摘要
Alzheimer’s disease (AD) is the most common form of dementia which mostly affects persons younger than 65 years old. Mounting findings showed that amyloid-β(Aβ) peptides, oxidative stress, neuroinflammation and insulin resistance may play central role in the pathogenesis of AD. There are very many methods to slow it through affecting these aforementioned factors. However, more efficient prevention of the progression of AD is still ambiguous. Fibroblast growth factor 21 (FGF21) is an endocrine hormone that is expressed by several organs. It increases insulin sensitivity and regulates lipid metabolism and energy homeostasis. Emerging evidence demonstrates that FGF21 has potential effects in the brain involving metabolic regulation, neuroprotection and cognition. Hence, we hypothesize that FGF21 may be a protective factor in AD by attenuating Aβ generation, inflammation, oxidative stress, and insulin resistance. Our hypothesis will shed new light on the understanding of pathogenesis of AD and help to find a new way to prevent the genesis and progress of AD.
Alzheimer’s disease (AD) is the most common form of dementia which mostly affects persons younger than 65 years old. Mounting findings showed that amyloid-β(Aβ) peptides, oxidative stress, neuroinflammation and insulin resistance may play central role in the pathogenesis of AD. There are very many methods to slow it through affecting these aforementioned factors. However, more efficient prevention of the progression of AD is still ambiguous. Fibroblast growth factor 21 (FGF21) is an endocrine hormone that is expressed by several organs. It increases insulin sensitivity and regulates lipid metabolism and energy homeostasis. Emerging evidence demonstrates that FGF21 has potential effects in the brain involving metabolic regulation, neuroprotection and cognition. Hence, we hypothesize that FGF21 may be a protective factor in AD by attenuating Aβ generation, inflammation, oxidative stress, and insulin resistance. Our hypothesis will shed new light on the understanding of pathogenesis of AD and help to find a new way to prevent the genesis and progress of AD.
