Can we restore sight by turning nerve cells into light sensors? What resonates with me about this remarkable study by José-Alain Sahel and colleagues in the New England Journal of Medicine, and the accompanying editorial by Nobel laureate Karl Deisseroth, is the possibility of restoring function even after the cells responsible for vision have been lost. In 10 individuals with advanced retinitis pigmentosa, an inherited disease that destroys the retina's light-sensing cells, researchers used optogenetics, a technique that introduces light-sensitive proteins into surviving nerve cells, combined w/ special goggles that translate visual information into light signals. Six of the 10 participants experienced clinically meaningful improvements in light sensitivity, and several demonstrated improvements in detecting or locating objects. This was a small, early-phase safety study, not a cure for blindness, and adverse events remind us that considerable work remains. What excites me most is the larger implication Deisseroth highlights: optogenetics is moving from a revolutionary laboratory tool toward a potential human therapy. We may not always need to replace every neuron lost to disease. Sometimes we may be able to reprogram surviving circuits to recover meaningful function. For those of us working in Parkinson's disease and deep brain stimulation, this is an especially powerful concept. The future of neurology may depend not only on protecting neurons, but also on learning how to restore the functions of circuits that survive. nejm.org/doi/full/10.1056/NE…

The Braak Paradox: When Parkinson’s pathology and clinical progression disconnect. For more than two decades, the Braak hypothesis has shaped how we think about Parkinson’s disease, suggesting that abnormal alpha-synuclein pathology spreads through the brain in a predictable sequence as the disease advances. What resonates with me about this new study by di Biase and colleagues, and the accompanying thoughtful editorial by Rodríguez-Violante in Neurology, is that the biology may be far more complicated than the model. In 61 people with autopsy-confirmed Parkinson’s disease, Braak stage did not correlate with motor disability, disease duration, age at death, or brain weight. In other words, having more widespread alpha-synuclein pathology did not necessarily mean having more advanced clinical disease. The editorial importantly reminds us that this finding does not invalidate Braak staging or the importance of alpha-synuclein, but rather exposes the limitations of using pathology as a clock for clinical progression. Parkinson’s is not one disease following one predictable path, and the frequent presence of other pathologies, including tau, amyloid, and vascular disease, further complicates the picture. For me, the lesson is that we must be careful not to confuse what we see under the microscope with what patients actually experience. As we develop biological staging systems, biomarkers, and disease-modifying therapies, we need to measure not only abnormal proteins but also neuronal loss, clinical disability, and the individual trajectories of people living with Parkinson’s. The patient, not the pathology, must remain at the center of our science. neurology.org/doi/10.1212/WN…

Could ADHD be a risk factor for dementia later in life? An important new study raises questions. What really resonates with me about this new study published in JAMA Psychiatry is the possibility that attention-deficit/hyperactivity disorder (ADHD), a condition we often associate with childhood, may also be an important risk factor for cognitive decline later in life. Researchers followed data from more than 187,000 adults and found that people diagnosed with ADHD had a substantially higher risk of developing mild cognitive impairment or dementia. In fact, 6.7% of those with ADHD developed cognitive impairment compared with 3.4% of those without ADHD, and the association remained significant even after accounting for several other health conditions and risk factors. Interestingly, genetic markers associated with ADHD also predicted a modest increase in risk. We must be careful here: this study does not prove that ADHD causes dementia, and having ADHD certainly does not mean you are destined to develop cognitive problems. What strikes me is that we may need to rethink ADHD as more than a disorder of attention and behavior and consider its potential implications across the lifespan. The message is not to create fear, but to recognize risk, pay attention to changes in memory and thinking, and invest in research to understand whether earlier recognition and better management of ADHD can improve long-term brain health. cutt.ly/UyWH9uHB

What Is Your Plan for Using Supplements for Parkinson's? Check out my newest Substack article on this important and highly relevant topic. A new clinical trial reveals why promising supplements may fail, sometimes cause harm, and why evidence matters more than hope. michaelokun.substack.com/p/w…

Africa's invisible Parkinson's crisis: When a diagnosis and levodopa become luxuries. Parkinson's disease is a growing global health challenge, however in parts of Africa, folks can live for years w/o a diagnosis or access to affordable treatment. Frank Burkybile describes in a compelling 2025 feature in The BMJ how Parkinson's disease in East Africa remains hidden by stigma, limited access to trained health care providers and the high cost of essential medications. Key points: - In Kenya, fewer than 20 neurologists serve more than 50 million folks, leaving enormous gaps in diagnosis and treatment. - Stigma can be devastating, as Parkinson's symptoms may be mistaken for curses or witchcraft, resulting in isolation, abandonment and loss of employment. - Levodopa, one of the most effective and affordable treatments for Parkinson's, remains inconsistently available, forcing some families into financial hardship simply to obtain medication. My take: What resonates most w/ me is that we are not talking about a disease for which we have no treatment. We have levodopa, a medication that has transformed millions of lives, yet access remains profoundly unequal. How can we accept a world where folks must sell their homes to obtain a medication that should be affordable and universally accessible? This is exactly why our Levodopa for All initiative matters. We must stop treating access to Parkinson's medications as a privilege and start treating it as a basic human right. Here are 5 points that resonated w/ me: 1- Parkinson's disease is not just a problem of wealthy countries. It is a global challenge that demands a global response. 2- A diagnosis can change a life, especially in communities where symptoms are misunderstood and stigma can tear families apart. 3- Levodopa should be available to 100% of folks who need it, regardless of where they live or what they can afford. 4- Training nurses, primary care teams and community health workers to recognize and manage Parkinson's could dramatically expand access to care. 5- We need better disease surveillance, stronger local medication supply chains and sustained advocacy. The Parkinson's community must insist that no one is left behind simply because of geography or poverty. The question is not whether we know what to do. The question is whether we have the collective will to do it. doi.org/10.1136/bmj.r1123