The finding of a common protein abnormality in these degenerative diseases supports a hypothesis among experts that abnormal deposition of proteins in many neurodegenerative disorders reflects an early change in these proteins.
“We have pinpointed a protein abnormality known as the ‘SOD1 fingerprint’ in regions of neuronal loss in the Parkinson’s disease brain,” said Associate Professor Kay Double who led the research published in Acta Neuropathologica.
“We believe this loss of neurons results from a combination of oxidative stress and a regional deficiency in copper, both of which occur specifically in vulnerable regions of the Parkinson’s disease brain.”
This new finding may offer hope to Parkinson’s disease patients, since therapies targeting abnormal SOD1 protein have resulted in substantial improvements in motor function and survival time in models of ALS, prompting their progression into human clinical trials in this disease. This new finding suggests that such therapies may also be useful to treat Parkinson’s disease.