Prof Michael Okun: My Take
Ebola survivors may carry neurological scars for years after the infection is gone. Neurological sequelae are long-lasting brain, nerve, thinking, mood, sleep, or movement symptoms that persist after recovery from an illness. Bridgette Billioux and colleagues describe in a new paper in JAMA Neurology the neurological manifestations observed in adult survivors of Ebola virus disease followed for more than 7 years in Liberia. Key points: - Ebola survivors experienced a broad range of neurological symptoms including headaches, memory loss, depression, sleep disturbances, fatigue, tremor, sensory symptoms, and sexual dysfunction. - Neurological abnormalities involving cranial nerves, sensation, movement, coordination, and cognition were detected on detailed examinations performed by trained neurologists. - Most neurological symptoms improved over time, however memory loss, irritability, and trouble concentrating remained significantly more common in survivors more than 7 years after infection. My take: This study is a reminder that viruses can leave a lasting imprint on the brain and nervous system. Ebola is frequently viewed through the lens of survival from an acute infection, however the story does not end when the virus clears. The long-term neurological burden can affect quality of life, relationships, employment, and overall well-being for years. Here are 5 points that resonated w/ me: 1- The brain appears to be a major target of Ebola virus disease, and the neurological consequences can persist for many years. 2- Memory loss was one of the most common and durable symptoms, affecting more than half of survivors at long-term follow-up. 3- Sleep disturbances, depression, fatigue, and cognitive symptoms frequently traveled together, reinforcing the interconnected nature of brain health. 4- The encouraging news is that many neurological symptoms and examination findings improved over time, suggesting resilience and recovery are possible. 5- Survivors of major infectious diseases deserve long-term neurological follow-up and access to rehabilitation, mental health support, and cognitive care. https://jamanetwork.com/journals/jamaneurology/fullarticle/2850237 #ebola
Childhood brain development may be shaped more by neighborhood opportunity than IQ. Socioeconomics refers to the social and economic conditions in which a person lives, including factors such as neighborhood opportunity, income, education, housing, and access to resources. Marek, Dosenbach and colleagues describe in a new paper in Science how socioeconomic factors may be the strongest predictors of brain organization in childhood, even exceeding measures such as IQ and psychopathology. Key points: - Across 649 behavioral, environmental, and demographic variables, socioeconomic measures showed the strongest and most reproducible associations w/ brain structure and function. - The strongest single brain association was linked to neighborhood opportunity, and these patterns were concentrated in motor and sensory brain regions rather than classic higher-order cognitive networks. - Brain patterns associated w/ socioeconomic status closely mirrored patterns linked to sleep, stress, arousal, and norepinephrine signaling, suggesting that environmental factors may influence brain development through these pathways. My take: This is a provocative and potentially paradigm-shifting study. For years, many brain-wide association studies have focused on IQ, cognition, or psychiatric symptoms. Marek and colleagues argue that socioeconomic conditions may be the dominant signal shaping childhood brain organization. The findings suggest that what we frequently attribute to cognition may partly reflect the cumulative effects of sleep, stress, opportunity, and environment. If these observations hold up, then improving childhood environments may be one of the most powerful brain health interventions available. Here are 5 points that resonated w/ me: 1- Neighborhood opportunity showed stronger brain associations than IQ, psychopathology, or most other measured variables. 2- The affected brain regions were primarily motor and sensory networks, not the classic frontal and parietal regions typically linked to higher-order cognition. 3- Sleep and stress emerged as plausible biological pathways connecting socioeconomic conditions to brain development.
The UF and UCSF east-coast and west coast collaboration has been meeting in Colorado Springs to create impact for persons with Spinocerebellar Ataxia Type 6. Spoiler alert: adaptive DBS system! Thanks to the Raynor Cerebellar Project.
