Abstract
Over the past decades, the human life span has dramatically increased, and therefore, a steady increase in diseases associated with age (such as Alzheimer’s disease and Parkinson’s disease) is expected. In these neurodegenerative diseases, there is a cognitive decline and memory loss, which accompany increased systemic inflammation, the inflamm-aging, and the insulin resistance. Despite numerous studies of age-related pathologies, data on the contribution of brain insulin resistance and innate immunity components to aging are insufficient. Recently, much research has been focused on the consequences of nutrients and adiposity- and nutrient-related signals in brain aging and cognitive decline. Moreover, given the role of metainflammation in neurodegeneration, lifestyle interventions such as calorie restriction may be an effective way to break the vicious cycle of metainflammation and have a role in social behavior. The various effects of calorie restriction on metainflammation, insulin resistance, and neurodegeneration have been described. Less attention has been paid to the social determinants of aging and the possible mechanism by which calorie restriction might influence social behavior. The purpose of this review is to discuss current knowledge in the interdisciplinary field of geroscience—immunosenescence, inflamm-aging, and metainflammation—which makes a significant contribution to aging. A substantial part of the review is devoted to frontiers in the brain insulin resistance in relation to neuroinflammation. In addition, we summarize new data on potential mechanisms of calorie restriction that influence as a lifestyle intervention on the social brain. This knowledge can be used to initiate successful aging and slow the onset of neurodegenerative diseases.
Highlights
It is a known fact that over the past decades, human life expectancy has greatly increased (Costantini et al, 2018)
If additional data confirm the occurrence of an initial increase and a final decrease in glucose metabolism in the brain, this shift can be visualized at an early stage and work to prevent the pathology
At the Alzheimer’s disease (AD) onset, Aβ oligomers activate microglia, which leads to the secretion of proinflammatory cytokines such as IL-1, IL-6, and tumor necrosis factor α (TNF-α) (Hemonnot et al, 2019). Such activation of microglia may play a key role in the AD pathogenesis, given the recent discovery that disabling a gene in AD model encoding a microglial receptor (i.e., NOD-like receptor 3) and perceiving inflammatory pathogens, including Aβ, prevent the development of AD and cognitive abnormalities that usually occur in this AD animal model (Heneka et al, 2013)
Summary
It is a known fact that over the past decades, human life expectancy has greatly increased (Costantini et al, 2018). The production of inflammatory cytokines through activation of TLR and NLRP3 Shin et al, 2015 contributes to the development of insulin resistance by suppressing insulin signaling.
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