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.
Encouraged by success in treating infant spinomuscular atrophy, researchers are redoubling their efforts to target genetic causes of age-related neurodegeneration.
Specific patterns of expression defined distinct subtypes of neurons, astrocytes, oligodendrocytes, and microglia in this early affected brain region.
Brain biopsy tissue reveals that their transcriptomes shift by location, age, and disease.
In a mouse tauopathy model, knocking out the NLRP3 inflammasome prevented toxic tau from forming.
Based on preclinical data, researchers gave this antibiotic a shot in a two-year clinical trial. It did nothing to slow cognitive decline.
Cataloguing enhancer-promoter interactions in the four major cell types of the brain, researchers found that Alzheimer’s risk variants predominantly appeared in microglial enhancers.
The same endothelial cell response is found in various models of brain disease.
New data suggest that while peptides translated from an expansion in the C9ORF72 gene are toxic, they don’t directly interfere with nucleocytoplasmic transport.
No link found with amyloid deposition.
DAPPD suppressed neuroinflammation and preserved cognition in mouse models of amyloidosis, suggesting potential for treating Alzheimer’s disease.
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.
GV-971, an oligosaccharide derived from marine kelp, was approved to treat AD in China. Preclinical studies suggest the drug soothes neuroinflammation by balancing the gut microbiome.
The rare ApoE3 Christchurch variant prevented tau tangles, neurodegeneration, and cognitive decline in a woman’s brain for decades, despite massive amyloid buildup from a familial presenilin AD mutation.
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.