Structural biologists at the Keck School of Medicine of USC are the first to measure the energy difference between protein...
Treatments for Parkinson’s disease, estimated to affect 1 million Americans, have yet to prove effective in slowing the progression of...
Long-term aim is to develop new treatments to block the spread of damaged proteins in the brain. Van Andel Institute...
Using a two-photon microscope capable of peering deep within living tissue, researchers at the University of California, San Diego School of Medicine have found new evidence that alpha-synuclein protein build-up inside neurons causes them to not only become leaky, but also to misfire due to calcium fluxes.
While evidence suggests pathological proteins linked to the onset and progression of neurodegenerative disorders are capable of spreading from cell-to-cell within the brains of affected individuals, new research shows no evidence to support concerns that these abnormal disease proteins are “infectious” or transmitted from animals to humans or from one person to another.
Researchers suggest the overexpression of a protein called alpha-synuclein appears to disrupt vital recycling processes in neurons. The study may have major implications for more fully understanding the causes and mechanisms of Parkinson’s disease.
Studying neurons derived from brain and skin cells of Parkinson's patients, researchers discover how the most common genetic mutations in familial Parkinson's disease damage brain cells.
Researchers discover alpha-synuclein proteins can morph into different strains. This can promote misfolding of other disease proteins associated with neurodegenerative diseases.
Researchers report of elevated alpha-synuclein levels detected on the skin of patients with Parkinson's disease. The findings could offer a new biomarker for the recognition of Parkinson's before the disease reaches advanced stage.
Researchers have succeeded in characterizing and producing two different types of alpha-synuclein aggregates. One of which is more toxic and has greater capacity to invade neurons.
Researchers have identified a novel Parkinson's disease drug target and a compound capable of repairing neurons derived from Parkinson’s patients.
A new study links a lack of SMG1 to protein aggregates associated with Parkinson's disease and other neurodegenerative diseases.
