Cycling may help restore neural connections damaged by Parkinson's

10-08-2025

Parkinson's disease negatively impacts the body's central nervous system, which includes the brain. A new study has found that cycling helps restore neural connections damaged by Parkinson's disease. This benefit was seen in as little as 12 cycling sessions over a four-week period.According to the Parkinson's Foundation, an estimated 10 million people around the world live with Parkinson's disease — a neurological condition that affects a person's ability to move. Parkinson's disease negatively impacts the body's central nervous system, which includes the brain. 'The brain is a dynamic and ever-evolving system, and Parkinson's disease disrupts this system in complex, continually changing ways,' Aasef Shaikh MD, PhD, professor and vice chair (research), director of the Research and Education Center in the Neurological Institute at University Hospitals Cleveland Medical Center, Department of Neurology at UH Cleveland Medical Center, explained to Medical News Today. 'Even in the absence of disease, the brain undergoes natural changes as it ages. When a degenerative condition like Parkinson's is introduced, it adds layers of complexity and nonlinear disruptions to brain function,' he said. Shaikh is the lead author of a new study recently published in the journal Clinical Neurophysiology that found cycling helps restore neural connections damaged by Parkinson's disease. Cycling and deep brain stimulation for Parkinson'sFor this study, researchers recruited nine adult participants with Parkinson's disease to undergo 12 cycling sessions over a four-week period. All participants had deep brain stimulation (DBS) devices that had already been implanted before the start of the study. 'This study … leveraged DBS for its unique ability to record neural activity in the brain regions surrounding the stimulation lead,' Shaikh said. 'Using this capability, the researchers examined how exercise influences and potentially rewires brain function.' Scientists utilized an adaptive cycling program where over time, the bike 'learned' how each participant performed while biking. For example, while a game screen allowed participants to know their pedaling intensity, the bike would add or remove resistance depending on each rider's effort level. Measurable changes after 12 cycling sessionsAt the study's conclusion, Shaikh and his team found that after 12 cycling sessions, study participants demonstrated a measurable change in the brain signals involved with both motor control and movement. 'This finding provided proof of principle that exercise changes the brain. It further informed us that change only happens when exercise is done persistently, consistently, and over (a) long period of time. From the mechanistic standpoint it told us that drivers of such change may reside outside of basal ganglia — the key structure involved in Parkinson's disease.' — Aasef Shaikh MD, PhD'(The) main takeaway from the patients' perspective is that one has to keep (an) active lifestyle, constantly doing physical 'exercise' to keep up with Parkinson's disease,' Shaikh explained. 'Analogous to this is doing 'mental exercise' — which will help one stay mentally healthy and cognitively healthy. The take away from scientific and mechanistic standpoint is that exercise induced change (plasticity) happens, but the driver is outside of the basal ganglia. We have yet to determine that driver, but it could very well be (the) proprioceptive system and/or the cerebellum.' 'We would like to broaden this mechanistic investigation with more imaging and structure to function correlation tool sets available to us,' Shaikh added. 'We would also like to expand the effort, disseminating bike technology in multicenter trials. We would like to explore whether other exercise modalities have similar benefits.'How much does exercise affect Parkinson's?MNT spoke with Daniel H. Daneshvar, MD, PhD, chief of Brain Injury Rehabilitation at Mass General Brigham and associate professor at Harvard Medical School, about this study. Daneshvar commented that this was an encouraging and creative study that answers a critical question: to what extent does exercise result in actual changes in the brain in patients with Parkinson's disease? 'There's a robust body of literature that shows that exercise is the best intervention for individuals with Parkinson's disease, and I often tell my patients that if there were a pill that worked as well as exercise for Parkinson's disease, it'd be a billion dollar pill. However, we don't have a complete understanding of how exercise works on the brain.' — Daniel H. Daneshvar, MD, PhD'For patients, this is promising evidence that exercise can help re-engage parts of the brain affected by Parkinson's disease,' Daneshvar continued. 'That alignment between a practical therapy and circuit-level readouts is what makes this noteworthy for clinicians counseling patients about why exercise works so well, and is so important, for patients with Parkinson's disease.' Benefits of exercise have a long-term effectMNT also spoke with Samer Tabbal, MD, a neurologist and director of the movement disorders program at Baptist Health Miami Neuroscience Institute, part of Baptist Health South Florida, about this research. 'The motor benefit of exercise on patients with Parkinson's disease was demonstrated in multiple previous studies,' Tabbal commented. 'This study is a good attempt to explain how exercise provides such motor benefits by demonstrating how exercise changes the behavior of cells even in a damaged brain. The ability of the behavior of brain cells to change, including forming new connections, is referred to as neuroplasticity.' 'Of interest is the finding that dynamic cycling had no significant immediate effects on the outcome measures, but had definite long-term effects,' he continued. 'This may suggest that the benefit of exercise is a long-term goal and that patients should exercise with a long-term hope without expecting immediate benefits. This reminds me very much of how a long-term social relationship builds a solid, healthy friendship.' Tabbal said that knowledge is power, defined as the ability to change, and the more we know about how exercise improves brain function, the better we will be able to use exercise effectively to improve the symptoms of patients.'In the longer term, if we know how exercise improves brain function, we could find other means of achieving the same or even better benefit through other means, such as using medication, electric stimulation, magnetic stimulation, music, or light therapy,' he added.

