α-synuclein tagged posts

Scientists at the Francis Crick Institute, UCL and the University of Edinburgh have uncovered how a build-up of harmful protein starts to happen within neurons in Parkinson’s disease, ultimately causing nerve cell death. By looking at how, where and why this build-up happens, the work provides unique insight into a key biological process driving Parkinson’s.

Parkinson’s is a progressive neurodegenerative disease that causes tremors, slowing of movements, stiffness and can progress to cause severe cognitive problems...

Immunohistochemistry for alpha-synuclein showing positive staining (brown) of an intraneural Lewy-body in the Substantia nigra in Parkinson’s disease. Credit: Wikipedia

New details learned about a key cellular protein could lead to treatments for neurodegenerative diseases, such as Parkinson’s, Huntington’s, Alzheimer’s, and amyotrophic lateral sclerosis (ALS). At their root, proteins misfold and accumulate in neurons, inflicting damage and eventually killing the cells. In a new study, researchers in the laboratory of Steven Finkbeiner, MD, PhD, at the Gladstone Institutes used a different protein, Nrf2, to restore levels of the disease-causing proteins to a normal, healthy range, thereby preventing cell death.

The researchers tested Nrf2 in 2 models of Parkinson’s disease: cells with muta...

Clumps of the protein a-synuclein in a Parkinsonian brain. Credit: Donghoon Kim/Johns Hopkins Medicine

Researchers at Johns Hopkins say they have gleaned 2 important new clues in the fight against Parkinson’s disease: that blocking an enzyme called c-Abl prevents the disease in specially bred mice, and that a chemical tag on a second protein may signal the disorder’s presence and progression. Their work, suggests a promising target for drug research and a tool that could speed Parkinson’s disease research more broadly.

“There were indications that c-Abl activity leads to Parkinson’s disease, and our experiments show there is indeed a connection,” says Prof. Ted Dawson, M.D., Ph.D...