Fighting Parkinson’s Disease with Exercise and Diet

Johns Hopkins Medicine

Doing your best to remain healthy and strong is key for everyone with Parkinson’s disease. Research has shown that following certain lifestyle modifications can help you accomplish two important goals:

  • Better control symptoms.
  • Slow progression of the condition.

Diet modifications and a focus on exercise can:

  • Keep you healthier longer.
  • Help you avoid secondary symptoms of Parkinson’s, like constipation.
  • Improve mobility and balance.
  • Enhance your overall quality of life.

The Role of Diet

Following a balanced diet improves general well-being and boosts your ability to deal with symptoms of the disease. Eating plenty of whole foods, such as fruits and vegetables, lean protein, beans and legumes, and whole grains, and staying hydrated are key ways to stay energized and healthy overall. That said, you should be aware of some special considerations.

  • Constipation: Many patients with Parkinson’s disease experience constipation due to a slowdown of the digestive system. At best, constipation is an annoyance, but at worst, your large intestine can become impacted. Combat constipation with a diet rich in fiber from sources such as fresh fruits and vegetables, whole grains, vegetables, legumes, and whole-grain breads and cereals. Drinking plenty of fluids and exercising can also help you avoid constipation.
  • Dehydration: Medications that treat Parkinson’s disease can dry you out. Not only can dehydration leave you more tired, over time, it can also lead to confusion, balance issues, weakness and kidney problems. Be sure to drink plenty of water and other fluids throughout the day.
  • Medication interaction: The drug most commonly used to treat Parkinson’s disease, carbidopa-levodopa, is absorbed in your small intestine. That absorption can be disrupted if you take your medication shortly after eating a high-protein meal, since it involves the same process. To help maximize the medication’s effects, eat high-protein foods at other times of the day. If you take your medicine in the morning, have oatmeal rather than high-protein eggs for breakfast, and save your protein intake for later in the day.

Study shows Parkinson’s affects brain circuits in different ways

Low dopamine levels can produce opposite changes

Written by Marisa Horak, MS | July 31, 2026

  • Parkinson's disease causes varied, even opposite, changes in brain circuits due to low dopamine levels.
  • Low dopamine levels correlate with motor symptoms; cognitive issues are linked to abnormalities in brain circuits.
  • Monitoring brain circuit activity may help track cognitive problems and treatment response.

Low dopamine levels disrupt nerve circuits in the brain in Parkinson’s disease — but a new study indicates that different brain circuits show different, even opposite, types of changes.

The study’s findings shed new light on how brain circuits are affected by Parkinson’s. The researchers said their data also suggest that looking at brain circuits may be a useful way to monitor certain Parkinson’s symptoms, particularly problems with cognition.

The study, “Dopamine-related alterations in functional brain network dynamic reconfiguration in Parkinson’s disease,” was published in npj Parkinson’s Disease.

Dopamine is a neurotransmitter, a signaling molecule that nerve cells in the brain use to communicate with each other. In Parkinson’s, the brain cells that are normally responsible for producing dopamine sicken and die, resulting in abnormally low dopamine levels.

Low dopamine levels in the brain disrupt neurological signaling, which ultimately gives rise to Parkinson’s symptoms. While this paradigm is well established, scientists don’t fully understand how low dopamine affects all the various neurological circuits throughout the brain.

FDA backs faster development path for Parkinson’s cell therapy

Sasineprocel gets regenerative medicine advanced therapy designation

Written by Marisa Horak, MS | Aug. 3, 2026

  • FDA granted RMAT designation to sasineprocel, a cell therapy for Parkinson's disease.
  • This therapy uses engineered stem cells to replace lost dopaminergic neurons.
  • Early trial data indicates sasineprocel is safe, improving patient function and quality of life.

The U.S. Food and Drug Administration (FDA) has granted regenerative medicine advanced therapy (RMAT) designation to sasineprocel (ANPD001), an experimental cell therapy to treat Parkinson’s disease.

The designation, given to promising regenerative therapies (treatments that aim to replace or restore disease-damaged tissue) that could substantially improve care for serious diseases, provides developer Aspen Neuroscience with perks such as more intensive FDA guidance.

“This significant milestone highlights the transformative nature of sasineprocel as a potentially disease-modifying therapy for patients facing a serious disease with substantial unmet medical need,” Damien McDevitt, PhD, president and CEO of Aspen, said in a company press release. “We stand with the Parkinson’s community realizing the urgency around the serious and growing unmet need in [Parkinson’s] and are unwavering in our commitment to bring sasineprocel to patients as soon as possible.”

