for a primary prevention study in people as young as 18.