Fact 13: The Potential Role of Inflammation in Diabetes and Dementia
Chronic inflammation, characterized by a long-term, persistent inflammatory response, can significantly contribute to the development of insulin resistance, a defining factor of type 2 diabetes. Insulin resistance arises when the body’s cells do not respond efficiently to insulin, leading to heightened glucose levels in the bloodstream. The immune system’s inflammatory response to this abnormality becomes chronic over time, exacerbating insulin resistance and advancing diabetes progression.
Beyond diabetes, inflammation has far-reaching consequences, notably playing a critical role in dementia’s pathogenesis, including Alzheimer’s disease. Chronic inflammation can have severe effects on brain health, with overactive microglia – the brain’s immune cells – potentially damaging healthy neurons and contributing to cognitive decline. Moreover, inflammation can interrupt neurogenesis, the formation of new neurons, weakening the brain’s plasticity and resilience, and making it more susceptible to aging and neurodegenerative diseases.
The interconnection of inflammation, diabetes, and dementia introduces the fascinating potential that certain diabetes medications could also safeguard against dementia. Some antidiabetic drugs like metformin and GLP-1 agonists exhibit anti-inflammatory properties. Metformin has demonstrated an ability to inhibit the production of inflammatory molecules and stimulate anti-inflammatory substances, potentially interrupting the inflammation-insulin resistance cycle. Similarly, GLP-1 agonists can decrease inflammatory responses in the brain, potentially mitigating cognitive decline and reducing dementia risk.(13)
