How walking poles can benefit those of us with Parkinson’s disease

Jun 16, 2026

Gut bacteria transplant may ease constipation in Parkinson’s

Jun 15, 2026

Evidence for motor and nonmotor benefits remains limited, researchers say

Written by Lila Levinson, PhD | June 10, 2026

• Fecal microbiota transplantation (FMT) shows promise for Parkinson’s-related constipation.
• FMT was generally safe and beneficial for gastrointestinal symptoms in people with Parkinson’s.
• Evidence for broader motor and nonmotor benefits is inconsistent, and more high-quality research is needed.

Fecal microbiota transplantation (FMT), a technique for replacing gut bacteria, may help with gastrointestinal symptoms of Parkinson’s disease, particularly constipation, according to a review study.

While the technique was found to be generally safe and beneficial for gastrointestinal symptoms in Parkinson’s disease, “at this stage, there is no convincing evidence that FMT produces a clinically relevant motor or non-motor symptomatic improvement on a group basis, at least in the short to medium term,” the researchers wrote.

Evidence on FMT remains limited

The researchers noted that available studies about FMT in Parkinson’s use a variety of different techniques, and many have methodological limitations. Future high-quality research could help clarify the potential benefits of FMT in this context.

The study, “Safety and efficacy of faecal microbiota transplantation in Parkinson’s disease,” was published in npj Parkinson’s Disease.

Parkinson’s is a neurological condition that leads to a variety of motor and nonmotor symptoms. Constipation and other gastrointestinal problems are among the possible nonmotor signs of the condition.

Parkinson’s and the digestive tract have a complex relationship. Not only can Parkinson’s cause gastrointestinal symptoms, but the bacteria and other microorganisms living in the intestines, collectively known as the gut microbiota, may influence certain disease processes. For example, the review noted that animal studies suggest that gut microbiota from people with Parkinson’s may promote inflammation and nerve degeneration.

These connections have led scientists to wonder whether altering the gut microbiota could be used as a treatment strategy for Parkinson’s. One way to do this is with FMT, which the researchers described as “an ultimate treatment for replacing the host microbiota with that of a healthy donor.”

There are several methods for performing FMT. Typically, they involve first collecting gut bacteria from donors’ stool. Patients receive the transplant as a capsule, an enema (a liquid placed into the rectum), or a procedure delivering the sample directly to the digestive system.

The team aimed to comprehensively examine existing research about FMT in Parkinson’s, which remains limited. “This review examines the current evidence on FMT in [Parkinson’s disease] concerning safety, efficacy, and microbiome changes, and analyses the data in the perspective of recommendations for future studies in this field,” they wrote.

Original Investigation 

Jun 12, 2026

Intermittent Theta-Burst Stimulation for Depressive Symptoms in Parkinson Disease

A Randomized Clinical Trial

JAMA Netw Open

Published Online: May 20, 2026

2026;9;(5):e2613580. doi:10.1001/jamanetworkopen.2026.13580

Miaomiao Hou, MD¹; Bingjie Tian, PhD²; Chen Qi, PhD¹ et al

Key Points

Question  Can the ultra-brief intermittent theta-burst stimulation (iTBS) protocol provide a time-efficient and effective alternative to standard high-frequency repetitive transcranial magnetic stimulation (HF-rTMS) for treating depressive symptoms in Parkinson disease (PD)?

Findings  In this randomized clinical trial including 54 patients with PD and depressive symptoms, both iTBS and HF-rTMS produced significant and comparable reductions in depressive symptoms compared with sham stimulation.

Meaning  This study suggests that the ultra-brief iTBS protocol achieved antidepressant efficacy comparable with that of standard HF-rTMS in PD while reducing treatment time, offering a pragmatic and patient-centered advancement for clinical management.

Importance  Depressive symptoms in patients with Parkinson disease (PD) are common and burdensome. High-frequency repetitive transcranial magnetic stimulation (HF-rTMS) targeting the left dorsolateral prefrontal cortex (DLPFC-L) is effective but time intensive, limiting practicality.

