Just What the Doctor Ordered? Polygenic Test Gauges Your Alzheimer’s Risk
The commercial test uses a few drops of saliva. It must be ordered by a physician. Plans are also in the works to use the test to select participants for clinical trials.
48 RESULTS
Sort By:
The commercial test uses a few drops of saliva. It must be ordered by a physician. Plans are also in the works to use the test to select participants for clinical trials.
White matter-associated microglia express similar genes to plaque-associated DAMs. They seem to be triggered by the myelin breakdown associated with aging and disease.
Some people with severe COVID-19 have neurovascular injury and elevated markers of neural damage in their blood and CSF. What’s going on in their brains?
This astrocytic glycoprotein greases glial phagocytosis and reduces plaque burden in mice. The circadian clock protein Bmal1 suppresses it.
Breaking familiar gene-disease patterns, HTT trinucleotide expansions lead to huntingtin aggregates in prefrontal cortex. Noncoding caveolin 1 variants suppress its expression.
This pathway may transmogrify microglia during neurodegeneration, without the help of TREM2.
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.
Sensor algorithms can accurately capture patterns of resting tremor and dyskinesia. This could help clinicians manage symptoms and medication.
Transcriptomic and epigenomic data pin PD risk genes in GWAS loci; six affect splicing, five expression, four are new.
Two cohorts—IDEAS and WHIMS—show Aβ accumulation and brain shrinkage in cognitively normal and impaired elderly who were exposed to levels of air pollution even within current EPA limits.
Researchers found that bits of tau from the protein’s microtubule-binding region can be detected in the cerebrospinal fluid. These, not phospho-tau or total tau, reflect neurofibrillary tangles in the Alzheimer’s brain.
Topline results suggested that the anti-inflammatory treatment stabilized cognition and function over six months. The trial did not include biomarkers.
Confronting unprecedented challenges this past year, scientists found ways to tide their research over and keep clinical trials mostly on track.
In cultured cells, lysosomal activity was necessary to enable tau seeds to break out of internalized exosomes and trigger the aggregation of tau in the cytosol.
Despite plaques and tangles in the brain, this group, on average, maintains their cognitive skills over two to four years, suggesting the presence of resilience factors.