In the Alzheimer’s brain, too, plaques trigger a coordinated inflammatory response from microglia and astrocytes. A preprint paper had shown the same for mice.
A 2018 report that had spotted extra copies of APP lurking in neuronal genomes has come under scrutiny, with claims that the result is due to contamination. Does a response from the original authors bolster their claim?
The designer chimera stabilizes synapses in various mouse models of neurodegenerative disease.
The circular transcripts correlate with AD pathology and dementia severity, suggesting potential roles in pathogenesis or as biomarkers.
The modeling approach reinforces the idea that tau pathology propagates through the brain’s physical architecture, including neuronal networks.
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.
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.