While former professional soccer players have less risk for heart disease and cancer than the general population, they are five times more likely to die with a neurodegenerative disease in old age.
The pattern varied from person to person, depending on the site of injury, in contrast to the stereotyped distribution of tau tangles seen in Alzheimer’s disease.
In animal models and patient-derived neurons, terazosin elevated ATP and warded off neurodegeneration. Men who take the drug to control prostate hyperplasia are less likely to get PD, or have milder symptoms.
The G2019S variant that boosts Parkinson’s risk helps mice survive infection, but raises α-synuclein in the brain and increases neuronal death.
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.
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 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.
What’s with all those head-to-head comparison studies of academic and commercial biomarker tests? Could we not just pick one that works, and be done?
In a tauopathy model, knocking out C3 spared synapses and neurons. In an amyloidosis model, deleting C3 preserved dendritic spines, but exacerbated plaque growth.
Older people who lived healthy lifestyles had a third lower risk of dementia than their unhealthy peers, but only if their genetic risk for the disease was low.
Loss of ataxin-1 intensifies BACE1 expression, Alzheimer’s pathogenesis. Is that how ataxin GWAS variants increase AD risk?