Parkinson's Insights

EP 41 - The Parkinson Weekly Helpdesk

🎙️ In Episode 41 of Parkinson Weekly, Prof. Bas Bloem opens the Helpdesk once again to answer questions submitted by listeners.In this fourth Helpdesk episode, Bas explores three very different but important topics. He begins with women and Parkinson’s, discussing the menstrual cycle, menopause, hormone replacement therapy and pregnancy, and why women with Parkinson’s may require more individualised approaches to care.He then looks at whether infections, stressful events or even mosquito bites could trigger Parkinson’s, explaining the difference between causing the disease and potentially unmasking symptoms that were already developing.Finally, Bas discusses delayed gastric emptying in Parkinson’s, how it can affect the absorption and reliability of oral medication, signs such as bloating and unpredictable medication response, and some of the approaches that may help manage it.Have a question you’d like Bas to answer in a future episode? Email us at parkinsonweekly@gmail.com – we’d love to hear from you.

EP 40 - A Faster Way to Find New Treatments for Parkinson’s?

In Episode 40 of Parkinson Weekly, Prof. Bas Bloem explores what he describes as one of the most exciting and encouraging developments in Parkinson’s clinical research: multi-arm, multi-stage (MAMS) clinical trial platforms.As our understanding of the biological processes underlying Parkinson’s disease continues to grow, so too does the number of potential treatments that could target these mechanisms and potentially slow disease progression. The challenge is how to test these promising therapies quickly, efficiently and reliably.Traditional clinical trials can take years, require large numbers of participants and often need a separate placebo group for every treatment being investigated. MAMS platforms offer a different approach, allowing several potential treatments to be tested simultaneously against a shared control group.Crucially, these platforms also incorporate planned interim analyses. Treatments showing little or no evidence of benefit can be stopped early and replaced by new candidates, while those showing promising signals can continue through the trial. The aim is to reduce costs, make better use of participants and, most importantly, identify promising therapies more quickly.Prof. Bloem discusses how this approach has already been successfully used in areas such as cancer and COVID-19, and looks at the growing international movement to bring the same model to neurological diseases.For Parkinson’s disease, he highlights the Edmond J. Safra Accelerating Clinical Trials in Parkinson’s Disease (EJS ACT-PD) platform in the UK, alongside similar initiatives emerging internationally. He also discusses some of the treatments being evaluated through these new trial approaches, including telmisartan, terazosin and UDCA.The episode also considers the challenges involved, from selecting appropriate placebo groups to identifying sensitive biomarkers that can provide an early indication of whether a treatment is working.While these platforms will not change clinical care tomorrow, Prof. Bloem explains why they represent genuine hope for the Parkinson’s community: a smarter, faster and more collaborative way of determining which potential treatments deserve to move forward.Could this new generation of clinical trials help accelerate the search for disease-modifying treatments in Parkinson’s?Have a question you’d like Bas to answer in a future episode? Email us at parkinsonweekly@gmail.com – we’d love to hear from you.

Could weight loss drugs also protect our brains? GLP-1 therapies, obesity and cognition. GLP-1 stands for glucagon-like peptide-1, a hormone that helps regulate blood sugar, appetite and metabolism. Drugs such as semaglutide mimic this hormone and are changing how we treat obesity and diabetes. But could they also change how we think, remember and age? Stina Börchers and colleagues describe in a new review in Science, part of the November 2026 special issue GLP-1 and Beyond, how obesity medications may influence cognition and brain health. The review explores whether these effects come from direct actions on brain circuits, improvements in metabolic health, or both. Key points: - GLP-1 therapies have been associated w/ lower rates of cognitive decline and dementia in some studies of folks w/ obesity and diabetes, but the evidence remains largely observational and results across clinical trials are mixed. - These medications may influence cognition through multiple pathways, including improved blood sugar regulation, vascular health, sleep and inflammation, as well as possible direct effects on brain cells and circuits. - Clinical trials in established Alzheimer's disease, including EVOKE and EVOKE+, have not demonstrated meaningful slowing of cognitive or functional decline, despite some encouraging changes in biomarkers. My take: This review resonated w/ me because it challenges us to think beyond weight loss and ask whether treating metabolic dysfunction could become part of our strategy for preserving brain health. The brain does not operate independently of the rest of the body. Obesity, diabetes, inflammation, vascular disease and sleep disorders all interact w/ brain function. However, we must resist the temptation to declare GLP-1 drugs the next breakthrough in dementia prevention before we have definitive evidence. The negative Alzheimer's trials are an important reminder that changing a biomarker is not the same as changing a patient's life.

When most people think of Huntington's disease, they picture chorea, the involuntary, dance-like movements that have become the hallmark of this condition. However, Huntington's is not simply a disease of too much movement. It is also a disease of too little movement, including bradykinesia (slowness), rigidity, impaired walking and difficulty initiating movements. This important new analysis from the PROOF-HD trial, published in Neurology, reminds us that suppressing chorea by reducing dopamine signaling may come at a price. Investigators examined patients in the placebo arm of the trial and found that those receiving antidopaminergic medications experienced greater worsening in functional capacity, cognition, overall motor performance and composite Huntington's disease scores compared with those not receiving these medications. Although chorea improved, other motor features, including bradykinesia, tended to worsen. Importantly, the associations were observed with both VMAT2 inhibitors, which reduce dopamine availability, and antipsychotics, which block dopamine receptors, with higher medication exposure also associated with greater decline. These findings do not prove that the drugs accelerate the underlying disease, since patients requiring treatment may already have more severe symptoms. My bottom line for clinicians is that treating Huntington's disease should never be reduced to treating chorea. The choice of medication, mechanism of dopamine suppression and dose all matter. We should use the lowest effective dose, reassess the need for treatment, and carefully monitor walking, swallowing, cognition, bradykinesia and everyday function. Our goal should not be simply to make the dancing stop. It should be to help the person with Huntington's disease function better and live better. https://www.neurology.org/doi/pdf/10.1212/WNL.0000000000218627