From more than 45,000 MRI scans, a typical pattern of brain aging emerges. Brains “age” faster in people who have a neurological disorder.
The G2019S variant that boosts Parkinson’s risk helps mice survive infection, but raises α-synuclein in the brain and increases neuronal death.
The circular transcripts correlate with AD pathology and dementia severity, suggesting potential roles in pathogenesis or as biomarkers.
The transcriptional repressor quiets neural activity and lengthens lifespan in worms. It is abundant in the brains of cognitively healthy centenarians.
Based on high school personality tests taken nearly 60 years ago, researchers associated certain traits with future risk of dementia.
Slow-wave sleep brings on coordinated oscillations in blood flow, which in turn are coupled to waves of cerebrospinal fluid. The data point to a mechanism linking deep sleep to the flow of CSF.
Two papers used different approaches to energize laggard lysosomal function in neurons derived from people with Parkinson’s. Both restored lysosomal trafficking and reduced α-synuclein accumulation.
Cognitive deficits in mice on a high-salt diet are due to tau phosphorylation, not reduced blood flow, according to a new study.
Brain biopsy tissue reveals that their transcriptomes shift by location, age, and disease.
Encouraged by success in treating infant spinomuscular atrophy, researchers are redoubling their efforts to target genetic causes of age-related neurodegeneration.
As gene therapy is making a comeback, scientists are exploring if it might prevent or reverse Alzheimer’s. Some of those treatments are permanent, heightening safety concerns.
The Phase 2 study missed its primary endpoint. While fewer developed dementia in the treatment group, the effect was not statistically significant. People on drug had less brain atrophy than those on placebo.
The study halted early when the primary endpoint was met, but an unusual trial design and lack of detailed data leave questions unanswered.
In neurons derived from FTD patients, morphological changes at the base of the axon render them hyperexcitable.
Negative findings for AVP-786 belie positive findings from a separate Phase 3 trial announced earlier this year.