Skip to main content

Sleep, beautiful sleep

Photo by S L on Unsplash

Human biology is systems biology; perturb one aspect of human biology and it will have downstream effects, which can be noted throughout the body. As you know sleep is critical for brain health; if you have poor sleep hygiene you are putting yourself at greater risk of developing dementia when you get older. Why? 

In this study of cognitively normal older Chinese adults, spinal fluid soluble TREM2 (sTREM2) was associated with self-reported poor sleep hygiene using the Pittsburgh Sleep Quality Index. sTREM2 is shed from activated microglia or macrophages and is thought to be a marker of microglial activation. The implications are that this association may be causal, i.e. poor sleep is pro-inflammatory, both in the periphery and central nervous system and the latter contributes to driving neurodegeneration.

Could improved sleep hygiene be anti-inflammatory? Or is the microglial activation simply a response to poorer clearance of CNS debris, which occurs when we are asleep? Whatever the reasons this study provides some evidence that the role poor sleep plays in driving neurodegeneration may be more complex than we realise.

I don’t think we can ignore poor sleep hygiene in our push to improve brain health. The question is how do we get the population to improve their sleep? What interventions work? How do we drive the necessary behavioural changes to get the whole country to improve their sleep quality?

I would be interested to know if we could use CSF sTREM levels as a response marker in trials designed to improve brain health.


Hu et al. Associations of Sleep Characteristics with Cerebrospinal Fluid sTREM2 in Cognitively Normal Older Adults: the CABLE Study. Neurotox Res . 2021 Jun 7. doi: 10.1007/s12640-021-00383-5. Online ahead of print.

As brain insults, sleep disorders could enhance microglial activation and aggravate neuroinflammation. Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) in cerebrospinal fluid (CSF) serves as a readout for TREM2-associated microglial responses. We aimed to study the association of sleep characteristics with CSF sTREM2 in cognitively normal (CN) older adults. Linear and non-linear regression analyses were conducted in 830 participants with measurements of sleep characteristics and CSF sTREM2, after adjusting for age, sex, education, the Chinese-Modified Mini-Mental State Examination (CM-MMSE) scores, and APOE4 status. These analyses were also performed in amyloid-negative (A -) and amyloid-positive (A +) individuals. Linear relationships between sleep characteristics and CSF sTREM2 were found. In all the participants, sleep efficiency score in Pittsburgh Sleep Quality Index (PSQI) (p = 0.037) showed a positive linear association with CSF sTREM2. In A + individuals, the grade of PSQI total score (p = 0.011) as well as subjective sleep quality score (p = 0.048) and sleep efficiency score (p < 0.001) in PSQI were positively associated with CSF sTREM2. Besides, several U-shaped relationships were revealed of sleep-time measures, such as insufficient or excessive nocturnal sleep duration, with CSF sTREM2 in A + individuals (the optimal model: bedtime 22:21 p.m., time to fall asleep 22:52 p.m., nocturnal sleep duration 7.36 h). In A - individuals, the above relationships were not found. Poor self-reported sleep characteristics and sleep indicators were associated with higher CSF sTREM2, suggesting that sleep might play an important role in the regulation of TREM2-associated microglial activity.

Conflicts of Interest

MS Research

Twitter

LinkedIn

Medium

General Disclaimer: Please note that the opinions expressed here are those of Professor Giovannoni and do not necessarily reflect the positions of the Barts and The London School of Medicine and Dentistry nor Barts Health NHS Trust and are not meant to be interpreted as personal clinical advice.
Labels:

Comments

Post a Comment

Popular posts from this blog

Are you ready for an EBV vaccine to prevent MS?

"Professor Giovannoni, you tell me that my daughter has a 1 in 40 chance of developing multiple sclerosis and that MS has reached epidemic proportions in parts of the world? Is there anything I can do to reduce her chances of getting MS? Is there anything we can do to stop other people from getting MS?" Although multiple sclerosis (MS) is a complex disease due to the interaction of genetic and environmental factors data on the occurrence of MS at the population level (epidemiology) supports the Epstein Barr Virus (EBV) as being necessary, but not sufficient, for someone to develop MS. In other words, EBV is probably the cause of MS. Of all the putative causative agents that have been proposed to be associated with MS, EBV is the only one where the risk of getting MS if you are EBV negative is close to zero or zero if you limit the analyses to those studies which use a technique called immunofluorescence microscopy as the gold-standard assay to detect anti-EBV antibodies. EBV ...
7 comments
Read more

Smoking: a major preventable MS risk factor

I have been complaining about my low productivity levels since I have gotten back to work after my accident. However, last night with a single one hour webinar we have managed to set-up a new international collaboration to study and address the social determinants of health (SDoH) and their impact on MS. Our focus is going to be on which SDoH can we modify and hence improve the outcome for people with MS (pwMS)? Smoking is one such modifiable factor and needs to be addressed at a (1) population level with policy and legislation, (2) at a local or community level, (3) with the family and (4) at an individual level target the people with MS (pwMS). We know that pwMS who smoke have a worse outcome than people who don’t smoke. The effect of smoking is equivalent to negating the treatment effect of being on an injectable therapy such as interferon beta. Put simply smokers with MS start using a walking stick (EDSS = 6.0) about 6 years earlier than pwMS who don’t smoke. Getting pwMS to stop s...
7 comments
Read more

Corpulence and poverty

Since stating my intention to join the  #BackTo21  campaign to get my BMI back to what it was when I was 21 years of age, I have had several emails and direct messages on social media questioning the wisdom of my intention.  Photo by NeONBRAND on Unsplash It is clear that despite BMI being a relatively poor metric of health there is overwhelming evidence that at a population level it predicts poor health outcomes. Importantly there is new data that indicates the target BMI for the prevention of type 2 diabetes and the metabolic syndrome depends on your ethnicity. For people of South Asian origin, there is a call to reset the BMI cutoff to 23.9, which for most people is within the normal range. At the same time, there is a call to classify obesity as an important social determinant of health. Arnaud Chiolero argues below for using BMI as a socioeconomic indicator. Do you agree? Isn’t it quite amazing that in a previous era corpulence was a sign of affluence, whereas in th...
4 comments
Read more