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Parkinson’s Disease May Share SOD1 Protein Anomaly with ALS, Study Finds

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ALS, Lou Gehrig's DiseaseParkinson's

Summary:

Parkinson’s disease and amyotrophic lateral sclerosis (ALS) may have more in common than previously thought. According to a recent study, a known ALS gene called SOD1 also may be involved in the development of Parkinson’s.

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Parkinson’s disease and amyotrophic lateral sclerosis (ALS) may have more in common than previously thought. According to a recent study, a known ALS gene called SOD1 also may be involved in the development of Parkinson’s.

This finding opens the possibility of treating Parkinson’s patients with therapies targeting SOD1 toxicity, which already have been investigated in clinical trials for ALS.

The study, “Amyotrophic lateral sclerosis-like superoxide dismutase 1 proteinopathy is associated with neuronal loss in Parkinson’s disease brain,” was published in the journal Acta Neuropathologica.

ALS is a neurodegenerative disease marked by loss of motor neurons, which control the muscles in the body. Previous studies have shown that about 20% of familial ALS cases carry mutations in the gene encoding SOD1. These mutations are responsible

for the faulty folding of the protein, which then aggregates in the brain, leading to impairment of motor neurons and ALS symptoms.

Now, researchers have found that abnormal SOD1 also may be involved in the development of Parkinson’s disease, leading to the formation of protein aggregates that “closely resembles that of neurotoxic SOD1 deposits in SOD1-associated familial amyotrophic lateral sclerosis (fALS),” researchers wrote.

The team also found that these aggregates of faulty SOD1 promote neuronal impairment and copper deficiency in the brain, similar to that seen in mutant SOD1 in fALS.

“We have pinpointed a protein abnormality known as the ‘SOD1 fingerprint’ in regions of neuronal loss in the Parkinson’s disease brain,” Kay Double, PhD, the study’s leading author, said in a press release. “We believe this loss of neurons results from a combination of oxidative stress [cell damage] and a regional deficiency in copper, both of which occur specifically in vulnerable regions of the Parkinson’s disease brain,” said Double, who is an associate professor of biomedical sciences at the University of Sydney, Australia.

Therapeutic strategies aiming to counteract the toxic effects of mutated SOD1 in ALS patients already have been investigated. According to researchers, the results found in this study may support the “potential translation of therapeutic approaches targeting SOD1 toxicity, already in clinical trials for ALS, into disease-modifying treatments for Parkinson’s disease,” which would speed-up the development of a novel treatment for this disease.

Abnormal protein aggregation is not a novel concept in the study for Parkinson’s disease. The disease is caused by the formation of aggregates of the protein alpha-synuclein, which are toxic to neurons and promote loss of brain function.

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