Rapid eye movement sleep

Sleep ‘boosts brain cell numbers’

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Scientists believe they have discovered a new reason why we need to sleep – it replenishes a type of brain cell.

Sleep ramps up the production of cells that go on to make an insulating material known as myelin which protects our brain’s circuitry.

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The findings, so far in mice, could lead to insights about sleep’s role in brain repair and growth as well as the disease MS, says the Wisconsin team.

The work is in the Journal of Neuroscience.

Dr Chiara Cirelli and colleagues from the University of Wisconsin found that the production rate of the myelin making cells, immature oligodendrocytes, doubled as mice slept.

The increase was most marked during the type of sleep that is associated with dreaming – REM or rapid eye movement sleep – and was driven by genes.

In contrast, the genes involved in cell death and stress responses were turned on when the mice were forced to stay awake.

Precisely why we need to sleep has baffled scientists for centuries. It’s obvious that we need to sleep to feel rested and for our mind to function well – but the biological processes that go on as we slumber have only started to be uncovered relatively recently.

Growth and repair

Dr Cirelli said: “For a long time, sleep researchers focused on how the activity of nerve cells differs when animals are awake versus when they are asleep.

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“Now it is clear that the way other supporting cells in the nervous system operate also changes significantly depending on whether the animal is asleep or awake.”

The researchers say their findings suggest that sleep loss might aggravate some symptoms of multiple sclerosis (MS), a disease that damages myelin.

In MS, the body’s immune system attacks and destroys the myelin coating of nerves in the brain and spinal cord.

Future studies could look at whether or not sleep affects the symptoms of MS, says Dr Cirelli.

Her team is also interested in testing whether lack of sleep, especially during adolescence, may have long-term consequences for the brain.

Sleep appears necessary for our nervous systems to work properly, says the US National Institute of Neurological Disorders and Stroke (NINDS).

Deep sleep coincides with the release of growth hormone in children and young adults. Many of the body’s cells also show increased production and reduced breakdown of proteins during deep sleep.

Since proteins are the building blocks needed for cell growth and for repair of damage from factors like stress and ultraviolet rays, deep sleep may truly be “beauty sleep”, says NINDS.

Source:BBC

Neurodegenerative disease status and post-mortem pathology in idiopathic rapid-eye-movement sleep behaviour disorder: an observational cohort study.

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Background

We postulated that idiopathic rapid-eye-movement (REM) sleep behaviour disorder (IRBD) represents the prodromal phase of a Lewy body disorder and that, with sufficient follow-up, most cases would eventually be diagnosed with a clinical defined Lewy body disorder, such as Parkinson’s disease (PD) or dementia with Lewy bodies (DLB).

Methods

Patients from an IRBD cohort recruited between 1991 and 2003, and previously assessed in 2005, were followed up during an additional period of 7 years. In this original cohort, we sought to identify the nature and frequency of emerging defined neurodegenerative syndromes diagnosed by standard clinical criteria. We estimated rates of survival free from defined neurodegenerative disease by means of the Kaplan-Meier method. We further characterised individuals who remained diagnosed as having only IRBD, through dopamine transporter (DAT) imaging, transcranial sonography (TCS), and olfactory testing. We did a neuropathological assessment in three patients who died during follow-up and who had the antemortem diagnosis of PD or DLB.

Findings

Of the 44 participants from the original cohort, 36 (82%) had developed a defined neurodegenerative syndrome by the 2012 assessment (16 patients were diagnosed with PD, 14 with DLB, one with multiple system atrophy, and five with mild cognitive impairment). The rates of neurological-disease-free survival from time of IRBD diagnosis were 65·2% (95% CI 50·9 to 79·5) at 5 years, 26·6% (12·7 to 40·5) at 10 years, and 7·5% (−1·9 to 16·9) at 14 years. Of the four remaining neurological-disease-free individuals who underwent neuroimaging and olfactory tests, all four had decreased striatal DAT uptake, one had substantia nigra hyperechogenicity on TCS, and two had impaired olfaction. In three patients, the antemortem diagnoses of PD and DLB were confirmed by neuropathological examination showing widespread Lewy bodies in the brain, and α-synuclein aggregates in the peripheral autonomic nervous system in one case. In these three patients, neuronal loss and Lewy pathology (α-synuclein-containing Lewy bodies and Lewy neurites) were found in the brainstem nuclei that regulate REM sleep atonia.