When tremor comes back after focused ultrasound: should you re-lesion or switch to DBS? Focused ultrasound thalamotomy creates a small lesion in a brain target involved in tremor control. Deep brain stimulation (DBS) uses an implanted electrode to deliver adjustable electrical stimulation to the same brain network. Nur Walker-Pizarro and colleagues describe in a new paper in Tremor and Other Hyperkinetic Movements how DBS can successfully rescue recurrent essential tremor following MRI-guided focused ultrasound thalamotomy. Key points: - Tremor recurrence after focused ultrasound does not necessarily mean the original procedure failed; it may reflect progression of a chronic neurological condition. - In this case, staged bilateral VIM DBS provided durable tremor control after tremor returned following an initially successful focused ultrasound procedure. - Therapeutic DBS stimulation was achieved even within a previously lesioned thalamic target, suggesting that focused ultrasound and DBS may complement one another over time. My take: This paper highlights an important reality. Essential tremor is a progressive disease, and no single intervention is likely to be the final chapter for every patient. Focused ultrasound and DBS should not be viewed as competing therapies. They may be different tools that can be deployed at different times in a person's journey. The ability to adjust DBS over time remains one of its greatest strengths, especially when symptoms evolve. I am biased as an author of this paper, so read for yourself and decide. Here are 5 points that resonated w/ me: 1- Tremor recurrence after focused ultrasound occurs in a subset of patients and should trigger a thoughtful reassessment rather than an automatic repeat procedure. 2- Essential tremor frequently progresses over time, and treatment plans should anticipate future needs. 3- DBS offers flexibility because stimulation can be adjusted as symptoms change. 4- Prior focused ultrasound does not necessarily prevent successful DBS therapy later in the disease course. 5- The future will likely be personalized, matching the right surgical approach to the right patient at the right stage of disease.
The Parkinson’s Plan is now available in Spanish. El plan para vivir con la enfermedad de Parkinson: Un nuevo enfoque para prevenirla y tratarla by RAY DORSEY, MICHAEL S. OKUN En esta obra, Ray Dorsey y Michael S. Okun, doctores y expertos en los últimos avances sobre la enfermedad de Parkinson, detallan los pasos necesarios para prevenir, ralentizar y tratar esta condición debilitante. Los autores exponen cómo prevenir la enfermedad a través de los alimentos que ingerimos, el agua que bebemos, el aire que respiramos y el estilo de vida que llevamos. Asimismo, nos presentan el Parkinson 25, la lista más detallada que existe para que cualquier persona pueda reducir el riesgo de padecerla. Los autores han entrevistado a los científicos, médicos y referentes en esta patología para ofrecer un plan detallado que incluye métodos innovadores y los más recientes avances médicos y tecnológicos. Una hoja de ruta con las estrategias necesarias para crear un mundo en el que esta enfermedad sea cada vez menos frecuente y los tratamientos más exitosos. https://cutt.ly/Xt2esco3
Can sitting too much change how you perceive your balance in Parkinson’s disease? Spoiler alert: Some folks underestimate their abilities and restrict activity, while others may overestimate their abilities and increase fall risk. Balance discordance refers to a mismatch between ‘how good’ folks think their balance is and ‘how good’ their balance actually is. Franziska Albrecht and colleagues describe in a new paper in npj Parkinson’s Disease how sedentary behavior may influence the effect of balance rehabilitation on balance discordance in Parkinson’s disease. Key points: - A highly challenging balance and gait training program improved balance performance however did not significantly change balance discordance across the entire study group. - Folks who were more sedentary before rehabilitation appeared more likely to improve the alignment between their perceived and actual balance abilities. - The findings suggest that physical rehabilitation alone may not be enough to recalibrate balance confidence and that psychological factors may also play an important role. My take: This paper reminds us that balance is not just about muscles and movement. It is also about perception. Some folks underestimate their abilities and restrict activity, while others may overestimate their abilities and increase fall risk. The future may require combining physical therapy, behavioral approaches and confidence building strategies to better align what the brain believes and what the body can do. Here are 5 points that resonated w/ me: 1- Parkinson’s disease can create a mismatch between actual balance ability and perceived balance confidence. 2- Simply improving physical performance may not automatically improve confidence or self-perception. 3- Sedentary individuals may have more room to recalibrate their understanding of their own abilities when exposed to challenging rehabilitation. 4- Fear of falling, anxiety and mood symptoms may influence balance confidence just as much as physical impairments. 5- The best rehabilitation programs of the future may target both the body and the brain by combining movement training w/ psychological strategies. https://www.nature.com/articles/
