From Obesity to Hippocampal Neurodegeneration: Pathogenesis and Non-Pharmacological Interventions.
Thomas Ho-Yin LeeSuk-Yu YauPublished in: International journal of molecular sciences (2020)
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.
Keyphrases
- cerebral ischemia
- adipose tissue
- insulin resistance
- weight loss
- type diabetes
- subarachnoid hemorrhage
- metabolic syndrome
- blood brain barrier
- brain injury
- high fat diet induced
- high fat diet
- physical activity
- mental health
- glycemic control
- bariatric surgery
- weight gain
- risk factors
- public health
- healthcare
- cardiovascular disease
- oxidative stress
- traumatic brain injury
- health information
- lipopolysaccharide induced
- temporal lobe epilepsy
- white matter
- cognitive impairment
- living cells
- fluorescent probe
- human health
- sensitive detection