Diabetes, Blood Sugar Linked to Biomarker of Nerve Cell Damage

Lindsey Shapiro, PhD avatar

by Lindsey Shapiro, PhD |

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Diabetes and high blood sugar were associated with elevated levels of neurofilament light (NfL) — a biomarker of nerve cell damage — and worse cognitive function among people with Parkinson’s disease, according to a recent study.

“Our study is the first to show that diabetes and [a measure of blood sugar management known as] HbA1c correlate with blood-based markers of neuroaxonal [nerve cell] damage in patients” with Parkinson’s disease, the researchers wrote.

The study, “Diabetes, Glycated Hemoglobin (HbA1c), and Neuroaxonal Damage in Parkinson’s Disease (MARK-PD Study),” was published in Movement Disorders

Diabetes is a chronic condition characterized by hyperglycemia, or high blood sugar levels. The disease has been associated with an increased risk of developing Parkinson’s. Further, diabetes and high blood sugar have both been implicated in a faster progression of Parkinson’s motor symptoms.

It has been suggested that controlling blood sugar levels with anti-diabetic treatments also can influence Parkinson’s symptoms.

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To learn more, researchers now further explored the relationship between diabetes, blood sugar, and Parkinson’s among patients participating in the Biomarkers in Parkinson’s Disease (MARK-PD) study.

The study involved 195 adults with Parkinson’s. Among them, 27 people had diabetes and 168 did not. The average disease duration in both groups was 10 years, and the average age among diabetic patients was 67.3. The non-diabetic patients had a mean age of 67.6.

Levels of glycated hemoglobin, or HbA1c, were measured in patients’ blood. HbA1c is formed when glucose (sugar) binds with hemoglobin — a protein found in red blood cells that carries oxygen. HbA1c levels are a reliable indicator of a person’s average blood sugar levels over the preceding two months.

Results showed that Parkinson’s patients with diabetes were more likely to have high blood pressure, elevated cholesterol, a history of stroke, and high HbA1c than those without diabetes.

Further, compared with non-diabetic patients, diabetic individuals had elevated blood levels of NfL — a Parkinson’s disease biomarker that indicates nerve cell damage, also called neuroaxonal damage. Similarly, those patients with high HbA1c also tended to have increased NfL levels, although this relationship did not reach statistical significance when accounting for potentially related vascular risk factors, like high blood pressure, cholesterol, or stroke.

“Our data suggest increased neuroaxonal damage in [Parkinson’s] patients with diabetes [is] independent of vascular risk factors, whereas the association of high HbA1c with neuroaxonal damage is not independent of vascular risk factors,” the researchers wrote.

The team observed that the presence of diabetes was weakly associated with levels of functional disability, as measured by the Hoehn and Yahr Scale (H & Y), but this relationship was not observed when using the MDS-UPDRS III, which assesses motor function.

The weakness of the observed relationship between diabetes and Parkinson’s disability compared with previous findings may be due to the relatively long disease duration and advanced disease stage of the participants in this study, the researchers wrote.

Diabetes was significantly associated with lower scores on the Montreal Cognitive Assessment (MoCA), indicating worse cognitive function among diabetic individuals than non-diabetic patients.

In contrast, while the results trended toward an association between HbA1c levels and cognitive function, the findings again were not statistically significant after accounting for other vascular risk factors.

While the results overall highlight a relationship between both diabetes and blood sugar with Parkinson’s symptoms, the team noted that the data suggest that “hyperglycemia might explain some, but not all, of the association of diabetes with [Parkinson’s],” adding that the relationship between the disorders is likely complex and involves several signaling pathways.

One other molecule that could be involved is glucagon-like peptide 1 (GLP-1), a gut hormone released in response to food. The actions of GLP-1 are mimicked by some anti-diabetic medications, which have been previously linked to a slower disease progression in Parkinson’s patients and a lower risk of developing the disease, the researchers noted.

HbA1c measurements reflect the compounded activities of this and other pathways, which may each have different effects on brain function. This highlights the complexity of the relationship between diabetes, blood sugar, and Parkinson’s disease, the team emphasized.

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