Can healthy eating prevent Parkinson's disease? A new 32-year study challenges assumptions. A dietary pattern is the overall way we eat, including combinations of foods such as fruits, vegetables, grains, dairy products and proteins rather than focusing on a single nutrient. Xiao Chen and colleagues describe in a new paper in Movement Disorders whether adherence to eight healthy dietary patterns influences the risk of developing Parkinson's disease. Key points: - Over 116,000 women and men were followed for up to 32 years and 1,179 participants developed Parkinson's disease. - Higher adherence to eight commonly recommended healthy dietary patterns, including Mediterranean, DASH, MIND and plant-based diets was NOT associated w/ a lower risk of Parkinson's disease. - Higher consumption of low-fat dairy products was associated w/ a higher risk of Parkinson's disease in this analysis. My take: This study is important because it is large, carefully performed and followed folks for more than three decades. The findings remind us that what is good for general health may not always translate into Parkinson's disease prevention. Healthy eating remains essential, however this study suggests we should be cautious about claiming that any specific dietary pattern prevents Parkinson's disease. The low-fat dairy signal is intriguing and deserves further study. Here are 5 points that resonated w/ me: 1- Healthy dietary patterns remain important because they lower the risk of many chronic diseases and support healthy aging. 2- Preventing Parkinson's disease is likely more complicated than following any single dietary strategy. 3- Environmental exposures, genetics and other biological factors may play a larger role in Parkinson's disease risk than previously appreciated. 4- The association between low-fat dairy intake and Parkinson's disease continues to appear across multiple studies and deserves closer investigation. 5- The future of Parkinson's prevention will likely require combining nutrition, environmental risk reduction, genetics and biomarker science into a more comprehensive strategy. https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.70358
Can we measure Parkinson's disease progression years before diagnosis? An ‘alpha-synucleinopathy’ is a brain disease linked to abnormal accumulation of the protein alpha-synuclein and includes Parkinson's disease, dementia w/ Lewy bodies and multiple system atrophy. Monica Roascio and colleagues describe in a new paper in Brain how clinical changes in REM sleep behavior disorder (RBD) may be tracked years before the emergence of overt Parkinson's disease or dementia. Key points: - Using longitudinal data from 766 individuals w/ isolated REM sleep behavior disorder, the authors developed a model that tracks disease progression over time rather than relying on a single conversion event. - The model identified three markers reflecting earlier or later onset of progression, faster or slower progression, and whether motor or cognitive symptoms emerge first. - These progression markers were linked to established dopamine imaging biomarkers and to EEG measures of brain network dysfunction. My take: This study tackles one of the biggest challenges in neurodegeneration. We need better ways to measure progression before a person develops obvious Parkinson's disease or dementia. The traditional approach of waiting for ‘phenoconversion’ may miss many years of meaningful biological and clinical change. Continuous progression markers could ultimately improve clinical trials and help us identify who is worsening and when. Here are 5 points that resonated w/ me: 1- REM sleep behavior disorder remains one of the strongest known risk states for future Parkinson's disease and related disorders. 2- Motor changes appeared to worsen approximately 35% faster than cognitive changes in this cohort. 3- Clinical progression could be detected many years before traditional diagnostic milestones were reached. 4- Abnormal dopamine transporter imaging and abnormal EEG synchronization were linked to earlier and faster disease progression. 5- The future of disease-modifying trials may depend on continuous progression markers rather than waiting for a binary diagnosis of Parkinson's disease or dementia. https://academic.oup.com/brain/advance-article/doi/10.1093/brain/awag193/8698219
Can fecal microbiota transplantation overcome antibiotic resistant superbugs? Spoiler alert: Not in this study. Fecal microbiota transplantation (FMT) is the transfer of healthy gut microbes from a donor to a recipient in an effort to restore a healthier microbial ecosystem. Narang and colleagues describe in a new paper in JAMA Internal Medicine whether a single FMT treatment could eliminate multidrug-resistant organisms (MDROs) from the gut in folks w/ gastrointestinal diseases. Key Points: - A single FMT treatment did not significantly improve elimination of multidrug-resistant organisms compared to a sham procedure. - FMT increased gut microbial diversity and enriched bacteria that produce beneficial short-chain fatty acids. - FMT appeared safe and was associated w/ only modest and transient changes in gut viruses and fungi. My take: This is an important reminder that changing the gut microbiome is more complicated than simply adding healthy bacteria. The study did not achieve its primary goal, however it showed that FMT can reshape the microbial ecosystem in potentially beneficial ways. The findings raise an important question: will future strategies require multiple FMT treatments, better donor matching, targeted microbial therapies, or combinations of approaches to successfully combat antibiotic resistance? Here are 5 points that resonated w/ me: 1- Antibiotic resistant bacteria living in the gut are a major global health challenge and increase the risk of serious infections. 2- A negative study is still valuable because it helps define what does and does not work. 3- FMT successfully changed the gut microbial community even when it did not eliminate resistant organisms. 4- Bacteria that produce short-chain fatty acids increased after FMT, suggesting potential benefits for gut health and resilience. 5- The future may involve precision microbiome therapies designed to restore healthy microbial ecosystems and reduce antibiotic resistance more effectively than current approaches.
