Abstract
Alzheimer’s disease (AD) is the sixth leading cause of death and is correlated with obesity, which is the second leading cause of preventable diseases in the United States. Obesity, diabetes, and AD share several common features, and inflammation emerges as the central link. High-calorie intake, elevated free fatty acids, and impaired endocrine function leads to insulin resistance and systemic inflammation. Systemic inflammation triggers neuro-inflammation, which eventually hinders the metabolic and regulatory function of the brain mitochondria leading to neuronal damage and subsequent AD-related cognitive decline. As an early event in the pathogenesis of AD, chronic inflammation could be considered as a potential biomarker in the treatment strategies for AD.
Highlights
Alzheimer’s disease (AD) is a progressive and irreversible brain disorder that begins well before the clinical symptoms appear
After cautiously considering the facts, we can suggest that obesity or diabetes-induced inflammation is associated with impaired mitochondrial health
The association between inflammation and cognitive decline could be the consequence of underlying disease conditions triggered by diabetes, obesity, or cardiovascular disease and their consequent comorbidities
Summary
Alzheimer’s disease (AD) is a progressive and irreversible brain disorder that begins well before the clinical symptoms appear. The numbers have been projected to grow from the current 55 million to 88 million [3], approximately doubling by 2050 [4] This alone depicts the magnitude of the burden of AD on health care and the overall society in the future. Pro-inflammatory cytokines activated by microglia can induce oxidative stress and compromised antioxidant defense [9] They contribute to impaired insulin signaling, synapses loss, reduced mitochondrial axonal transport [10], mitochondrial fragmentation, dynamics, and eventual dysfunction [11]. Mitochondrial dysfunction has been considered as an early event for AD pathogenesis and is associated with a metabolic syndrome including obesity, diabetes, insulin resistance, and cardiovascular diseases [8]. It is possible that mitochondrial dysfunction has an evident role in the initiation and development of the metabolic disorder, and it is worthy to investigate to what extent inflammation and mitochondrial health affect the progression of AD
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