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).
Researchers investigate how toxic proteins associated with Alzheimer's disease spread throughout the brain.
Researchers have identified how specific brain areas change over time in patients with Parkinson's disease.
A new study reports appoptosin initiates a path that leads to tau accumulation in neurodegenerative disorders.
An inflammatory trigger like one present during viral infections is elevated in those with Alzheimer's disease and progressive supranuclear palsy (PSP).
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.
People who later developed Alzheimer's disease scored poorly on memory and logic-based tests, as well as reaction times and grip tests. They were also more likely to have experienced a fall within the past 12 months. Those who developed PSP were twice as likely to experience a fall.
Researchers have identified multiple new risk genes for Alzheimer's disease and progressive supranuclear palsy (PSP).
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.
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 report people with PSP experience more severe and extensive cognitive impairments than those with Parkinson's disease.
