Abstract
Diet and exercise influence the risk of cognitive decline (CD) and dementia through the food metabolome and exercise-triggered endogenous factors, which use the blood as a vehicle to communicate with the brain. These factors might act in concert with hippocampal neurogenesis (HN) to shape CD and dementia. Using an in vitro neurogenesis assay, we examined the effects of serum samples from a longitudinal cohort (n=418) on proxy HN readouts and their association with future CD and dementia across a 12-year period. Altered apoptosis and reduced hippocampal progenitor cell integrity were associated with exercise and diet and predicted subsequent CD and dementia. The effects of exercise and diet on CD specifically were mediated by apoptosis. Diet and exercise might influence neurogenesis long before the onset of CD and dementia. Alterations in HN could signify the start of the pathological process and potentially represent biomarkers for CD and dementia.
Highlights
Diet and exercise influence the risk of cognitive decline (CD) and dementia through the food metabolome and exercise-triggered endogenous factors, which use the blood as a vehicle to communicate with the brain
3.1 Cell death during differentiation is associated with future CD while the association of hippocampal stem cell integrity with CD is modified by regular exercise
We found a significant interaction between baseline levels of %sex determining region Y (SRY)-Box Transcription Factor 2 (SOX2)-positive cells and physical exercise on CD (p = .049), such that reduced baseline levels of %SOX2 were significantly associated with CD but only in participants who did not regularly exercise (p = .04; Figure 2A: Model 1B; Figure 2C)
Summary
Cognitive decline (CD) is an increasing concern, due to the resulting deterioration in overall quality of life and independence worldwide,[1] and because of the well-known elevated risk to develop dementia.[2]. Several clinical studies have documented the protective effects of increased exercise against CD/ dementia,[7] and revealed how higher adherence to a Mediterranean diet slowed CD and reduced dementia risk.[8,9] There is evidence of a protective association between certain candidate nutrients and foods (e.g., folate and flavonoids in dark leafy vegetables, omega-3 fatty acids, and vitamin D in seafood, caffeine) and cognitive outcomes in aging human populations.[10] In this respect, we recently identified a signature of metabolites predictive of CD and found a protective role of coffee, cocoa, fish, and red wine.[11] before we can effectively exploit the effects of exercise and incorporate protective bioactive compounds into targeted dietary interventions to attenuate/prevent CD and potentially dementia, the role of exercise, and of these dietary modulators, needs to be better understood at the neurobiological level. We: (1) determined whether markers of HN were associated with CD and/or dementia 12 years after the samples were taken, and (2) whether exercise and key nutritional factors, including our previously identified metabolites[11] and lipids,[19] could modulate the neurogenic process
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