Study identifies specific chemical features of tau that may cause it to accumulate in the brain and trigger Alzheimer's disease.
Gantenerumab, an investigational drug for Alzheimer's disease, reduced amyloid plaques and lowered tau levels in the brains of people with genetic risk factors for the neurodegenerative disorder.
Elderly monkeys treated with CpG ODN had 59% fewer deposits of Alzheimer's related plaques in their brains compared to those who did not receive the treatment. The treatment also helped improve cognitive function and slow the progression of Alzheimer's symptoms.
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.
Sevoflurane, an anesthetic, causes tau to leave neurons and enter microglia. This stimulates the production of interleukin-6, leading to inflammation and cognitive impairment.
Eating a Mediterranean-style diet can help protect the brain from tau protein build-up and brain shrinkage associated with Alzheimer's disease.
Researchers have identified four distinct subtypes of Alzheimer's disease. The findings could lead to more individualized treatments for those with the neurodegenerative disorder.
An increase in bad gum bacteria and a decrease in good bacteria is associated with amyloid-beta in cerebral spinal fluid samples of older adults. The findings add to the growing body of evidence linking periodontal disease to the development of Alzheimer's.