Objective  To evaluate the antidepressant efficacy and neurofunctional effects of the ultra-brief intermittent theta-burst stimulation (iTBS) protocol for patients with PD depression (PD-D) compared with active HF-rTMS and sham stimulation.

Design, Setting, and Participants  This triple-arm, randomized, sham-controlled single-center clinical trial was conducted at Xinhua Hospital, Shanghai Jiao Tong University School of Medicine in China from August 1, 2024, to January 31, 2025. Patients with PD aged 50 to 80 years with 24-item Hamilton Depression Rating Scale (HAMD-24) scores of 8 to 20 were randomized 1:1:1 to iTBS, HF-rTMS, or sham iTBS. Outcomes were assessed at baseline, week 1, week 2, and week 6. Data analysis was finalized in February 2026.

Interventions  Ten daily sessions over 2 weeks: active iTBS (3 minutes and 20 seconds), active HF-rTMS (20 minutes), or sham iTBS.

Main Outcomes and Measures  The primary outcome was the HAMD-24 score at week 2. Secondary outcomes included anxiety (measured by the 14-item Hamilton Anxiety Rating Scale [HAMA-14]), motor symptoms (measured by the Movement Disorder Society–Unified Parkinson Disease Rating Scale), quality of life (measured by the 8-item Parkinson’s Disease Questionnaire [PDQ-8]), and prefrontal hemodynamics (measured using functional near-infrared spectroscopy). Primary analysis followed the principle of intention to treat.

Results  Of 54 randomized participants (mean [SD] age, 70.1 [5.3] years; 29 men [53.7%]), 50 (92.6%) completed the trial. Linear mixed-effects models revealed a significant group × time interaction for the HAMD-24 (F_6,145 = 4.84; P < .001). At week 2, both active interventions were superior to sham (HAMD-24 score mean difference: iTBS, −4.97 [95% CI, −7.71 to −2.23]; P < .001; and HF-rTMS, −5.73 [95% CI, −8.95 to −2.51]; P < .001). Effects persisted at week 6 (HAMD-24 score mean difference: iTBS vs sham, −6.05 [95% CI, −9.26 to −2.83]; P < .001; and HF-rTMS vs sham, −5.57 [95% CI, −9.36 to −1.78]; P = .002), with no between-group differences. Both interventions improved PDQ-8 scores at week 2 (mean difference: iTBS vs sham, −2.33 [95% CI, −3.33 to −1.33]; P < .001; and HF-rTMS vs sham, −2.43 [95% CI, −4.60 to −0.26]; P = .02). iTBS also alleviated anxiety (mean difference: HAMA-14 score vs sham, −4.04 [95% CI, −7.73 to −0.35; P = .03). Active stimulations increased DLPFC-L activation (estimated adjusted difference: iTBS vs sham, 151.18 [95% CI, 51.24-251.11]; P = .004; and HF-rTMS vs sham, 173.26 [95% CI, 71.92-274.60]; P = .001) and reduced time in low-efficiency connectivity states (iTBS: median change, −0.12 [IQR, −0.29 to 0.02]; false discovery rate–corrected P = .045; and HF-rTMS: −0.12 [IQR, −0.32 to 0]; false discovery rate–corrected P = .02).

Conclusions and Relevance  In this randomized clinical trial of patients with PD-D, the ultra-brief iTBS achieved antidepressant efficacy comparable with that of standard HF-rTMS while markedly reducing treatment time, supporting its use as a pragmatic therapy for PD-D. This study suggests the promise of symptom-stratified neuromodulation for personalized treatment protocols.

Trial Registration  Chinese Clinical Trial Registry Identifier: ChiCTR2100044421

Introduction

Depressive symptoms affect 20% to 50%¹ of patients with Parkinson disease (PD), worsening quality of life, motor function, and cognitive trajectory.² Although selective serotonin reuptake inhibitors are first-line pharmacotherapy, their adverse effects (eg, nausea and headache) often limit tolerability.^3,4 High-frequency repetitive transcranial magnetic stimulation (HF-rTMS) over the left dorsolateral prefrontal cortex (DLPFC-L) offers an effective alternative with guideline support.^5-7 However, the standard 20-minute session duration of HF-rTMS poses a practical barrier for patients with PD, who frequently contend with complex medication regimens, mobility challenges, and time-intensive care schedules.

