Scientists have gained new insights into how exercise protects against neurodegenerative diseases.
A special issue of the magazine. brain plasticity explores research on how exercise-induced activation of peripheral systems can improve cognitive function and delay or prevent the onset of neurodegenerative diseases.
A growing body of research shows that exercise can improve brain function and delay, or even prevent, the onset of neurodegenerative diseases such as Alzheimer’s Y Parkinson’s disease. Although the underlying mechanisms remain unclear, recent research indicates that exercise-induced activation of peripheral systems, such as muscle, gut, liver, and adipose tissue, may affect neural plasticity. a special problem From the newspaper brain plasticity presents new research and insights into neural plasticity and the role of peripheral factors in cognitive health.
“At least a dozen peripheral factors have been identified that affect neurotrophin levels, adult neurogenesis, inflammation, synaptic plasticity, and memory function,” explained the journal’s Guest Co-Editor and Editor-in-Chief Henriette van Praag, PhD, Charles E. Schmidt. College of Medicine and Brain Institute, Florida Atlantic University.
Cathepsin B (CTSB), a myokine, and brain-derived neurotrophic factor (BNDF) have been found to possess strong neuroprotective effects. in a new studio Featured in the special issue, researchers examined whether increasing the intensity of aerobic exercise would increase the amount of CTSB and BDNF circulating in the blood. Sixteen healthy young subjects were selected as participants and completed treadmill-based aerobic exercise at maximum capacity and then at 40%, 60%, and 80% capacity.
After each exercise session, blood samples were taken to measure circulating CTSB and BDNF, and the expression of CTSB protein, BDNF protein, and mRNA in skeletal tissue was measured. The scientists found that high-intensity exercise elevates circulating CTSB in young adults immediately after exercise, and that skeletal muscle tissue expresses both the CTSB and BDNF message and protein.
In response to a variety of stimuli, skeletal muscle can communicate with the central nervous system (CNS) in a number of ways, including the following: (1) by secreting signaling proteins (myokines) that can bind to receptors in the blood and the brain. barrier (BBB) and brain cells (neurons and/or glia), with the consequent induction of downstream signaling; (2) releasing extracellular vesicles such as exosomes that contain signaling factors; (3) releasing metabolites (myometabolites) that enter the brain via solute transporters present in the BBB and brain cells; (4) secreting enzymes that produce signaling factors in muscle, in the circulation, and/or in the brain; and (5) through indirect effects derived from the modulation of muscle metabolism and/or myokine signaling to tissues other than the brain. Regulated processes include enhancement of cerebral blood flow, brain metabolic functions, mitochondrial biogenesis, and neurogenesis, while protective signaling reduces oxidative stress, cellular senescence, and neuroinflammation. Together, the action of muscle-brain signaling on these cellular processes improves cognitive functions. Credit: Mamta Rai and Fabio Demontis, Brain Plasticity
“CTSB and BDNF are promising therapeutic targets that may delay the onset and progression of cognitive impairments,” said lead investigator Jacob M. Haus, PhD, University of Michigan School of Kinesiology. “Future studies are needed to elucidate the mechanisms that regulate its fiber type-specific release, processing, and function in skeletal muscle tissue.”
The special number of brain plasticity also shares new research that CTSB may play a role in cognitive control by modulating processing speed, and that both moderate-intensity and high-intensity interval exercise increase serum BDNF levels and memory performance of work in young adult women.
Five review articles cover interorgan crosstalk between muscle, liver, adipose tissue, the gut microbiome, and the brain. While it is well known that exercise protects the central nervous system, it was only recently discovered that it depends on the endocrine capacity of skeletal muscle. In their review, co-authors Mamta Rai, PhD, and Fabio Demontis, PhD, both from the Department of Developmental Neurobiology, St. Jude Children’s Research Hospital, highlight the impact of myokines, metabolites, and other unconventional factors that mediate the effects of the musculature – the communication between the brain and the muscle-retina on neurogenesis, neurotransmitter synthesis, proteostasis, mood, sleep, cognitive function and eating behavior after exercise.
They also raise the possibility that detrimental myokines resulting from inactivity and muscle disease states may become a novel focus for therapeutic intervention. “We propose that adapting central nervous system signaling to muscle by modulating myokines and myometabolites can combat age-related neurodegeneration and brain diseases that are influenced by the system’s signals,” they said.
Men and women exhibit differences in their biological responses to physical activities and also in their vulnerabilities to the onset, progression, and outcomes of neurodegenerative disease. A review by co-authors Constanza J. Cortes, PhD, University of Alabama at Birmingham, and Zurine De Miguel, PhD, California State University, discusses emerging research on sex-specific differences in the immune system response to exercise as a potential mechanism by which physical activity affects the brain.
“Individual findings suggest that the immune response to exercise might be increased in women, but further study is needed,” Dr. Cortés and Dr. de Miguel note. “Interdisciplinary research integrating neuroscience, exercise physiology, and geroscience is needed to explain sex differences in cognitive aging and age-related neurodegenerative diseases, and to develop new therapeutic targets.”
Research on cross-talk between brain and adipose tissue, particularly on a hormone that can cross the BBB and has been shown to improve neuronal function in animal models of[{” attribute=””>Alzheimer’s disease; accumulating evidence that neurogenesis can be regulated by the gut microbiome; and research on effects of exercise and diet on hippocampal BDNF signaling, which suggest approaches to the treatment of neurodegenerative conditions are also reviewed.
“The research collected in this issue corroborates the importance of exercise for memory function,” said co-Guest Editor Christiane D. Wrann, PhD, DVM, Massachusetts General Hospital and Harvard Medical School. “We are pleased to share this exciting special issue. In the coming years likely many more systemic molecules relevant to the brain will be discovered and may provide a basis for novel therapeutic approaches to neurodegenerative diseases.”
References:
“High Intensity Acute Aerobic Exercise Elicits Alterations in Circulating and Skeletal Muscle Tissue Expression of Neuroprotective Exerkines” by Corey E. Mazo, Edwin R. Miranda, James Shadiow, Michael Vesia and Jacob M. Haus, 21 October 2022, Brain Plasticity.
DOI: 10.3233/BPL-220137
“Muscle-to-Brain Signaling Via Myokines and Myometabolites” by Mamta Rai and Fabio Demontis, 21 October 2022, Brain Plasticity.
DOI: 10.3233/BPL-210133
“Precision Exercise Medicine: Sex Specific Differences in Immune and CNS Responses to Physical Activity” by Constanza J. Cortes and Zurine De Miguel, 21 October 2022, Brain Plasticity.
DOI: 10.3233/BPL-220139
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