Fragmented tau that accumulates in neurons in those with Alzheimer's disease may be a new target for drugs to treat the neurodegenerative disease.
mRNA decay may facilitate tau-induced damage to the brain and associated apoptosis that contributes to a range of neurodegenerative disorders. Researchers found the mechanism can be altered pharmacologically, providing a new target for the development of therapeutics to prevent or slow the progression of some neurodegenerative disorders.
Degeneration of neurons associated with wakefulness, and not a lack of sleep, makes Alzheimer's patients more drowsy. The degeneration of these neurons is caused by the tau protein. In PSP, the damage to the neurons was associated with symptoms of sleep deprivation.
Alpha2-NKA, a protein that drives toxicity in astrocytes, was discovered in higher levels of brain samples from people who died of PSP, Alzheimer's and other tau-related neurodegenerative disorders. Treatment with an FDA-approved drug called digoxin may suppress the inflamed astrocytes and halt disease progression for those with tauopathy disorders.
Researchers have identified a link between misshapen, fast replicating tau proteins, and accelerated cognitive decline. The findings shed new light on the development and progression of Alzheimer's disease.
Researchers have identified a rare population of potentially toxic senescent cells that may be a novel target for Alzheimer's disease therapies.
A new framework reveals Alzheimer's disease is far more complex than previously believed. Rather than being a disease where the same causes produce the same outcomes, researchers found three different models for the disease, each with its own characterizations and dynamics.
Older adults who sleep less than 4.5 hours, or more than 6.5 hours per night and who experience sleep disruptions are at greater risk of cognitive decline, researchers report.
Inhibiting the NHE6 gene abolished the formation of amyloid-beta plaques in mouse models of Alzheimer's disease.