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Breakthrough discovery could slow or reverse Parkinson's disease

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The Independent

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A low- oxygen environment similar to the air around Mount Everest 's base camp could be key to tackling and even reversing Parkinson's disease, a new study suggests. The research, published in the journal Nature Neuroscience, shows that faulty cellular processes in the brain cause a build-up of excess oxygen molecules, leading to Parkinson's symptoms. The excess oxygen appears to drive the breakdown of cells in the brain, suggesting that limiting oxygen intake could help slow or reverse symptoms, say researchers from Harvard Medical School. Parkinson's patients experience a progressive loss of neurons in the brain, leading to tremors and slowed movements, with the disease affecting over 10 million people worldwide. Neurons affected by Parkinson's also tend to accumulate toxic protein clumps called Lewy bodies, with some research suggesting that these clumps interfere with the function of mitochondria, the powerhouse of the cell, . Anecdotal case studies have shown that people with Parkinson's seem to fare better at high altitudes. 'Based on this evidence, we became very interested in the effect of hypoxia on Parkinson's disease,' said study author Fumito Ichinose. 'We first saw that low oxygen could alleviate brain-related symptoms in some rare diseases where mitochondria are affected, such as Leigh syndrome and Friedreich's ataxia... That raised the question: Could the same be true in more common neurodegenerative diseases like Parkinson's?' said Vamsi Mootha, another author of the study. In the research, scientists induced Parkinson's-like conditions in mice by injecting them with clumps of the α-synuclein proteins that seed the formation of Lewy bodies. They then split the mice into two groups – one breathing normal air with 21 per cent oxygen, and the other continuously housed in chambers with 11 per cent oxygen, comparable to living at an altitude of about 4,800 metres (16,000 ft). Researchers found that just three months after receiving the α-synuclein protein injections, mice breathing normal air had high levels of Lewy bodies, dead neurons, and severe movement problems. On the other hand, the mice kept in low-oxygen conditions didn't lose any neurons and showed no movement problems, despite developing Lewy bodies. The results show that while hypoxia couldn't stop the formation of Lewy bodies, it was protecting neurons from the damaging effects of these protein clumps. Researchers hope the findings could serve as a new way to interpret and treat Parkinson's without targeting α-synuclein or Lewy bodies. Scientists also found that the low-oxygen treatment still worked even when hypoxia was introduced six weeks after the injection, when symptoms were already appearing. After six weeks, the mice's motor skills rebounded, their anxiety-like behaviours faded, and the loss of neurons in the brain stopped, researchers found. When scientists analysed the brain cells of the mice, they discovered that mice with Parkinson's symptoms had much higher levels of oxygen in some parts of the brain than control mice and those that had breathed low-oxygen air. They suspect the excess oxygen likely resulted from mitochondrial dysfunction. With the damaged cell powerhouses unable to use oxygen efficiently, oxygen was building up to damaging levels, researchers say. 'Too much oxygen in the brain turns out to be toxic. By reducing the overall oxygen supply, we're cutting off the fuel for that damage,' Dr Mootha said. Scientists are working on 'hypoxia in a pill' drugs which mimic the effects of low oxygen to treat disorders stemming from mitochondrial dysfunction. But while the results are encouraging, researchers caution that more research is needed before the findings can be directly used to treat Parkinson's in humans. 'It may not be a treatment for all types of it's a powerful concept – one that might shift how we think about treating some of these diseases,' Dr Mootha said.

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