What if “sleeping well” didn’t mean “sleeping longer”?


What really happens in our brain while we sleep?


Every evening, we do something quite extraordinary: we close our eyes, gradually lose awareness of our surroundings, and remain almost completely still for several hours.
We might think that our brain simply switches off and rests until the next morning.
In reality, it is almost the opposite.
While we sleep, the brain remains active. It changes how it functions, consolidates certain memories, reorganizes its activity, and helps eliminate waste produced during the day.
And most importantly, we do not sleep in the same way throughout the entire night.
Our brain moves through several very different states. And in Parkinson’s disease, some of these mechanisms take on particular significance.
Let’s take a look inside the brain during a night’s sleep.

A night’s sleep is not one long, uniform state
Our sleep is organized into several cycles of approximately 90 minutes, which repeat throughout the night.
During each cycle, we gradually move from light sleep to deeper sleep before reaching a very particular state: rapid eye movement sleep, during which the most vivid dreams notably occur.

Then the cycle begins again. But not all cycles are identical.
Deep sleep is generally more prominent at the beginning of the night, while periods of rapid eye movement sleep (also known as REM sleep) gradually become longer as morning approaches.

Why is this organization interesting?
Because these different stages do not appear to serve exactly the same functions. During deep sleep, for example, the activity of millions of neurons becomes much more synchronized.

In Parkinson’s disease: less stable sleep?

When living with Parkinson’s disease, the different stages of sleep sometimes appear to be less clearly separated.

A study published in 2025, involving 280 people with early-stage Parkinson’s disease and 158 people without Parkinson’s, observed greater “mixing” between wakefulness and deep sleep.
And this phenomenon appears to matter: the people in whom this mixing was most pronounced also experienced greater motor and cognitive difficulties and, over the course of the follow-up period, more rapid progression of motor symptoms.

This does not mean that disorganized sleep accelerates Parkinson’s disease. But the way a person sleeps could reflect certain changes occurring in the brain.

Another small study published in 2024 provides an additional clue. Using electrodes that had already been implanted in the brains of four people with Parkinson’s disease, researchers were able to directly observe their brain activity while they slept.
They noticed that a type of brain activity characteristic of Parkinson’s disease increased a few seconds before certain nighttime awakenings. This activity could therefore contribute to more fragmented sleep.
The study involved only four people, so its findings still need to be confirmed.
But this research shows us something interesting: for people with Parkinson’s disease, the issue may not simply be sleeping less. The brain may also have greater difficulty maintaining deep, stable, and well-organized sleep.

And this brings us to another fascinating discovery: what the brain may be doing during these periods of deep sleep.
 

During deep sleep, does the brain clean itself?


Our brain is constantly active and, like any active organ, it produces metabolic waste.
It therefore has mechanisms that help remove this waste. One of them is the glymphatic system, a network in which the movement of fluid through the brain helps eliminate certain molecules that accumulate in brain tissue.
And this system appears to be particularly active during sleep, especially during deep sleep.

This phenomenon has been particularly well demonstrated in animals. In humans, research and imaging techniques are also providing increasingly interesting evidence.

But what does this have to do with Parkinson’s disease?
In this neurodegenerative disease, a protein called α-synuclein accumulates abnormally in the brain.
The “cleaning” system we have just discussed may play a role in eliminating certain forms of this protein.

This raises a question that researchers are currently investigating: if sleep is regularly disrupted, does this cleaning system function less effectively?

A study published in 2025 provides an initial clue. Researchers studied the sleep of 54 people who had recently been diagnosed with Parkinson’s disease, then used MRI scans to look for indirect indicators of how well their glymphatic system was functioning.
They observed an interesting trend: the more participants’ sleep was disrupted by awakenings or breathing problems, the more signs they showed suggesting less efficient functioning of this system.

Importantly, this does not prove that poor sleep causes α-synuclein to accumulate. The study did not directly measure its clearance during the night.

However, it strengthens an interesting hypothesis: this neurological condition could disrupt sleep, and disrupted sleep could, in turn, make certain nighttime brain functions less efficient.
A possible vicious cycle that researchers are now trying to better understand.


REM sleep: The brain dreams, but the body becomes paralyzed


At other times during the night, our brain enters a completely different state: rapid eye movement sleep.
Its name comes from a rather remarkable phenomenon. The brain becomes highly active, sometimes almost as active as when we are awake, while the body does exactly the opposite: our muscles become temporarily paralyzed.

