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 layer of genetic material involved in controlling the production of tau in the brain. The material is part of a larger family of non-coding genes that regulate and control other brain proteins associated with neurodegenerative disorders, such as Alzheimer's disease, Parkinson's, and PSP. The findings could lead to the development of new therapeutics to treat a range of neurodegenerative disorders.
Progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS), two atypical parkinsonian syndromes, may be twice as common as previously believed, researchers report.
Tau accumulations disrupt wake-promoting neurons. The findings help explain why day-time napping and sleep disruptions are often reported in Alzheimer's patients.
Cortice Biosciences announced today results from placebo-controlled, double-blinded Phase 1 studies evaluating TPI 287, a brain penetrable microtubule stabilizing agent, for the treatment of Alzheimer’s disease, progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS).
A new study reports appoptosin initiates a path that leads to tau accumulation in neurodegenerative disorders.
Researchers report people with PSP experience more severe and extensive cognitive impairments than those with Parkinson's disease.