Intermittent theta-burst stimulation (iTBS) condenses therapeutic stimulation into an ultra-brief 3-minute session while using potent plasticity mechanisms.⁸ Although iTBS has demonstrated efficacy comparable with that of HF-rTMS in major depressive disorder,⁹ its use for PD depression (PD-D) remains unknown.

Therefore, we conducted this 3-arm, randomized, sham-controlled clinical trial to evaluate the clinical use of iTBS for PD-D. We aimed to determine whether the ultra-brief iTBS protocol could achieve antidepressant efficacy comparable with that of the standard HF-rTMS and to examine the underlying neural mechanisms. Using functional near-infrared spectroscopy (fNIRS) during a verbal fluency task (VFT),¹⁰ we measured prefrontal cortical activation via oxygenated hemoglobin (HbO) concentration changes, and we complemented this with dynamic functional connectivity analysis to capture temporal network dynamics. We hypothesized that both active interventions would be superior to sham stimulation in alleviating depressive symptoms and that the clinical response to iTBS would be underpinned by measurable modulation of prefrontal network dynamics. Confirmation of these hypotheses would position iTBS as a pragmatic, patient-centered advancement in the management of PD-D.

Methods

Study Design

This double-blind, 3-arm, randomized, sham-controlled clinical trial compared iTBS, HF-rTMS, and sham stimulation for PD-D (trial protocol in Supplement 1). The protocol consisted of 10 daily sessions over 2 consecutive weeks, with clinical assessments at baseline, on the day of session 5 (week 1) and session 10 (week 2), as well as 4 weeks after session 10 ended (week 6) (eFigure 1A in Supplement 2). This study was conducted at Xinhua Hospital affiliated with Shanghai Jiao Tong University School of Medicine in China from August 1, 2024, to January 31, 2025. The Ethics Committee of Xinhua Hospital affiliated with Shanghai Jiao Tong University School of Medicine approved the experiments, and written informed consent was obtained from all the participants. The study protocol was preregistered with the Chinese Clinical Trial Register (ChiCTR2100044421). This 3-arm, randomized, sham-controlled clinical trial followed the Consolidated Standards of Reporting Trials (CONSORT) reporting guideline.

Gene therapy strategy may ease Parkinson’s disease dyskinesia

Jun 11, 2026

Mouse study targets GluN2B receptor subunit in movement-control neurons

Written by Marisa Wexler, MS | June 8, 2026

• Many people with Parkinson’s disease develop dyskinesia, or uncontrolled movements, after long-term levodopa treatment.
• In a mouse model, dyskinesia was linked to abnormal levels of the GluN2B receptor subunit in specific movement-control neurons.
• An experimental gene therapy strategy that reduced GluN2B levels in mice prevented and eased dyskinesia without reducing levodopa’s benefits.

Levodopa, a standard treatment for Parkinson’s disease, can cause uncontrolled movements called dyskinesia — and this side effect may be driven by changes in a specific receptor component in certain brain cells, a new study shows.

Scientists found that an experimental gene therapy strategy aimed at decreasing levels of this receptor component in those specific brain cells could blunt dyskinesia’s development and substantially ease established dyskinesia in a mouse model.

“This is a way that we might be able to control dyskinesia with a completely novel strategy,” D. James Surmeier, PhD, senior author of the study at Northwestern University, said in a university news story. “Nearly 80 percent of Parkinson’s disease patients will develop dyskinesia. At present, we have a very limited set of tools to help these patients right now. This work points to the possibility of a non-invasive gene therapy that would be transformative.”

The study, “Cell- and state-specific plasticity of striatal glutamatergic synapses is critical to the expression of levodopa-induced dyskinesia,” was published in Neuron.

