21 – This is the time when one should start paying attention to maintain equilibrium of the body balanced food, sleep and exercise. If you are in 30s, still there is a chance, start exercise! Running, swimming, real sports (Not cricket but basketball, football, hockey for 30 minutes at least), hiking, climbing, digging!

Exercise, plays vital role. Especially endurance exercise. Exercise, especially endurance exercise, is known to have beneficial effects on brain health and cognitive function. This improvement in cognitive function with exercise has been most prominently observed in the aging population. Exercise has also been reported to ameliorate outcomes in neurological diseases like depression, epilepsy, stroke, Alzheimer’s disease, and Parkinson’s disease.

As per this research [1] , endurance exercise induces FNDC5, a muscle protein. This induced protein helps inducing Bdnf (Brain-derived neurotrophic factor), a secreted protein, a growth factor. BDNF activity is correlated with increased long term potentiation and neurogenesis, which can be induced by physical activity. Long term potentiation is shown to improve learning and memory by strengthening the communication between specific neurons.

If you do not want your brain cells (neurons) to die prematurely, If you have started feeling midlife crisis, started forgetting things; Exercise is your ultimate solution.

One more study notes[2]:

Learning, memory, and brain repair depend on the ability of our neurons to change with experience.

“We provide the first demonstration that moderate levels of physical activity enhance neuroplasticity in the visual cortex of adult humans,” says Claudia Lunghi of the University of Pisa in Italy.

“Our study suggests that physical activity, which is also beneficial for the general health of the patient, could be used to increase the efficiency of the treatment in adult patients,” Lunghi says. “So, if you have a lazy eye, don’t be lazy yourself!”

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Research

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[1] Exercise Induces Hippocampal BDNF through a PGC-1α/FNDC5 Pathway

http://www.sciencedirect.com/science/article/pii/S155041311300377X

Exercise can improve cognitive function and has been linked to the increased expression of brain-derived neurotrophic factor (BDNF). However, the underlying molecular mechanisms driving the elevation of this neurotrophin remain unknown. Here we show that FNDC5, a previously identified muscle protein that is induced in exercise and is cleaved and secreted as irisin, is also elevated by endurance exercise in the hippocampus of mice. Neuronal Fndc5 gene expression is regulated by PGC-1α, and Pgc1a^−/− mice show reduced Fndc5 expression in the brain. Forced expression of FNDC5 in primary cortical neurons increases Bdnf expression, whereas RNAi-mediated knockdown of FNDC5 reduces Bdnf. Importantly, peripheral delivery of FNDC5 to the liver via adenoviral vectors, resulting in elevated blood irisin, induces expression of Bdnf and other neuroprotective genes in the hippocampus. Taken together, our findings link endurance exercise and the important metabolic mediators, PGC-1α and FNDC5, with BDNF expression in the brain.

A cycling lane for brain rewiring

http://www.cell.com/current-biology/abstract/S0960-9822%2815%2901288-9?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0960982215012889%3Fshowall%3Dtrue

Brain plasticity, defined as the capability of cerebral neurons to change in response to experience, is fundamental for behavioral adaptability, learning, memory, functional development, and neural repair. The visual cortex is a widely used model for studying neuroplasticity and the underlying mechanisms. Plasticity is maximal in early development, within the so-called critical period, while its levels abruptly decline in adulthood [1] . Recent studies, however, have revealed a significant residual plastic potential of the adult visual cortex by showing that, in adult humans, short-term monocular deprivation alters ocular dominance by homeostatically boosting responses to the deprived eye [2–4] . In animal models, a reopening of critical period plasticity in the adult primary visual cortex has been obtained by a variety of environmental manipulations, such as dark exposure, or environmental enrichment, together with its critical component of enhanced physical exercise [5–8] . Among these non-invasive procedures, physical exercise emerges as particularly interesting for its potential of application to clinics, though there has been a lack of experimental evidence available that physical exercise actually promotes visual plasticity in humans. Here we report that short-term homeostatic plasticity of the adult human visual cortex induced by transient monocular deprivation is potently boosted by moderate levels of voluntary physical activity. These findings could have a bearing in orienting future research in the field of physical activity application to clinical research.