Phase 3 Trial Suggests Pimavanserin Assuages Psychosis in Dementia
The study halted early when the primary endpoint was met, but an unusual trial design and lack of detailed data leave questions unanswered.
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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.
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.
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.
Using a new optogenetic model for TDP-43 phase transitions, scientists see the protein aggregate outside, not inside stress granules. The model distinguishes physiological from abnormal phase transition.
Different polymorphisms in MS4A genes up- or downregulate levels of TREM2, modulating levels of the shed ectodomain in the cerebrospinal fluid and AD risk.