
Recapping MDS 2026: Biomarkers, Aging, and Prodromal Movement Disorders
Odinachi Oguh, MD, movement disorder specialist at the Cleveland Clinic Lou Ruvo Center for Brain Health, shares clinical perspectives on biomarkers, aging, non-motor symptoms, and prodromal disease from the 2026 MDS Congress.
Held October 4 to 8 in Seoul, South Korea, the
Biomarker-defined disease, prodromal PD, and non-motor symptoms were also prominent throughout the program, reflecting a field that is increasingly focused on earlier diagnosis and more individualized care. Shortly after the meeting, NeurologyLive sat down with Odinachi Oguh, MD, a movement disorder specialist at the
Oguh answered questions on her overall impressions of the meeting, how the aging theme is shaping her practice, and whether non-motor symptoms are getting enough attention. As part of a new iteration of NeuroVoices, she also covered where prodromal PD and biomarkers stand and the main takeaway she brought back to her patients and colleagues.
NeurologyLive: What was the overall feeling coming out of the conference, and was there a single moment or session that stood out to you personally?
Odinachi Oguh, MD: I think the big picture was incremental but meaningful progress in movement disorders, rather than one transformative breakthrough. Based on the meeting, the field is moving simultaneously toward more biomarker-defined disease, earlier diagnosis, and genotype- and pathway-specific therapies. That means more individualized therapies, perhaps better delivery of dopaminergic therapy, and also a look at nondopaminergic and nonpharmacological treatments in movement disorders. AI and digital biomarkers have entered the field as well. There is also greater recognition of the impact of environmental and systemic factors on disease etiology and triggers, particularly in Parkinson disease and other movement disorders.
One of the overarching themes this year was aging and movement disorders. Did anything presented at the conference genuinely shift how you think about that relationship?
This is something I have been doing in my practice over the last few years. We are seeing an aging population more and more being diagnosed with PD, so we have to think about the fragility of aging and how it modifies our diagnostic process and our treatment. There was a lot of talk about this, and I found one lecture very exciting, because that is how I see treatment in movement disorders.
Not everything is related to the primary diagnosis of PD, and some things just happen because of aging. It can be difficult to differentiate aging and fragility from the primary diagnosis. We also have to keep in mind all the things that can happen with aging, from vascular risk factors to mechanical and orthopedic risk factors, deconditioning, and muscle wasting. These can throw off balance and gait and create a multifactorial picture that can sometimes mimic PD.
That emphasizes how I think about practicing in the future, because we are going to increasingly see an aging population. How do we balance the treatment of PD and aging, and how do we encourage our patients to look beyond PD and think about how aging interacts with their disease? I am glad we are seeing more of this. We have to treat the patient as a unit rather than as different parts of the body.
One thing I want to add is that we are also seeing more co-pathologies rather than simple PD. You could have PD and then develop memory changes that might be a co-pathology with Alzheimer disease. That is where biomarker-driven diagnosis might come into play. As we age, we are not just seeing one disease. When we were trained as fellows, we were taught that you can’t have more than one diagnosis, but we are clearly seeing something different in clinical practice. We are seeing more than one co-pathology in a patient, and we really have to think about the fragility of aging rather than making just one pathological diagnosis.
Cognitive impairment and non-motor features were prominent in several sessions. Are those areas finally getting the attention they deserve, or is there still a gap between what we know and how we manage them clinically?
I think there is still a gap. I usually group this in the nondopaminergic pipeline, which is getting more interesting. There is increasing recognition that simply giving more dopamine won’t adequately treat cognitive impairment, autonomic dysfunction, or other non-motor symptoms, from anxiety and mood disorders to sleep problems.
We are increasingly seeing that nondopaminergic pipeline become interesting in research, but of course the wheels of research turn very slowly. It is important that we are talking more about it and how it interferes with the treatment of motor symptoms in many of our patients. There is still a gap, but the fact that we are talking about it more is a pleasant improvement from where we were a few years ago.
Where do we stand with prodromal PD and identifying patients early, and what role are biomarkers starting to play?
During the meeting there was a substantial emphasis on biomarkers for earlier, biologically defined PD. The direction is moving away from patients simply meeting clinical criteria for PD and toward a biological subtype or pathology.
For prodromal patients, CSF and other biomarkers will increasingly be investigated for things like alpha-synuclein pathology, tau pathology, and genetic pathways, particularly LRRK2 pathway activation, as well as GBA, which is another biological substrate for PD. There is also increasing focus on neuroinflammation, which is the foundation of all neurodegenerative diseases, and on the synaptic injury that results from it. Stem cells are in the picture as well. I think we will be better able to diagnose prodromal synucleinopathies and follow these patients over time.
The gap that remains is what we do when we find this out and how we treat these patients. I do know that the Parkinson’s Progression Markers Initiative (PPMI) is running a path-to-prevention study right now, harnessing some of those prodromal patients to see what we do with them in terms of a treatment pathway. Over the next few years we are going to be better at diagnosing biological subtypes of PD through the multitude of biomarkers available to us. But the gap remains, because all we have now for many prodromal patients is exercise and diet and lifestyle. To better harness what we are doing with biomarkers, we still have to create novel treatment pathways for these patients.
As someone who treats patients every day, what was the one thing you took home from MDS Congress 2026 that you would relate to your patients or your clinician colleagues?
My biggest takeaway is that it was a meaningful meeting for the field, but it still brings us back to the foundation of our practice. That means clearer phenotypic differentiation in PD and other movement disorders, and the use of biomarkers in my practice for better diagnostics.
There is still a big question mark about what we do with prodromal patients. Once we have these patients, we might put them in clinical trials that are currently available, whether observational studies like PPMI or treatment trials like the LRRK2 and GBA trials that are ongoing.
It also buys into the world of genetics. If I test my patients and we have a genetic substrate, I can individualize their treatment in the future. For advanced therapies in patients with existing diagnoses, there is better delivery. How do I make clinical judgments about who is better suited to a particular type of therapy versus a surgical type of therapy?
I also still don’t use a lot of digital monitoring in my practice because of my older population, who are not very computer savvy, so how do I incorporate this into my clinical practice to follow patients over time? I have probably thrown out a lot, but the key thing is how I treat patients in a transformative way that will be more meaningful to them, as we are going to increasingly see more patients with PD over time.
Transcript edited for clarity. For more MDS 2026 coverage,
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