A Proteomics Dive into Cause of Frontotemporal Dementia
Proteomics and protein-protein interaction research may yield clues to etiology, tracking, and treatment of granulin-related and other forms of FTD/ALS.
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Proteomics and protein-protein interaction research may yield clues to etiology, tracking, and treatment of granulin-related and other forms of FTD/ALS.
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.
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...
In PASSPORT study, the antibody failed to slow progressive supranuclear palsy. Alzheimer’s trial to continue.
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.
New genes linked to early and late-onset AD offer up mechanistic insight, potential targets for treatment.
Scientists are tweaking immune pathways to scavenge amyloid and curb symptoms in Alzheimer’s mice.
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.
NIH Summit Sets Agenda for AD-Related Dementias Alzheimer's Disease Research Summit 2019 ...
Bringing the total NIH funding for Alzheimer’s research up to $2.8 billion, the Senate continued its steady upward climb in spending for the disease.