From Obesity to Hippocampal Neurodegeneration: Pathogenesis and Non-Pharmacological Interventions.
From Obesity to Hippocampal Neurodegeneration: Pathogenesis and Non-Pharmacological Interventions.
复制标题
从肥胖到海马神经变性:发病机制和非药物干预。
DOI:
10.3390/ijms22010201
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发表时间:
2020-12-28
影响因子:
5.6
通讯作者:
Yau SY
中科院分区:
文献类型:
--
作者:
Lee TH;Yau SY
High-caloric diet and physical inactivity predispose individuals to obesity and diabetes, which are risk factors of hippocampal neurodegeneration and cognitive deficits. Along with the adipose-hippocampus crosstalk, chronically inflamed adipose tissue secretes inflammatory cytokine could trigger neuroinflammatory responses in the hippocampus, and in turn, impairs hippocampal neuroplasticity under obese and diabetic conditions. Hence, caloric restriction and physical exercise are critical non-pharmacological interventions to halt the pathogenesis from obesity to hippocampal neurodegeneration. In response to physical exercise, peripheral organs, including the adipose tissue, skeletal muscles, and liver, can secret numerous exerkines, which bring beneficial effects to metabolic and brain health. In this review, we summarized how chronic inflammation in adipose tissue could trigger neuroinflammation and hippocampal impairment, which potentially contribute to cognitive deficits in obese and diabetic conditions. We also discussed the potential mechanisms underlying the neurotrophic and neuroprotective effects of caloric restriction and physical exercise by counteracting neuroinflammation, plasticity deficits, and cognitive impairments. This review provides timely insights into how chronic metabolic disorders, like obesity, could impair brain health and cognitive functions in later life.