This paralysis serves a very useful purpose. We can run, fight, or jump in our dreams without physically reproducing those movements in bed. Normally, then, the brain dreams while the body remains still.

But in some people, this protective mechanism no longer works properly. They may talk, shout, gesture, kick, or actually “act out” their dreams while asleep. This is known as REM sleep behavior disorder, or RBD.

REM sleep behavior disorder (RBD) is of particular interest to researchers because it is strongly associated with certain neurological diseases, including Parkinson’s disease. Most notably, it can appear several years, and sometimes even several decades, before the first motor symptoms.

A study published in 2024 helps us better understand why. Researchers in Barcelona analyzed, after death, the brains of 20 people who had experienced RBD when they still showed no motor or cognitive signs of a neurodegenerative disease.
Among other findings, the results showed that all 20 brains contained abnormal deposits of α-synuclein, the protein that also accumulates in the brain in Parkinson’s disease.
Even more interestingly, in people who had not developed motor symptoms, these deposits were already present in brain regions involved in controlling REM sleep. In those who later developed Parkinson’s disease or a related condition, they had spread more widely throughout the brain.

In other words, certain biological changes associated with Parkinson’s disease can be present long before the onset of tremor, stiffness, or slowed movement.
This does not mean that everyone who talks or moves during sleep will develop Parkinson’s disease. RBD is a specific disorder that must be diagnosed by a healthcare professional.
But when it is truly present, it can be a very early sign of neurological changes that, in some people, precede Parkinson’s disease by many years.

In some cases, sleep may therefore provide clues about what is happening in the brain long before changes in movement become apparent.


Sleep, much more than simply taking a break


For a long time, we have tended to think about sleep mainly in terms of duration: did I get enough sleep last night?

But the research we have just explored shows that this question tells only part of the story. While we sleep, our brain continues to work. It moves through different states, activates certain clearance mechanisms, and undergoes profound changes in its activity. And in Parkinson’s disease, several of these processes appear to be disrupted.

What is particularly interesting is that the relationship appears to work in both directions. Parkinson’s disease can make sleep more fragmented, while researchers are now investigating whether disrupted sleep could, in turn, affect certain functions normally carried out during the night.

Sleep may even sometimes tell us something about what is happening in the brain before certain motor symptoms appear.

So, rather than asking ourselves only: “How many hours did I sleep?”
It may be just as interesting to ask: “How well did I sleep?”

Because spending eight hours in bed does not necessarily mean getting eight hours of stable, restorative sleep. And this naturally brings us to our next question: can we take action to improve sleep quality when living with Parkinson’s disease?

That is what we will explore in our next newsletter…

Understanding what happens in the brain during the night is one thing. But perhaps the most relevant question in everyday life remains: can we actually improve sleep quality when living with Parkinson’s disease?

In the next newsletter in our The Power of Sleep series, we will move from understanding to practical action: which habits can genuinely support better sleep, which ones may need to be adapted when living with Parkinson’s disease, and what role could AtremoPlus play?

We look forward to sharing it with you very soon!


References for the studies used:

Dodet P, During E, Arnulf I, et al. (2025). Sleep stage mixing is associated with poor prognosis in early Parkinson’s disease. npj Parkinson’s Disease, 11, 275. DOI: 10.1038/s41531-025-01105-w.

Anjum MF, Smyth C, Zuzuárregui R, et al. (2024). Multi-night cortico-basal recordings reveal mechanisms of NREM slow-wave suppression and spontaneous awakenings in Parkinson’s disease. Nature Communications, 15, 1793. DOI: 10.1038/s41467-024-46002-7.

Nepozitek J, Marecek S, Rottova V, et al. (2025). Glymphatic dysfunction evidenced by DTI-ALPS is related to obstructive sleep apnea intensity in newly diagnosed Parkinson’s disease. npj Parkinson’s Disease, 11, 160.

Mayà G, Iranzo A, et al. (2024). Post-mortem neuropathology of idiopathic rapid eye movement sleep behaviour disorder: a case series. The Lancet Neurology, 23, 1238–1251.

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Please note that this blog provides information about our AtremoPlus supplement and related topics.

This blog is not intended to provide medical advice. If you have medical questions, please consult your healthcare professional.

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