Decreased Brain Levels of Vitamin B12 in Aging, Autism and Schizophrenia

Zhang, Yiting; Hodgson, Nathaniel; Trivedi, Malav Suchin; Abdolmaleky, Hamid M.; Fournier, Margot; Cuénod, Michel; Quang, Kim; Deth, Richard C.

doi:10.1371/journal.pone.0146797

Cited by 136 publications

(100 citation statements)

References 87 publications

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“…We have previously shown that decreased GSH levels and elevated oxidative stress can subsequently result in altered epigenetic changes, specifically DNA methylation levels via the vitamin-B12-dependent enzyme methionine synthase [29]. In agreement, we observed that sleep deprivation increased the global DNA methylation levels.…”

Section: Discussionsupporting

confidence: 88%

Short-term sleep deprivation leads to decreased systemic redox metabolites and altered epigenetic status

et al. 2017

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Sleep is critical for repair as well as the rejuvenation processes in the body and many of these functions are regulated via underlying cellular metabolic homeostasis. Changes in sleep pattern are reported to alter such metabolic function resulting in altered disease susceptibility or behavior. Here, we measured the extent to which overnight total sleep deprivation (SD) in young adult humans can influence systemic (plasma-derived) redox-metabolism including the major antioxidant, glutathione as well as DNA methylation levels. Nineteen participants (n = 19, μ age = 21, SD = 3.09) underwent morning testing before and after overnight total SD. Biochemical measures before and after SD revealed that glutathione, ATP, cysteine, and homocysteine levels were significantly reduced following one night of sleep deprivation (all p’s < 0.01). Parallel to the well-recognized fact that sleep deprivation (maintaining wakefulness) uses up metabolic reserves, we observed that morning cortisol levels were blunted after sleep deprivation. There were no significant correlations between self-reported or actigraphy-measured sleep and the biochemical measurements, strongly indicating that prior sleep behavior did not have any direct influence on the biochemical measures taken at baseline or after sleep deprivation. Results from the current investigation supports the previous literature implicating the induction of oxidative stress and ATP depletion with sleep deprivation. Furthermore, such altered antioxidant status can also induce downstream epigenetic changes. Although we did not measure the specific genes that were altered under the influence of such sleep deprivation, such epigenetic changes could potentially contribute towards disease predisposition.

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Section: Discussionsupporting

confidence: 88%

Short-term sleep deprivation leads to decreased systemic redox metabolites and altered epigenetic status

et al. 2017

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“…Subcutaneous methyl‐B12 in children with autism has shown improvement with the clinician‐rated score on the Clinical Global Impressions Scale, and was positively correlated with increases in plasma methionine, and decreases in S‐adenosyl‐1‐HCy and improvement in the S‐adenosylmethionine‐to‐S‐adenosyl‐1‐HCy ratio . This is consistent with the observation that the levels of B12 were threefold lower in the brains of autistic subjects compared with age‐matched controls ( n = 12) …”

Section: Future Directionssupporting

confidence: 85%

Genetics and epigenetics of autism: A Review

Waye

Cheng

2017

Psychiatry Clin Neurosci

122

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Autism is a developmental disorder that starts before age 3 years, and children with autism have impairment in both social interaction and communication, and have restricted, repetitive, and stereotyped patterns of behavior, interests, and activities. There is a strong heritable component of autism and autism spectrum disorder (ASD) as studies have shown that parents who have a child with ASD have a 2-18% chance of having a second child with ASD. The prevalence of autism and ASD have been increasing during the last 3 decades and much research has been carried out to understand the etiology, so as to develop novel preventive and treatment strategies. This review aims at summarizing the latest research studies related to autism and ASD, focusing not only on the genetics but also some epigenetic findings of autism/ASD. Some promising areas of research using transgenic/knockout animals and some ideas related to potential novel treatment and prevention strategies will be discussed.

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“…Subsequently vitamin B 12 deficiency leads to elevated homocysteine, and impaired folate metabolism [306]. Decreased vitamin B 12 concentrations have been demonstrated in postmortem human frontal cortex from patients with autism and schizophrenia, as well as to decline with age (range from 19 weeks pregnancy to 80 years) [307].…”

Section: The Role Of Trace Elements and Micronutrients In Agingmentioning

confidence: 99%

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence

et al. 2017

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Aging is a complex phenomenon and its impact is becoming more relevant due to the rising life expectancy and because aging itself is the basis for the development of age-related diseases such as cancer, neurodegenerative diseases and type 2 diabetes. Recent years of scientific research have brought up different theories that attempt to explain the aging process. So far, there is no single theory that fully explains all facets of aging. The damage accumulation theory is one of the most accepted theories due to the large body of evidence found over the years. Damage accumulation is thought to be driven, among others, by oxidative stress. This condition results in an excess attack of oxidants on biomolecules, which lead to damage accumulation over time and contribute to the functional involution of cells, tissues and organisms. If oxidative stress persists, cellular senescence is a likely outcome and an important hallmark of aging. Therefore, it becomes crucial to understand how senescent cells function and how they contribute to the aging process. This review will cover cellular senescence features related to the protein pool such as morphological and molecular hallmarks, how oxidative stress promotes protein modifications, how senescent cells cope with them by proteostasis mechanisms, including antioxidant enzymes and proteolytic systems. We will also highlight the nutritional status of senescent cells and aged organisms (including human clinical studies) by exploring trace elements and micronutrients and on their importance to develop strategies that might increase both, life and health span and postpone aging onset.

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Decreased Brain Levels of Vitamin B12 in Aging, Autism and Schizophrenia

Cited by 136 publications

References 87 publications

Short-term sleep deprivation leads to decreased systemic redox metabolites and altered epigenetic status

Short-term sleep deprivation leads to decreased systemic redox metabolites and altered epigenetic status

Genetics and epigenetics of autism: A Review

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence

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