Metabolic Changes Accelerate Cognitive Decline in Type 2 Diabetics

Article

Examining evidence from epidemiologic, clinical, and animal studies, a team of researchers discussed the connection between neural dysfunction and metabolic disorders related to type 2 diabetes in the February 2014 issue of Current Diabetes Reports.

Previous research has demonstrated patients with metabolic disorders have significantly increased risks of experiencing cognitive decline, vascular dementia, and Alzheimer’s disease (AD). In addition, individuals with type 2 diabetes mellitus (T2DM) have a nearly two-fold higher risk of developing AD than non-diabetics.

Examining evidence from epidemiologic, clinical, and animal studies, a team of researchers discussed the connection between neural dysfunction and T2DM-related disease in the February 2014 issue of Current Diabetes Reports.

Metabolic, inflammatory, vascular, and oxidative changes were among the underlying mechanisms examined in the report. The authors noted that women may be at greater risk of cognitive decline and AD compared to men, and they also indicated that patients with comorbid diabetes and depression appear to experience accelerated decline.

According to the authors, several modifiers regulate the relationships between T2DM and neural dysfunction, of which the genetic risk factor apolipoprotein E and low testosterone (low T) are considered to be key. Both of those factors represent independent risk factors for AD and may accelerate pathology. Researchers have only recently identified andropause as a significant risk factor for AD, clarifying that men with low blood or brain testosterone levels appear to be at increased risk of dementia. Of note, low T has also been linked to insulin resistance.

Although the article did not address effective therapeutic strategies, the authors said the scientific community’s increasing understanding between metabolic disease and dementia may lead to better approaches in the clinic. While conventional T2DM-related approaches have been shown to reduce neural damage, new strategies may target implicated pathways independently and interactively. Reducing metabolic, inflammatory, and oxidative changes may reduce deleterious effects on the brain.

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