Interpretation

Most IRBD individuals from our cohort developed a Lewy body disorder with time. Patients who remained disease-free at follow-up showed markers of increased short-term risk for developing PD and DLB in IRBD, such as decreased striatal DAT binding. Our findings indicate that in most patients diagnosed with IRBD this parasomnia represents the prodromal phase of a Lewy body disorder. IRBD is a candidate for the study of early events and progression of this prodromal phase, and to test disease-modifying strategies to slow or stop the neurodegenerative process.

Source: Lancet

More Evidence Links REM Sleep Behavior Disorder and Neurodegenerative Disease.

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Most patients diagnosed with idiopathic REM sleep behavior disorder advance to a neurodegnerative disease associated with alpha synuclein deposition (Lewy body disease) within a decade.

Several longitudinal studies have demonstrated a consistent association between idiopathic rapid eye movement (REM) sleep behavior disorder (IRBD) and the development of neurodegenerative disorders associated with alphasynucleinopathy, including Parkinson disease (PD), dementia with Lewy bodies (DLB), and multiple systems atrophy (MSA). In one previously described cohort of 44 patients with symptomatic IRBD for a median interval of 11 years and followed clinically for a median of 4.5 years, 45% met criteria for a neurodegenerative disorder. Now, the investigators report their findings in this cohort after an additional 7-year interval.

The conversion to a defined neurodegenerative diagnosis was 82% (16 PD, 14 DLB, 1 MSA, and 5 mild cognitive impairment). Four cohort members were lost to follow-up. Three patients in the cohort underwent autopsy during the period of study, which demonstrated characteristic pathological changes confirming diagnoses of PD in 2 and DLB in 1. Compared with healthy controls without IRBD, 4 patients who did not meet criteria for a neurodegenerative disorder demonstrated decreased striatal uptake of dopamine transporter, a biomarker associated with alphasynucleinopathies.

Comment: Although the sample size is relatively small, this report emphasizes the importance of longitudinal observations in slowly progressive neurodegenerative disorders. The findings highlight an opportunity to identify at-risk individuals and potentially intervene as disease-modifying therapies become available. However, clinicians should look carefully for other causes of dream-enactment behavior, such as medications or concomitant sleep disorders. In the absence of such factors, clinicians should confirm the diagnosis with polysomnography. As the authors suggest, idiopathic RBD may be more accurately termedisolated RBD. Patients who have REM sleep behavior disorder but are asymptomatic for parkinsonism or dementia should be made aware of the risk and the need for continued clinical follow-up.

 

Source:Journal Watch Neurology

Idiopathic REM sleep behaviour disorder in the development of Parkinson’s disease.

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Parkinson’s disease is a progressive neurodegenerative disorder associated with Lewy body disease pathology in central and peripheral nervous system structures. Although the cause of Parkinson’s disease is not fully understood, clinicopathological analyses have led to the development of a staging system for Lewy body disease-associated pathological changes. This system posits a predictable topography of progression of Lewy body disease in the CNS, beginning in olfactory structures and the medulla, then progressing rostrally from the medulla to the pons, then to midbrain and substantia nigra, limbic structures, and neocortical structures. If this topography and temporal evolution of Lewy body disease does occur, other manifestations of the disease as a result of degeneration of olfactory and pontomedullary structures could theoretically begin many years before the development of prominent nigral degeneration and the associated parkinsonian features of Parkinson’s disease. One such manifestation of prodromal Parkinson’s disease is rapid eye movement (REM) sleep behaviour disorder, which is a parasomnia manifested by vivid dreams associated with dream enactment behaviour during REM sleep. Findings from animal and human studies have suggested that lesions or dysfunction in REM sleep and motor control circuitry in the pontomedullary structures cause REM sleep behaviour disorder phenomenology, and degeneration of these structures might explain the presence of REM sleep behaviour disorder years or decades before the onset of parkinsonism in people who develop Parkinson’s disease.

Source: Lancet