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Released from hippocampal neurons in response to experience, the cytokine prompted microglia to eat extracellular matrix around synapses. This facilitated growth of new spines, and sharpened memory.
This early marker distinguishes Alzheimer’s from controls and other neurodegenerative diseases more accurately than other biomarkers.
In large population datasets, people who had been vaccinated against influenza or pneumonia appeared less likely to develop AD.
Comprising mostly Aβ40, these large plaques are shot through with strange tubular structures and BBB markers. They are common in early onset AD.
Expert panel concludes there’s little risk based on current evidence.
AMX0035, a mix of sodium phenylbutyrate and taurursodiol, slowed functional decline over six months by about as much as the approved ALS drug edaravone.
P-tau217 appears sooner than p-tau181 in the brain, and it distinguishes AD from controls and other dementias even more cleanly.
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.
Not Just Blood Pressure—Dietary Salt Linked to Tau Phosphorylation Time to Try Again: Gene-Based Therapy for Neurodegeneration Gene Therapies Enter Trials for Many Brain Pathologies—What about AD? Organized around 10 major themes, this year’s annual ...
Based on preclinical data, researchers gave this antibiotic a shot in a two-year clinical trial. It did nothing to slow cognitive decline.
In PASSPORT study, the antibody failed to slow progressive supranuclear palsy. Alzheimer’s trial to continue.
Using mass spectrometry to detect teensy amounts of phospho-tau species in plasma, researchers reported that p-tau-217 and p-tau-181 picked out people with Aβ pathology. Differences between groups appear to be huge. An MS-based test for plasma Aβ42 corresponded to brain amyloid, and is going in for regulatory approval.
Apabetalone, an epigenetic drug that tamps down vascular inflammation, slowed cognitive decline in people with MCI. A new statistical analysis of results from AMBAR claimed the plasma-exchange therapy might boost cognition by removing pathogenic proteins from blood.
