Researchers detail the complex interaction between alpha synuclein and the prion protein PrPc.
According to researchers, an antidepressant that has been available for more than 50 years could help slow the progression of Parkinson's disease. The drug, nortiptyline, has been shown to stop the growth of alpha synuclein.
Even during early stages of the disease, gut bacteria in those with Parkinson's differs significantly from those without the disease, a new study reports.
Researchers report klotho, a life extending protein, improved working memory, spatial memory and learning in mice. The researchers also noted a single injection of klotho was sufficient to improve cognitive ability and the effects were long lasting.
A Nature Neuroscience study reveals the normal role of alpha-synuclein, a protein implicated in Parkinson's disease. Researchers say understanding how the protein normally acts may give insights into how it might fail.
Researchers report T cells in Parkinson's disease patients respond to alpha synuclein to a greater degree than those without the disease. The Nature study reports four genetic variations are associated with T cell reactivity to alpha synuclein. More than 50% of Parkinson's patients carry at least one of the gene variants.
A common misconception is that Alzheimer's disease and dementia are the same thing. Alzheimer's disease is simply one form of dementia. Researchers from Texas A&M describe how Alzheimer's and other forms of dementia impact the lives of both patients and their families, and provide new insights into minimizing the risks of developing neurodegenerative conditions.
Researchers have implicated an enzyme that appears to make both Tau and alpha synculein more toxic in Alzheimer's and Parkinson's disease. Inhibiting this enzyme has already proved helpful in treating animal models of Alzheimer's disease. The researchers report they are moving on to testing drugs that inhibit AEP in animal models of Parkinson's disease.
T cells may be tricked into thinking dopamine neurons are foreign due to the build up of damaged alpha-synuclein, a new study reports.
Researchers suggest an agent in the gut could interfere with alpha-synuclein in endocrine cells, deforming the proteins which then may spread to the brain in Parkinson's patients.
CRISPR technology allows researchers to illuminate and monitor alpha synuclein in the brain.
Findings may explain how neurodegenerative diseases spread throughout the brain and disrupt normal functions. Additionally, treatment for one disease could possibly work for the other two also.
