NIH Funds Translational Research Centers to Accelerate AD Drug Discovery
$73 million to transform big data into open-access targets and drugs for testing in clinical trials.
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$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.
New data suggest that while peptides translated from an expansion in the C9ORF72 gene are toxic, they don’t directly interfere with nucleocytoplasmic transport.
Can genetics please parse the confusing spectrum of frontotemporal dementias? Whole genome sequences make a start.
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.
In patient-derived neurons, tau mutations scupper lysosomes and SORLA shunts APP through different types of endosomes.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.