There is a hobby rare thing that makes people act out their dreams. They can yelling, hitting, or making sudden movements while sleeping. More specifically, these behaviors occur in the REM sleep phase.
It is known as “Isolated rapid eye movement sleep behavior disorder” or they also call it iRBD by its acronym in English.
During sleep, the body should lose muscle tone and prevent movement. But in people with the disorder, physical and vocal actions can occur.
Now, a study carried out by researchers from Spain and Austria noted that the disorder could suggest a “early stage of neurodegenerative diseases related to the protein α-synuclein”. The work was published in the magazine The Lancet Neurology.
The research was led by Alex Iranzo y Gerard Mayàof the Clinical Hospital of Barcelona-IDIBAPStogether with a multidisciplinary team. It aimed to confirm, through post-mortem analysis, the connection between iRBD disorder and neurodegenerative diseases related to the protein α-sinuclein.
The researchers analyzed postmortem brain and spinal cord tissue from 20 patients diagnosed with iRBD. He 95% of the cases presented deposits of α-sinuclein in brain regions responsible for the regulation of REM sleep.
In dialogue with Infobaethe doctor Marcelo Merellohead of the Abnormal Movements service of sleep and researcher in medical sciences Conicetexpressed caution when considering the results of the new study.
“Isolated rapid eye movement sleep behavior disorder can be confused with other conditions such as sleep-walking. Therefore, when someone has vivid dreams and awakeningsyou should keep in mind that they are symptoms shared by different disorders,” he said.
The scientist stressed that the new study, in which he was not involved, was based only on a limited series of cases. “iRBD disorder could be heraldic symptom of Parkinson’s disease or some kind of cognitive impairment in the elderly. But that possibility must be taken with extreme caution, since even many medications used for sleep or mood control can induce iRBD,” he said.
A person who has iRBD today at age 30 or 40 may never develop Parkinson’s or dementia in the future. “You can’t generalize. Therefore, patients should not live with a sword of Damocles in the presence of this disorder. “A health professional should be consulted,” the researcher clarified.
He isolated REM sleep behavior disorder (iRBD) was first described in humans in 1986 by a research group led by Carlos Schenck in the United States.
It was classified as a parasomniathat is, a sleep disorder characterized by abnormal physical or vocal behaviors during the REM sleep phase, linked to the loss of muscle atonia typical of this stage of rest.
Previous studies have estimated that the global prevalence of iRBDits isolated form, oscillates between 0.74% and 2.01% in adults over 60 years of age, depending on the population studied and the methodologies used.
In 2006, researchers in Spain and Austria had already suggested that iRBD is a sleep disorder that could be a precursor to neurodegenerative diseases. However, evidence was lacking.
To find out, they examined in detail the postmortem brains and spinal cords of 20 patients diagnosed with iRBD before they died. Their tissues were donated for analysis to the biobank, called IDIBAPS Neurological Tissue Bank in Spain.
One of the findings was the identification of deposits of the protein α-synuclein in brain regions critical for the regulation of REM sleep, including the coeruleus-subcoeruleus complex, the gigantocellular reticulated nucleus, the laterodorsal tegmentum and the amygdala.
These areas are responsible for controlling muscle atonia or relaxation during REM sleep, and their dysfunction is known to be related to the development of typical involuntary movements during iRBD sleep, the researchers commented in a statement.
In patients who had not developed symptoms of dementia or parkinsonism, α-synuclein deposits were located in the brain stem and limbic system.
However, in patients who had developed Parkinson’s or dementia with Lewy bodies, α-synuclein deposits were much more extensive, suggesting disease progression toward more widespread neuronal damage.
“These findings are consistent with previous studies that have suggested that iRBD could be an early manifestation of synucleinopathies, but this study provides the strongest neuropathological evidence to date,” he explained. Gerard Mayà.
Furthermore, the researchers found that α-synuclein deposits were not only present in neurons, but also in glial cells (astrocytes and oligodendrocytes), suggesting that glia also play a key role in disease progression.
Another observation of the study is the identification of a series of coexisting pathologies that affect the majority of people with iRBD.
“In particular, we observed a high prevalence of neuropathological changes typical of Alzheimer’s disease. The 20 patients with iRBD had a-synuclein in the brain. But 70% presented these pathological characteristics associated with Alzheimer’s, which could suggest that iRBD could be linked to a higher risk of also developing Alzheimer’s, although its implication is still unclear,” he said. Mayà.
For the authors of the work, the study provided evidence that α-synuclein deposits in brain structures involved in REM sleep could serve as early biomarkers to identify individuals at risk of developing neurodegenerative diseases.
They also acknowledged that the study is based on a relatively small sample. They also considered that the results could be used for the design of clinical trials.
“Our findings could inform the design of clinical trials of compounds targeting specific pathological proteins (e.g., α-synuclein and β-amyloid) in people with iRBD,” they wrote.