The Power of UConn Collaborating for Parkinson’s Disease Patients

July 29, 2026 | Lauren Woods

UConn Health Parkinson's disease patients like Jose Figueroa are experiencing the power of a UConn-made protein shake being tested by the UConn research team in an FDA clinical study.

Jose Figueroa, 66, of New Britain is “so grateful” for UConn and its powerful cross-campus collaboration helping improve the health and quality of life of Parkinson’s disease patients just like him.

Figueroa has been battling Parkinson’s disease for 16 years since being diagnosed in 2012 following his visit to the Emergency Department when a provider noticed his legs and arms were continuously shaking. He is a longtime patient at UConn Health and now its Brain and Spine Institute with Dr. Bernardo Rodrigues.

“Dr. Rodrigues is excellent. Anytime there is a new program or resource for Parkinson’s patients he always tells us,” says Figueroa. “It has helped so much.”

His wife also sees a big difference in the last year.

“Jose’s Parkinson’s used to be like an Earthquake,” says his wife, Emily. “But now there has been a big improvement. He no longer needs to use a cane to walk.”

His successful progress is all thanks to a UConn cross-campus collaboration to advance research between the Brain and Spine Institute’s faculty like Rodrigues at UConn School of Medicine with the researchers of UConn Storrs’ Department of Kinesiology and its dedicated Movement for Life Lab.

Just a year ago Figueroa started participating in an initial, three-week nutritional supplement study beginning to test the benefits of consuming a targeted, amino-acid protein shake developed by the Storrs research team led by Dr. Jacob Earp and Dr. C. Colon-Semenza. Their goal was to find a new way to assist PD patients like Figueroa by using a nutritional supplement designed specifically for those with Parkinson’s disease that is intended to be easier to consume than conventional supplements, reduce inflammation, and provide nutrients that support an active lifestyle.

“I felt really good while taking the shake. I definitely had more energy,” reports Figueroa. “A healthy shake can feel better than medicine. I would still take the shake if it was still available to me,” says Figueroa who also has learned the true benefits of not only the shake but adding daily exercise too.

Turmeric compound may protect motor function in Parkinson’s mouse model

Preclinical study links curcumin’s effects to cellular recycling pathways

Written by Marisa Horak, MS | Aug. 4, 2026

  • Curcumin pretreatment helped protect motor function in a Parkinson’s mouse model.
  • It activated autophagy and reduced cuproptosis, a copper-dependent form of cell death.
  • The findings point to curcumin, autophagy, and cuproptosis as possible targets for further Parkinson’s research.

Pretreatment with curcumin, a compound found in the spice turmeric, helped protect motor function in a mouse model of Parkinson’s disease, a new study found.

Findings suggest that curcumin helped protect dopamine-producing nerve cells by activating autophagy, a process cells use to recycle unneeded material. This cellular recycling process, in turn, appeared to reduce cuproptosis, a copper-dependent form of regulated cell death. The researchers proposed that these biological pathways might be useful targets for new Parkinson’s treatments.

The study, “Curcumin Attenuates Cuproptosis via Activating Autophagy Through Inhibition of the AKT/mTOR/P70S6K-Signaling Pathway in Parkinson’s Disease Models,” was published in Molecular Neurobiology. 

Turmeric compound studied as a possible Parkinson’s therapy

Parkinson’s is a neurological disease characterized by the progressive loss of brain cells that produce dopamine, a chemical messenger involved in movement. The loss of these dopamine-producing cells disrupts normal nerve signaling in the brain, ultimately leading to disease symptoms.

Turmeric is an herb native to southern Asia that is widely used in food and has been used for millennia in Ayurvedic medicine, a traditional medical system that originated in India. One of turmeric’s main compounds is the antioxidant curcumin, which is largely responsible for the spice’s characteristic bright-yellow color.

There is no conclusive evidence that curcumin benefits people with Parkinson’s disease. However, because of its historical use in traditional medicine and antioxidant properties, researchers have been studying whether this naturally occurring compound could help treat Parkinson’s.

In this study, scientists at Taihe Hospital in China conducted a series of tests in a mouse model in which Parkinson’s-like symptoms are triggered by exposure to the chemical MPTP, which is toxic to dopamine-producing brain cells. MPTP exposure causes mice to lose weight and develop motor problems that resemble some features of Parkinson’s disease.

The researchers found that mice given curcumin before each MPTP exposure lost less weight and performed better on tests of motor function than mice given MPTP without curcumin pretreatment.