The transcription factor NFATc2 mediates this response.
By looking for SNPs that affect how transcription factors bind DNA, researchers nominated causal genes for 30 Alzheimer’s and Parkinson’s GWAS hits.
A new single-nucleus RNA-Seq study of 3,900 endothelial cells finds a boost in angiogenesis and antigen presentation genes, drawing attention to the vascular component of AD.
In a retrospective study, people with vitiligo had 12 times the risk of developing Alzheimer’s disease than did healthy controls. Why is that?
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 ...
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.
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.
Exposure, Exposure, Exposure? At CTAD, Aducanumab Scientists Make a Case Fluid AD Biomarkers Link P-Tau to Synapses, Inflammation Blood Tests of Phospho-Tau, Aβ42, Track With Brain Amyloid Amyloid Clearance: Check. Cognitive Benefit: Um … Maybe. Picking ...
Besides further broadening the Alzheimer’s therapeutic pipeline, researchers urge a return to Phase 2, using artificial intelligence tools to streamline aspects of trials.
An expanded set of CSF biomarkers exposed tight connections between p-tau, synaptic dysfunction, and neuroinflammation in people with brain amyloid.
Positive allosteric modulators improve learning and memory in mouse models of AD and epilepsy.
In early Alzheimer’s disease, the pattern of tau deposition also strongly predicts areas destined for subsequent degeneration.