TRP cation channels combine with extrasynaptic NMDA glutamate receptors to set off mitochondrial meltdown and cell death. Blocking the interaction stops excitotoxicity.
The modeling approach reinforces the idea that tau pathology propagates through the brain’s physical architecture, including neuronal networks.
The designer chimera stabilizes synapses in various mouse models of neurodegenerative disease.
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.
Three studies found no link between vascular disease and cerebral amyloidosis.
Two epigenetic proteins accelerated age-related behavioral decline in worms and in mice, at least partly by dampening mitochondrial function. Orthologs in the human brain ramped up with aging and with AD progression.
In motor neurons of TMEM106b knockout mice, swollen vacuoles piled up in axons near the soma, rendering the mice wobbly and slow to react. The finding contradicts prior reports.
Different forms of p-tau in cerebrospinal fluid reflect worsening plaque load, metabolism, and atrophy in the brain. They could help stage Alzheimer’s disease.
In people with Alzheimer’s biomarkers, the basal forebrain shrinks early, foreshadowing microglial neurotoxicity, atrophy in the medial temporal lobe, and cognitive decline.