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.
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.
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.
Happy New Year, readers! Yes, 2019 has passed, but so much happened last year that capturing the essence took longer than usual. Our mega year-end story is now posted for your reading pleasure.
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.
For people with Parkinson’s, carrying Alzheimer’s genetic risk variants upped their odds of harboring Aβ and tau pathology and getting dementia. In people with DLB, Aβ plaques worsened tau and Lewy pathology, and cognition.
Avid’s postmortem validation data indicate Alzheimer’s can be diagnosed by visual examination of flortaucipir PET scans.