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Exercise changes the brain in many ways at once, and a review paper lays out how those changes might protect it from neurodegenerative disease. The authors' conclusion is hedged: exercise has neuroprotective effects, the signaling behind them is not completely worked out, and it cannot be used alone to handle diseases such as Alzheimer's (AD) and Parkinson's (PD). As an add-on therapy, though, they say it has great potential.
Figure 1 of the review: effects of exercise on the human brain (CC BY 4.0).
Why it matters
Aging is the most important risk factor for most neurodegenerative diseases. In the United States, AD affects about 50% of people aged 95 and over, and PD affects 2 to 3% of people aged 65 and over. Epidemiological studies cited in the review found that physical activity reduces the risk of AD by 45% and of dementia by 28%. A meta-analysis of 29 randomized controlled trials (2049 people) found improved memory, attention, processing speed and executive function with aerobic exercise.
What studies in people found
- Parkinson's disease. The review reports that only high-intensity treadmill training improved motor symptoms in a recent clinical finding. Aerobic walking in mild to moderate PD was safe and well accepted and improved fitness, fatigue, motor function, mood and quality of life. Eight weeks of multi-component training improved gait speed and functional status. In a preliminary study of 36 patients, a year of 30 minutes of daily activities such as dry-land swimming and para-spinal muscle stretching improved balance, mobility and cardiac function compared with a group that did not exercise regularly.
- Alzheimer's disease. Exercise helps stabilize and improve cognitive function and reduces and delays severe neuropsychiatric symptoms such as apathy, confusion and depression.
- Across brain disorders. A meta-analysis covering Huntington's disease, AD, PD, multiple sclerosis, unipolar depression and schizophrenia found no complications from exercise in 69% of the studies, and exercise did better than usual treatment for quality of life, depressive symptoms, attention, working memory and psychomotor speed.
- Structure. In people aged 55 to 79, the age-related loss of cortical tissue density in temporal, frontal and parietal areas was reduced as cardiovascular fitness rose. Midlife physical activity may help maintain cognition and delay or reduce late-life dementia.
The pathways
| Pathway | What the review reports |
|---|---|
| Stress hormones | Exercise of enough intensity or duration activates the neuroendocrine system, changing hormones such as vasopressin, cortisol, β-endorphin and ACTH; the greater the exercise volume, the greater the response. Regular training lowers the hormonal stress response to sub-maximal exercise. |
| Neurotransmitters | Dopamine, noradrenaline and serotonin are the three main monoamines modulated by exercise. Effects on serotonin depend on brain region, duration and intensity: four weeks of moderate treadmill exercise lowered hippocampal serotonin, while seven days of high-intensity exercise raised it. |
| Brain insulin signaling | Insulin and growth factors such as BDNF, IGF-1, IGF-2 and VEGF keep hippocampal neurons working. Exercise enhances insulin signaling there. In 20-month-old rats, two weeks of forced daily running reversed memory loss and inflammatory changes. |
| BDNF | This protein regulates plasticity in the hippocampus and supports learning and memory. In mice bred to model AD, ten weeks of treadmill training increased dendritic branching and improved memory and raised BDNF-related signaling. |
| Irisin | A hormone released by muscle during exercise. In work cited by the review, raising its precursor FNDC5 increased BDNF in neurons and in the hippocampus, irisin limited neuronal injury in models of ischemia, and in cell cultures it protected neurons from amyloid-β toxicity. |
| Inflammation and oxidative stress | Exercise raises antioxidant enzymes such as superoxide dismutase and releases heat shock protein 70, which may help neurons defend themselves. A mouse study of exercise plus the antioxidant NAC found the exercise helped in the long term only, with the combination's extra benefit due to NAC alone. |
| Cell survival | Voluntary running triggers new cells to form in the hippocampus's dentate gyrus. In rats with cerebral ischemia, moderate-intensity treadmill exercise protected neurons, and high intensity did not. |
| Autophagy | The cell's recycling process. Voluntary exercise induces it, and in AD-model mice it helped clear amyloid-β and protect memory. |
Figure 2 of the review: effect of exercise on neurons involving BDNF and irisin (CC BY 4.0).
Caveats
Much of the mechanistic work the review cites was done in rats and mice, and the review notes that a complete understanding of the molecular mechanisms is still lacking. Neuroplastic changes in people show wide variation between individuals. Intensity matters, and results differ by region of the brain.
Sources
- Possible Neuroprotective Mechanisms of Physical Exercise in Neurodegeneration, PubMed Central article, licensed CC BY 4.0. Changed here: condensed and reworded, with the references and most study details left out; figures 1 and 2 are reproduced from the article; rewritten in hubnx's own words.
- Authors of the original: Mahalakshmi B, Maurya N, Lee SD, Bharath Kumar V.
ライセンス： CC BY 4.0 · 出典 pmc.ncbi.nlm.nih.gov
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