A broadening drug development pipeline now contains Phase 1 or 2 drugs on targets unrelated to Aβ or tau.
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 ...
Null results ended the development of the neuroprotective drugs edonerpic and abeotaxane, the AMPA receptor modulator S47445, and the dietary formulation tricaprilin.
Researchers reported negative findings from three trials at ICFTD 2016.
Based on preclinical data, researchers gave this antibiotic a shot in a two-year clinical trial. It did nothing to slow cognitive decline.
The Canadian pharmaceutical company Bellus Health has begun to sell the would-be prescription drug tramiprosate over the counter as a nutritional supplement...
Working with human microglia is fraught with technical challenges, but that didn’t stop researchers at Keystone from sharing a flurry of data on how these cells act in neurodegenerative disease.
In PASSPORT study, the antibody failed to slow progressive supranuclear palsy. Alzheimer’s trial to continue.
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
At AAIC, researchers touted phospho-tau species, especially p217 and p181. They tick up in CSF as an early response to amyloid accumulation.
At this year’s AAIC, no sooner had scientists reported that phospho-tau in the CSF might reflect early responses to amyloid, than they reported parallel data for phospho-tau in blood.
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
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.
Plaque-busting antibodies reset the time course of amyloid accumulation, but so far provide only hints of a clinical benefit in mild AD. Good news: once gone, plaque stays gone for a while.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.