Alzheimer’s disease (AD) is the only common chronic disease that has no known cure or way to prevent its development. This is a critical problem because the rates of AD are expected to increase over the next several decades. In the United States, approximately 5.3 million people have AD, which comprises up to 80% of all dementia cases. That number is expected to increase to 13.8 million people by 2050.
The belief that AD does not respond to any intervention has largely disproven over the last 10 years. This belief was grounded in the idea that the nervous system is static and unchanging. Numerous drug trials were conducted over the last several decades, which has led to a significant conclusion: AD has multiple factors that develop over decades before the onset of symptoms and is a result of lifestyle.
The concept of neuroplasticity is gaining acceptance rapidly. A 2014 study by UCLA showed a reversal of mild to moderate AD using a comprehensive approach of individualized diet and lifestyle recommendations (improvement in 9 out of 10 participants). Of all of the systemic factors, one of the most important to address is insulin resistance.
Insulin resistance and the brain
An important finding of the pathology of AD is the strong correlation between AD and insulin resistance, metabolic syndrome, and type 2 diabetes. As much as 40% of AD pathology can be related to hyperinsulinemia. Higher HbA1c levels correlate with lower cognitive capacity and changes in hippocampal microstructure, and positive APOE e4 genetic status (a genetic determinant of AD risk) is correlated with increased risk of type 2 diabetes, altered lipid profiles, and cardiovascular disease. Research suggests that early intervention to address impaired cerebral glucose metabolism may be critical for the outcome success in treating AD. In addition, treating diabetes in later life reduces the conversion of mild cognitive impairment to AD and all-cause dementia.
It is also well known that the brain regions (especially the hippocampus) that rely most heavily on insulin and insulin-like growth factor (IGF) signaling are the most vulnerable to AD pathology. Impairments in brain insulin/IGF signaling lead to increased expression of amyloid-β precursor protein (AβPP) and accumulation of AβPP-Aβ aggregates.
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