Lifestyle Modulators of Neuroplasticity: How Physical Activity, Mental Engagement, and Diet Promote Cognitive Health during Aging

Abstract

The number of the elderly across the globe will approximate 2.1 billion by 2050. Juxtaposed against this burgeoning segment of the population is evidence that nonpathological aging is associated with an increased risk for cognitive decline in a variety of domains, changes that can cause mild disability even before the onset of dementia. Given that pharmacological treatments that mitigate dementia are still outstanding, alternative therapeutic options are being investigated increasingly. The results from translational studies have shown that modifiable lifestyle factors—including physical activity, cognitive engagement, and diet—are a key strategy for maintaining brain health during aging. Indeed, a multiplicity of studies has demonstrated relationships between lifestyle factors, brain structure and function, and cognitive function in aging adults. For example, physical activity and diet modulate common neuroplasticity substrates (neurotrophic signaling, neurogenesis, inflammation, stress response, and antioxidant defense) in the brain whereas cognitive engagement enhances brain and cognitive reserve. The aims of this review are to evaluate the relationship between modifiable lifestyle factors, neuroplasticity, and optimal brain health during aging; to identify putative mechanisms that contribute positive brain aging; and to highlight future directions for scientists and clinicians. Undoubtedly, the translation of cutting-edge knowledge derived from the field of cognitive neuroscience will advance our understanding and enhance clinical treatment interventions as we endeavor to promote brain health during aging.

Current understandings of the trajectory and emerging correlates of cognitive impairment in bipolar disorder: An overview of evidence

“…However, diet and nutrients may influence several biological pathways that are dysregulated in BD but relevant to cognition, such as monoaminergic activity, inflammation, oxidative stress, neuroplasticity and the gut microbiome . Growing preclinical and clinical evidence has shown that diet and physical activity are key to maintaining brain health and cognitive function, especially during ageing . Nutritional factors in particular, may stimulate adult neurogenesis and help to protect cognitive function in the elderly, as well as those with brain disorders .…”

Dementia in China (2015–2050) estimated using the 1% population sampling survey in 2015

“…Furthermore, we should make efforts to improve the quality of care, and to seek a cure. Primary prevention could be focused on beneficial interventions, such as physical activity, mental engagement and diet, to promote slowing of the progression of dementia in the older community . Researchers also need to pay attention to the relationship between cardiovascular diseases and dementia.…”

Role of phytochemicals as nutraceuticals for cognitive functions affected in ageing

“…Thus it prevents protein disulfide isomerase‐resistant misfolded protein forms that accumulate with oxidative stress that are implicated in the pathogenesis of AD (Howes & Perry, ). Relevant to both cognitive functions in ageing and dementia, curcumin rescued age‐related loss of hippocampal synapse input specificity of LTP via favouring NMDA receptor activity (Phillips, ). With respect to the suggested link between hypercholesterolaemia and AD risk, the hypocholesterolaemic effects of curcumin, as observed in different animal studies, have also been suggested as an additional basis to reduce dementia risk and cognitive decline with ageing (Goozee et al, ).…”

“…‐Reverses age‐related loss of hippocampal synapse input specificity of LTP via favouring NMDA receptor activity (Phillips, )…”

“…Resveratrol's neuroprotective effects may also be due to activation of the sirtuin 1 miR‐134 pathway and up‐regulation of CREB/BDNF expression (Shen, Xu, Qu, Sun, & Zhang, ). Another study revealed that resveratrol enhanced proliferative states in neuronal stem cells in rat hippocampus and via BDNF restoration, it attenuated stress‐induced learning deficits and hippocampal degeneration in vivo (Phillips, ).…”