REM sleep and demetia risk: there are relations but still no explanations

REM, or “rapid eye movement,” is one of four stages of sleep, which also include two phases of light sleep and a deeper sleep phase called slow-wave-sleep (slow wave sleep). REM sleep is characterized by vivid dreams and high levels of brain activity, similar to the state of the awake brain. Man goes through different periods of REM sleep every night, among other phases of sleep. In the new study published in the journal Neurology (Pase MP et al., 2017), the researchers found that people who developed dementia had a lower REM sleep activity, examining the study carried out in previous years on a sample of people compared to those who do not develop cognitive problems. The study does not demonstrate that low levels of REM sleep cause dementia; rather, it shows an association between the two, said study lead author Matthew Pase, a research leader at the University of Swinburne in Australia.

Pase has advanced several hypotheses for how REM sleep and dementia could be linked. While REM sleep can help protect connections within the brain that are vulnerable to damage with aging and Alzheimer’s disease, on the other hand, perhaps the least REM activity is caused by other potential risk factors of dementia, such as accentuated anxiety and stress. Doctors have long recognized that a lack of sleep can cause mental and emotional health problems. But the details about which types of sleep are associated with dementia and long-term cognitive decline have been lacking. More than 10% of Americans over age 65 have a certain form of dementia, according to the Centers for Disease Control and Prevention. In the new study, the researchers looked at more than 320 American patients with a mean age of 67, who were already part of an ongoing, more extensive study on heart health. Researchers collected sleep data approximately halfway through this study and for about 12 years.

During this time, 32 people (about 10%) were diagnosed with some form of dementia; among these, for 24 was diagnosed with Alzheimer’s disease. People who developed dementia spent an average of 17% of their sleep time in REM sleep, compared to 20% of those who did not develop dementia. The researchers found that for every 1% reduction in REM sleep, there was a 9% increase in the risk of dementia. The results remained unaffected even after the researchers took into consideration other factors that could have influenced the risk of dementia or decreased sleep, such as heart disease, depression and medication use. Pase and his team would like to understand why a lower amount of REM sleep is linked to an increased risk of dementia. He hopes to tap into a larger sample of data to examine the relationship between sleep and signs of accelerated brain aging, such as memory problems and loss of brain volume.

But Alzheimer’s disease does not seem the only pathology that could be affected by the quality of sleep, implying REM sleep also for the pathogenesis of Parkinson’s disease. The disturbance of REM sleep behavior (RBD) is a parasomnia, in which a loss of atony of REM sleep manifests itself as a promulgation of the often violent dream. Regardless of its importance as a predictor of Parkinson’s, RBD in Parkinson’s may involve more than simply screaming at night and experiencing sleep fragmentation. A systematic review of the literature was performed to probe its significance as a prognostic factor. The analysis of prospective studies reveals that baseline RBD confers a greater risk of developing dementia and hallucinations. In transversal studies, RBD is associated with the predominant motor phenotype without tremor and with autonomic dysfunction.

Previous studies already published (Nomura T et al., 2013; Suzuki K et al., 2013; 2017; Chung SJ et al., 2017) had already investigated various aspects of the symptoms and typical signs of Parkinson’s disease related to the quality of REM sleep. But for at least a decade it has been hypothesized that REM sleep if disturbed, could have compromised cognition. For this reason this hypothesis was tested on parkinsonian subjects, but without cognitive decline (Vendette M et al., 2007). Out of 34 patients with Parkinson’s, half had a RBD disorder and half did not. All parkinsonian patients with RBD had poor neurological and cognitive performance compared to those without REM sleep disorders. Finally, some Authors just this year have confirmed the impact of a bad REM sleep on cognitive processes in active clinical disease (Jozwiak N et al., 2017; Barber TR et al., 2017). The cohort used was higher in number than in previous studies (more than 280 subjects with RBD).

The reasons why REM sleep disturbance should cause a clinical worsening of Parkinson’s or cognitive decline appear to be unclear. Some very likely hypotheses speculate that the molecular mechanisms of dopamine-regulated memory enhancement have to do with it. This neurotransmitter, normally, does not regulate memory during the diurnal phases, being the major role entrusted to glutamate and to acetylcholine. But there is still no knowledge that dopamine, on the other hand, can regulate or consolidate the memory of the day during nighttime sleep. And it is for this reason that the hypotheses have been oriented towards this direction. There are few studies that prove that certain substances or drugs can affect the expression or redistribution of dopamine D1 and D2 receptors in rats, during the occurrence of processes that involve learning. But there is no scientifically valid causal link to state that they are directly connected to the memory, even less in the case of nocturnal sleep.

However, for precautionary purposes and as a medical advice, it is also important to take care of yourself at night. As you can read from these discoveries, the key to maintaining the brain’s functioning could be the quality of sleep rather than its quantity.

  • edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.

Scientifiche

St Louis EK, Boeve BF. Mayo Clin Proc. 2017 Nov; 92(11):1723-36. 

Högl B, Stefani A, Videnovic A. Nat Rev Neurol. 2017 Nov 24.

Pase MP et al. Neurology. 2017 Sep 19; 89(12):1244-1250.

Al-Qasset  A et al. Curr Treat Options Neurol. 2017 Jun;19(6):22.

Rahmani F et al. Conf Proc IEEE Eng Med Biol Soc. 2016:1124-26. 

Chung SJ et al. Eur J Neurol. 2017; 24(10):1314-19. 

Grima N et al. J Clin Sleep Med. 2016; 12(3):419-28. 

Suzuki K et al. BMC Neurol. 2013 Feb 9; 13:18.

Nomura T et al. Sleep Med. 2013 Feb; 14(2):131-35.

Informazioni su Dott. Gianfrancesco Cormaci 2479 Articoli
- Laurea in Medicina e Chirurgia nel 1998 (MD Degree in 1998) - Specialista in Biochimica Clinica nel 2002 (Clinical Biochemistry specialty in 2002) - Dottorato in Neurobiologia nel 2006 (Neurobiology PhD in 2006) - Ha soggiornato negli Stati Uniti, Baltimora (MD) come ricercatore alle dipendenze del National Institute on Drug Abuse (NIDA/NIH) e poi alla Johns Hopkins University, dal 2004 al 2008. - Dal 2009 si occupa di Medicina personalizzata. - Detentore di un brevetto sulla preparazione di prodotti gluten-free a partire da regolare farina di frumento immunologicamente neutralizzata (owner of a patent concerning the production of bakery gluten-free products, starting from regular wheat flour). - Responsabile del reparto Ricerca e Sviluppo per la società CoFood s.r.l. (leader of the R&D for the partnership CoFood s.r.l.) - Autore di un libro riguardante la salute e l'alimentazione, con approfondimenti su come questa condizioni tutti i sistemi corporei. - Autore di articoli su informazione medica, salute e benessere sui siti web salutesicilia.com e medicomunicare.it