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.
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.
A $400,000 prize is to be awarded as part of the new Rainwater program, and $63 million of NIH money will support a research consortium on frontotemporal dementias.
Evidence from postmortem human brains and cultured human microglia suggests the immune cells make a meal out of synapses, especially near plaques.
New data suggest that while peptides translated from an expansion in the C9ORF72 gene are toxic, they don’t directly interfere with nucleocytoplasmic transport.
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
Negative findings for AVP-786 belie positive findings from a separate Phase 3 trial announced earlier this year.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.
In patient-derived neurons, tau mutations scupper lysosomes and SORLA shunts APP through different types of endosomes.