Can a brain MRI reveal the biology behind Parkinson’s disease? Diffusion MRI is a specialized MRI technique that measures microscopic changes in brain tissue and may provide clues about neurodegeneration before major structural damage is visible. Shannon Chiu and colleagues describe in a new paper in Annals of Neurology how diffusion MRI findings relate to α-synuclein seed amplification assay (SAA) status in early Parkinson’s disease. Key points: - Most folks w/ Parkinson’s disease who were SAA positive showed MRI patterns consistent w/ Parkinson’s disease using the Automated Imaging Differentiation for Parkinsonism (AIDP) approach. - SAA positive participants had worse smell function and a shorter duration of motor symptoms prior to imaging. - Only limited MRI differences were observed between SAA positive and SAA negative groups, suggesting that α-synuclein positivity alone may not explain the broader patterns of neurodegeneration detected by diffusion MRI. My take: This study highlights an important lesson in Parkinson’s disease research. Biomarkers and imaging may each be measuring different pieces of the same puzzle. A positive α-synuclein test tells us that abnormal protein aggregation is present, however diffusion MRI may be capturing downstream effects on brain structure and circuitry. The future will likely require combining molecular biomarkers, imaging and clinical features to fully understand the biology of Parkinson’s disease. I was biased as an author so please read and decide for yourself. Here are 5 points that resonated w/ me: 1- A positive α-synuclein seed amplification assay does not necessarily mean a person will show widespread MRI changes early in the disease. 2- Smell loss continues to emerge as one of the strongest clinical clues linked to underlying α-synuclein pathology. 3- Advanced MRI techniques such as free-water imaging may provide information different from biomarker testing and the two approaches may be complementary. 4- Artificial intelligence tools such as AIDP continue to show promise in identifying Parkinson-related patterns of neurodegeneration from routine MRI scans. 5- Image plus may be important!
Kristine Meldrum is an exercise professional, Parkinson’s advocate and her signature concept has been the 'PD Exercise Cocktail Plan' which combines different exercise ingredients such as aerobic training, strength training, balance work, dual-task activities, boxing, cycling, treadmill training, and flexibility exercises all into an individualized program rather than relying on a single exercise modality. “Parkinson’s exercise is not generic. It should be specific, targeted, and individualized based on assessments. That is how we build exercise plans that reduce symptoms and help slow disease progression.” Page 14 captures the core message and highlights the importance of understanding the difference between physical activity and exercise dosage in Parkinson’s disease. Thanks to Margaret Preston for the photo. Margaret Preston is the President of the nonprofit organization Power Over Parkinson's, a Virginia-based Parkinson's advocacy and support organization. She founded the organization after her father, Gary Rogliano, was diagnosed with Parkinson's disease in 2019. Here is the link to the book: https://cutt.ly/zt0ujNX9
Parkinson’s disease may not be just one disease protein. Co-pathology means multiple abnormal proteins and disease processes may exist together in the same brain. Matarazzo and colleagues describe in a new paper in Movement Disorders how Parkinson’s disease frequently includes overlapping pathologies such as tau, beta amyloid, TDP-43, vascular disease and inflammation, in addition to alpha-synuclein. Key points: - Most folks w/ Parkinson’s disease appear to have multiple co-existing brain pathologies rather than a pure alpha-synuclein disorder. - Tau, beta amyloid and TDP-43 pathologies were linked to faster progression, cognitive decline and more severe symptoms in many studies. - The review highlights how genetics, inflammation, vascular disease, microbiome changes and immune dysfunction may all interact to shape Parkinson’s progression. My take: This paper is important because it challenges the old idea that Parkinson’s disease is simply a dopamine disorder or just a synuclein disorder. The future of Parkinson’s treatment may require us to target multiple biological pathways simultaneously. We may need to think less about a single culprit and more about an entire ecosystem of interacting disease processes. Here are 5 points that resonated w/ me: 1- Parkinson’s disease is likely more biologically complex than we previously imagined. 2- Co-pathologies may help explain why symptoms and progression differ so dramatically between folks. 3- Tau and beta amyloid pathology may contribute importantly to thinking and memory decline in Parkinson’s disease. 4- Inflammation, vascular disease and immune dysfunction may not just accompany Parkinson’s disease, they may actively shape progression. 5- Precision medicine approaches that combine biomarkers, genetics and pathology may ultimately help us personalize therapies and improve outcomes. https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.70324