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.
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.
At AAT-AD/PD, scientists showed that correlated amyloid patches are an even earlier marker than brain-wide positivity, while others puzzled over why tau signals are lower in older people.
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.
This past year, therapeutic antibodies massively reduced brain amyloid, blood tests came into their own, and systems-based approaches transformed the study of gene expression, glial cells, and selective vulnerability.
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.