Michael J. Fox has just received the Bob Hope Humanitarian Award. At the 78th Emmy Awards, the honor was bestowed not only on an actor but, above all, on his decades-long commitment to people with Parkinson’s and to Parkinson’s research. Fox was diagnosed as early as 1991, at the age of just 29. In 2000, he founded The Michael J. Fox Foundation for Parkinson’s Research (MJFF), which , together with the Parkinson’s Progression Markers Initiative (PPMI) that grew out of it , has since become one of the most important private players in Parkinson’s research. It wasn’t until 2026 that it evolved into the Parkinson’s Precision Medicine Initiative.
His story raises an interesting question that goes far beyond his personal illness:
What actually happens in the brain long before Parkinson’s can be diagnosed?
Because we now know that the clinical diagnosis likely does not mark the onset of the disease. Biological changes can begin years before the typical motor symptoms appear. And sleep, of all things, provides a remarkable clue in this regard.
However, it is important to make a key distinction: this is not about sleep disorders in general. And there is no solid evidence that poor sleep or sleep problems cause Parkinson’s disease. This concerns a very specific disorder of REM sleep: REM Sleep Behavior Disorder (RBD).
When the Body Slows Down in a Dream
REM sleep is the sleep stage during which vivid dreams occur particularly frequently. REM stands for “Rapid Eye Movement.”
During this phase, something remarkable happens: Although the brain is, in part, highly active and we can dream of complex movements, skeletal muscle activity is normally largely suppressed. This so-called REM atonia effectively prevents us from physically acting out our dreams. For example, someone who runs away from a lion in a dream does not actually run around the bedroom. The muscles are essentially “off.”
In REM Sleep Behavior Disorder (RBD), this motor inhibition does not function—or does not function sufficiently—during REM sleep. As a result, movements, loud vocalizations, or full-fledged actions related to dreams may occur during sleep. People may hit, kick, speak, or even jump out of bed, often in a way that corresponds to the events in their dreams.
It is crucial to note that RBD is not diagnosed solely on the basis of a person reporting particularly vivid or unusual dreams. The loss of normal muscle atonia— REM Sleep Without Atonia (RSWA)— can be objectively detected through polysomnography. A definitive diagnosis should therefore be confirmed by a video sleep study.
And that’s when Parkinson’s comes into play
This is where it gets scientifically interesting. In people with so-called isolated RBD—that is, RBD in which no manifest neurodegenerative disease has initially been diagnosed—there is an unusually strong link to disorders within the α-synucleinopathy spectrum. These include Parkinson’s disease, Lewy body dementia, and multiple system atrophy. They are referred to as α-synucleinopathies because, in these diseases, the α-synuclein protein undergoes pathological changes and can accumulate in nerve cells, among other places.
α-synuclein acts, in a sense, as a regulator of the “replenishment” and release of neurotransmitters at the synapse. Under certain conditions, the protein can change its structure. A normally soluble or membrane-bound protein can give rise to “misfolded” forms that can assemble into oligomers and eventually into larger aggregates. It is precisely these pathological forms that are at the heart of α-synucleinopathies.
Isolated RBD is therefore now considered one of the most important so-called prodromal markers of these diseases. “Prodromal” means that a symptom appears at a stage when the actual disease is not yet clinically detectable, or not yet fully detectable. And this is precisely the key point:
There is no evidence that RBD causes Parkinson’s disease.
Rather, the available data suggest that some people with isolated RBD may already exhibit biological changes indicative of a developing α-synucleinopathy long before it becomes clinically apparent.
RBD would then be less of a cause and more of an early visible sign of a process that may have begun long before. That is a fundamental difference.
Does RBD automatically mean Parkinson’s?
Definitely NO! That’s also important so as not to overinterpret the connection.
RBD can have various causes and may, for example, occur in connection with certain medications or other neurological disorders. The group of particular interest to Parkinson’s research is isolated RBD, especially when it has been objectively confirmed by a sleep laboratory examination.
However, these individuals have a strikingly high risk of developing α-synucleinopathy later in life. This is precisely why RBD is currently being studied intensively as a window into the so-called prodromal phase of neurodegenerative diseases. This is what makes RBD so valuable to research.
After all, if we can identify a biological process before the classic symptoms appear, this could open up an entirely new possibility: we could study the disease before it becomes clinically apparent.
RBD may be just the tip of the iceberg
What is particularly exciting is that research has now taken another step forward. A small study published in 2026 in *npj Parkinson’s Disease* examined 25 people with early-stage, untreated Parkinson’s disease. The study found that changes in REM atonia can also occur in people who do not meet the clinical criteria for RBD. Increased muscle activity during REM sleep was observed in some of the Parkinson’s patients.
This opens up an interesting possibility: Perhaps clinically evident RBD is actually just the visible tip of a broader spectrum of changes in REM sleep.
A key question, therefore, is: When does the normal regulation of REM sleep begin to change in measurable ways, or is the postnatal development of atonia already disrupted?
Where Is Research Headed?
We know much more today about the connection between RBD and Parkinson’s disease than we did a few decades ago, thanks in no small part to Michael J. Fox. However, we still do not know exactly when and how the abnormality in REM atonia develops.
Does the normal regulation of REM sleep begin to change only as we age—perhaps as part of a neurodegenerative process that has already begun—or might the cause lie much earlier?
The muscle atonia characteristic of adult REM sleep develops during late fetal development and, above all, during postnatal development, and continues to mature over many years. Therefore, another possibility is conceivable: that in some people, the neural mechanisms that later become responsible for REM atonia are already structured differently or incompletely formed during this developmental period.
If the neural systems underlying REM atonia develop and mature over such a long period of time, could there not also be individual developmental differences that arise very early on? In other words, we should not only ask , “When does the normal regulation of REM sleep begin to change?” but also consider: “Was it perhaps different from the very beginning in these individuals?”
This does not yet explain Parkinson’s disease, and it certainly does not provide evidence that early disruption of REM atonia would foreshadow or even cause Parkinson’s later in life. Rather, it is an open research question that opens up a temporal dimension that has received little attention to date: Does the abnormality first arise later in life—or could an individual peculiarity in the development of the REM sleep system already be present much earlier?
This is precisely where there is a gap in our knowledge. The RBD cohorts that have been particularly well studied to date consist mainly of older adults. By contrast, we know much less about what happens to REM sleep regulation decades earlier. The intriguing question, then , is when the specific characteristics begin that we later recognize as a marker of this disorder.
And what about Michael J. Fox?
Through his dedication, Michael J. Fox has helped create a research and data ecosystem that makes it increasingly possible to investigate precisely these kinds of questions. His foundation has funded research for years, connected scientists, and focused on detecting Parkinson’s earlier and better understanding the disease. Fox has now been honored with the Bob Hope Humanitarian Award for his contributions.
Perhaps that is why, at some point, we will no longer just know when Parkinson’s is diagnosed. Perhaps one day we will know when the first biological changes begin—and what signs might alert us to them. Michael J. Fox has, in a sense, planted the seed for this tree. We do not yet know how tall this tree will grow.
And maybe Fox himself will never be able to live up to his legacy.
Quellen
Michael J. Fox Honored at the Emmys for His Advocacy for Parkinson’s, by Danielle Broadway, September 14, 2026, https://www.reuters.com/business/media-telecom/michael-j-fox-honored-emmys-parkinsons-advocacy-2026-09-15/
Dauvilliers, Y., Schenck, C.H., Postuma, R.B., et al. REM sleep behavior disorder. Nat Rev Dis Primers 4, 19 (2018). https://doi.org/10.1038/s41572-018-0016-5
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