Levodopa treatment can trigger dyskinesia

Parkinson’s is a neurological disorder marked by the degeneration and death of brain cells that make dopamine, a signaling molecule that’s key for coordinating movements. Low dopamine levels ultimately drive Parkinson’s symptoms.

Levodopa and its derivatives primarily work by being converted into dopamine in the brain. These medications have for decades been a gold standard of Parkinson’s treatment, and they can be highly effective for easing disease symptoms — but as with any medical treatment, levodopa can cause side effects. In particular, many people who take levodopa long term develop dyskinesia, defined by jerky, uncontrollable movements.

Although it’s well-established that levodopa can trigger dyskinesia, the precise molecular mechanisms by which this drug causes this side effect have been obscure.

Working in a mouse model, researchers found that repeated levodopa treatment that induced dyskinesia led to molecular abnormalities in a subset of brain cells called indirect pathway spiny projection neurons, or iSPNs. Under normal circumstances, these nerve cells are thought to help the brain prevent unwanted movements.

The researchers specifically found that dyskinesia was linked to increased levels of N-methyl-D-aspartate (NMDA) receptors containing a specific subunit called GluN2B in iSPNs. NMDA receptors normally help nerve cells communicate with each other, but changes in these receptors can disrupt nerve-to-nerve communication.

“Connections between neurons dictate when they become active and how they perform their duties in controlling movement. In late-stage [Parkinson’s] patients, levodopa begins to ‘scramble’ these connections, which we think leads to uncontrolled movement or dyskinesia,” Surmeier said. “When we induce dyskinesia, we see this change in NMDA receptors in this subset of striatal neurons thought to be responsible for suppression of unwanted movement.”

Can You Drive If You Have Parkinson’s?

Jun 10, 2026

Medically reviewed by Meredith Goodwin, MD, FAAFP — Written by The Healthline Editorial Team — Updated on June 16, 2025

Key takeaways

• Parkinson’s disease can impair driving ability due to its effects on vision, motor function, memory, and spatial awareness, though the degree and timing vary for each individual.
• People with Parkinson’s can remain safe while driving by managing their symptoms, getting regular evaluations, and making certain adjustments to their driving habits.
• Even if driving is no longer an option, individuals with Parkinson’s can maintain independence through alternative transportation and support services.

Parkinson’s disease is a central nervous system disorder that causes certain cells in your brain to decline over time. This can affect your movement, reaction times, memory, and visual-spatial perception. It may also lead to dementia.

All of these challenges can interfere with a person’s ability to drive.

Yet it may take many months or years after diagnosis for Parkinson’s to interfere with activities of daily living, including the ability to drive a vehicle.

It’s important to know when driving will become a concern and what you can do once it’s no longer safe to get behind the wheel.

How does Parkinson’s affect your driving?

There is no one-size-fits-all answer for how long you can drive with Parkinson’s or how your condition is affecting your driving now. Many people can drive long after they first receive a diagnosis, while others will need to stop driving sooner.

It depends on:

• the person
• progression of the disease
• how severe the symptoms are

Some Parkinson’s symptoms that specifically interfere with safe driving may include:

• tremors, or uncontrollable shaking, in the hands and arms
• lack of coordination
• decreased reaction times
• attention deficits
• visual impairment
• muscle stiffness
• daytime sleepiness, often due to nighttime sleeping issues
• drowsiness, dizziness, or blurred vision resulting from Parkinson’s medications

Driving may be riskier than it might seem, because your symptoms may become more or less severe depending on the particular day.

Even the earliest stages of Parkinson’s can affect a person’s driving.

That said, people who aren’t experiencing cognitive impairments (such as vision changes or visuospatial processing issues) might be able to drive for many years.

A 2018 review of studies found that in 50 studies, people with Parkinson’s were 6 times more likely to fail an on-the-road driving test compared with people who did not have the condition. Those with Parkinson’s were also more than 2 1/2 times as likely to crash in a simulated test.