P-tau217 appears sooner than p-tau181 in the brain, and it distinguishes AD from controls and other dementias even more cleanly.
Researchers have devised a way to measure how long ago a reporter transcript was made. It allows them to detect distinct transcriptional events within a cell.
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.
Amyloids of AIMP2 found in Parkinson’s disease may seed α-synuclein aggregation.
By pinpointing where tau pathology starts in a person’s brain, researchers better predicted future spread and determined small changes in tangle load.
In mice, forebrain neurons with hobbled retromers ooze fragments of tau and several BACE1 substrates into the CSF. Similar proteins are up in CSF from people with MCI and Alzheimer’s disease.
Breaking familiar gene-disease patterns, HTT trinucleotide expansions lead to huntingtin aggregates in prefrontal cortex. Noncoding caveolin 1 variants suppress its expression.
This astrocytic glycoprotein greases glial phagocytosis and reduces plaque burden in mice. The circadian clock protein Bmal1 suppresses it.
Among a growing number of blood-based tauopathy markers, this new immunoassay may offer a way to catch preclinical disease just before symptoms show up.
In a retrospective study, people with vitiligo had 12 times the risk of developing Alzheimer’s disease than did healthy controls. Why is that?
This pathway may transmogrify microglia during neurodegeneration, without the help of TREM2.
Sensor algorithms can accurately capture patterns of resting tremor and dyskinesia. This could help clinicians manage symptoms and medication.
People who report not participating in social or cognitive activities are more likely to develop dementia within the next few years, but not after that. The findings cast nonparticipation as a consequence, not a cause, of neurodegeneration.