Type 2 Diabetes Linked to Increased Risk of Parkinson’s

Type 2 Diabetes Linked to Increased Risk of Parkinson’s
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People with type 2 diabetes may have an increased risk of developing Parkinson’s disease and for experiencing faster Parkinson’s progression, according to a large-scale analysis of past research.

The study, “Type 2 Diabetes as a Determinant of Parkinson’s Disease Risk and Progression,” was published in the journal Movement Disorders.

Type 2 diabetes and Parkinson’s both affect aging populations and share several biological similarities, including toxic protein accumulation, lysosomal and mitochondrial dysfunction, and chronic systemic inflammation.

Many studies have explored a possible relationship between the two illnesses, but the studies often have reached conflicting conclusions.

Researchers from Queen Mary University of London sought to reconcile these conflicts by conducting a large-scale review of all available studies on the topic.

From 33,408 articles, the researchers selected 28 that were either observational studies that specifically investigated possible effects of type 2 diabetes on Parkinson’s, or studies analyzing how diabetes in general might affect Parkinson’s progression.

From nine studies that focused on type 2 diabetes specifically, the investigators calculated that people with type 2 diabetes were 1.21 times more more likely to develop Parkinson’s.

Including studies that evaluated any diabetes in the analysis showed “an overall null effect,” suggesting that only type 2 diabetes raised one’s Parkinson’s risk.

In both cases, the researchers saw no influence from either age or sex.

The analysis also revealed an association between type 2 diabetes and a faster progression of both motor symptoms and cognitive decline in Parkinson’s.

To gain insight into whether the relationships the team had discovered were truly causal or merely coincidental, they applied a technique called mendelian randomization to a separate analysis. Mendelian randomization relates well-understood genetic variation to observable outcomes such as disorders.

This analysis supported the link between type 2 diabetes (T2D) and faster motor symptom progression in Parkinson’s but found “no convincing evidence” to support the possible link to cognitive decline.

“This research brings together the results from many other studies to provide convincing evidence that type 2 diabetes likely affects not only Parkinson’s risk, but also Parkinson’s progression,” Alastair Noyce, PhD, the study’s senior author, said in a press release.

“There are many treatment strategies for type 2 diabetes, including prevention strategies, which may be re-purposed for the treatment of Parkinson’s,” he added.

Although this study did not examine the potential effects of diabetes medications, past studies have found evidence that antidiabetic therapies lower the risk and severity of Parkinson’s.

“Treating T2D may slow down the progression of [Parkinson’s],” the researchers concluded. “Thus, careful screening for T2D and early treatment of T2D in patients with [Parkinson’s] may be advisable.”

Forest Ray received his PhD in systems biology from Columbia University, where he developed tools to match drug side effects to other diseases. He has since worked as a journalist and science writer, covering topics from rare diseases to the intersection between environmental science and social justice. He currently lives in Long Beach, California.
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Ana holds a PhD in Immunology from the University of Lisbon and worked as a postdoctoral researcher at Instituto de Medicina Molecular (iMM) in Lisbon, Portugal. She graduated with a BSc in Genetics from the University of Newcastle and received a Masters in Biomolecular Archaeology from the University of Manchester, England. After leaving the lab to pursue a career in Science Communication, she served as the Director of Science Communication at iMM.
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Forest Ray received his PhD in systems biology from Columbia University, where he developed tools to match drug side effects to other diseases. He has since worked as a journalist and science writer, covering topics from rare diseases to the intersection between environmental science and social justice. He currently lives in Long Beach, California.
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