Parkinson's Insights

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.

EP 39 - Can Blue Light Therapy Improve Sleep in Parkinson’s Disease?

🎙️ We’re back with the 39th episode of Parkinson Weekly, hosted by Prof. Bas Bloem - on this week’s episode, Prof. Bas Bloem explores an intriguing new approach to one of the most common challenges faced by people with Parkinson’s disease: poor sleep.Could something as simple as blue light therapy make a difference?Prof. Bloem discusses a recent placebo-controlled study investigating blue light delivered through specially designed glasses in people with Parkinson’s experiencing sleep problems. Participants received either blue or red light therapy for two weeks, with the results showing a significantly greater improvement in sleep quality and daytime sleepiness among those receiving blue light.In this episode, Prof. Bloem explores:Why blue light may help regulate the body’s biological clock and sleep–wake cycleThe improvements seen in sleep quality and daytime sleepinessWhy the lack of improvement in motor symptoms may actually strengthen the findingsThe potential for blue light therapy as an easy, home-based interventionWhy larger and longer Phase III studies are still needed before it can become an established treatmentWhile the study involved only 30 participants and further research is required, the findings offer an encouraging glimpse at a potentially safe, non-invasive way of improving sleep for people living with Parkinson’s disease.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.

What resonates most with me about Carey Gillam’s deeply reported piece is not simply the continuing concern about paraquat and Parkinson’s disease, but the question of whether our regulatory system has been working with the full deck of cards. Newly released internal records described by Gillam indicate that Syngenta possessed information on worker exposure, skin and clothing penetration, surfactants, and potential effects on the brain that was not provided to the EPA; Syngenta disputes that it withheld information it was required to disclose and continues to dispute a causal link between paraquat and Parkinson’s. As a Parkinson’s neurologist, this is what keeps me up at night: if a chemical may contribute to a disease that is largely incurable, progressive and increasingly common, shouldn't we demand complete transparency and independent science before exposing another generation? More than 70 countries have banned paraquat, while it remains available for restricted use in the United States. Prevent the preventable. We need the data, we need transparency, and we need to put people and brain health first. https://www.thenewlede.org/2026/09/syngentas-secrets-paraquat-pesticide/

Could the human brain begin as two different developmental programs? And what could this mean for Parkinson’s, Alzheimer’s and ALS? Neural ectoderm progenitors are very early cells that ultimately give rise to the brain. Jokhai, Dundes and colleagues describe in a new paper in Nature Neuroscience evidence challenging the traditional idea that the entire brain emerges from one common neural progenitor. Instead, their mouse lineage-tracing and human pluripotent stem cell experiments support two parallel progenitors; an anterior lineage committed to forebrain/midbrain and a posterior lineage committed to hindbrain. They also generated hindbrain motor neurons that have previously been difficult to produce in the laboratory. Key points: - Two distinct neural ectoderm progenitors emerged during very early development, one destined largely for forebrain/midbrain and the other for hindbrain. - These developmental identities appeared remarkably early and were supported by distinct gene regulatory and chromatin programs. - Mapping the hindbrain pathway enabled the investigators to generate specific human hindbrain motor neurons from pluripotent stem cells, opening an important experimental door for studying diseases affecting these neurons. My take: This paper made me rethink something very basic; perhaps we should not always think of the brain as one organ following one developmental roadmap. Why does this matter for neurodegeneration? Parkinson’s, Alzheimer’s and ALS attack different populations of neurons and different brain regions, and understanding how these cells acquired their identities in the first place may help us understand their selective vulnerability later in life. For ALS the connection is particularly intriguing because degeneration of hindbrain motor neurons contributes to swallowing and other bulbar problems. For Parkinson’s and Alzheimer’s, the implications are more indirect, but this developmental roadmap could help us build better disease models and ultimately generate more precisely specified cells for studying degeneration and testing therapies. https://www.nature.com/articles/s41593-026-02433-7