No alteration in leukocyte telomere length in schizophrenia; evidence from a meta-analysis

Omidpanah, Nafiseh; Darvishi, Farshad; Saadat, Mostafa

doi:10.1016/j.schres.2019.04.004

Cited by 5 publications

(4 citation statements)

References 10 publications

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“…Further, cellular aging can be assessed using telomere length, where SCZ patients have shorter telomeres compared to healthy subjects ( Czepielewski et al, 2016 ; Omidpanah et al, 2019 ). Follow-up investigation from one of the groups showed similar results while also correlating with the decreased brain gray matter volume measured using MRI described by other groups ( Czepielewski et al, 2018 ; Carrier et al, 2020 ).…”

Section: Evidence Of Accelerated Aging In Sczmentioning

confidence: 99%

“…Follow-up investigation from one of the groups showed similar results while also correlating with the decreased brain gray matter volume measured using MRI described by other groups ( Czepielewski et al, 2018 ; Carrier et al, 2020 ). It is important to mention though that the findings appear conflictual across studies [see for example ( Omidpanah et al, 2019 )], possibly due to differences in medication or subsets of patients with SCZ. Another hallmark of cellular aging measured in SCZ patients is oxidative stress ( Okusaga, 2013 ).…”

Section: Evidence Of Accelerated Aging In Sczmentioning

confidence: 99%

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Emerging epigenetic dynamics in gut-microglia brain axis: experimental and clinical implications for accelerated brain aging in schizophrenia

Ben-Azu

VanderZwaag

et al. 2023

Front. Cell. Neurosci.

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Brain aging, which involves a progressive loss of neuronal functions, has been reported to be premature in probands affected by schizophrenia (SCZ). Evidence shows that SCZ and accelerated aging are linked to changes in epigenetic clocks. Recent cross-sectional magnetic resonance imaging analyses have uncovered reduced brain reserves and connectivity in patients with SCZ compared to typically aging individuals. These data may indicate early abnormalities of neuronal function following cyto-architectural alterations in SCZ. The current mechanistic knowledge on brain aging, epigenetic changes, and their neuropsychiatric disease association remains incomplete. With this review, we explore and summarize evidence that the dynamics of gut-resident bacteria can modulate molecular brain function and contribute to age-related neurodegenerative disorders. It is known that environmental factors such as mode of birth, dietary habits, stress, pollution, and infections can modulate the microbiota system to regulate intrinsic neuronal activity and brain reserves through the vagus nerve and enteric nervous system. Microbiota-derived molecules can trigger continuous activation of the microglial sensome, groups of receptors and proteins that permit microglia to remodel the brain neurochemistry based on complex environmental activities. This remodeling causes aberrant brain plasticity as early as fetal developmental stages, and after the onset of first-episode psychosis. In the central nervous system, microglia, the resident immune surveillance cells, are involved in neurogenesis, phagocytosis of synapses and neurological dysfunction. Here, we review recent emerging experimental and clinical evidence regarding the gut-brain microglia axis involvement in SCZ pathology and etiology, the hypothesis of brain reserve and accelerated aging induced by dietary habits, stress, pollution, infections, and other factors. We also include in our review the possibilities and consequences of gut dysbiosis activities on microglial function and dysfunction, together with the effects of antipsychotics on the gut microbiome: therapeutic and adverse effects, role of fecal microbiota transplant and psychobiotics on microglial sensomes, brain reserves and SCZ-derived accelerated aging. We end the review with suggestions that may be applicable to the clinical setting. For example, we propose that psychobiotics might contribute to antipsychotic-induced therapeutic benefits or adverse effects, as well as reduce the aging process through the gut-brain microglia axis. Overall, we hope that this review will help increase the understanding of SCZ pathogenesis as related to chronobiology and the gut microbiome, as well as reveal new concepts that will serve as novel treatment targets for SCZ.

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Section: Evidence Of Accelerated Aging In Sczmentioning

confidence: 99%

Section: Evidence Of Accelerated Aging In Sczmentioning

confidence: 99%

Emerging epigenetic dynamics in gut-microglia brain axis: experimental and clinical implications for accelerated brain aging in schizophrenia

Ben-Azu

VanderZwaag

et al. 2023

Front. Cell. Neurosci.

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“…In addition, three studies (Cui et al, 2017;Maurya et al, 2017a;Nieratschker et al, 2013) found an opposite result: increased TL in subjects with schizophrenia. Several meta-analyses have been published on TL in schizophrenia leading to different conclusions (Lin, 2015;Omidpanah et al, 2019;Polho et al, 2015;Rao et al, 2016;Russo et al, 2018). Three of them conclude that TL is decreased in schizophrenia while, two others (Li et al, 2015;Omidpanah et al, 2019) do not.…”

Section: Introductionmentioning

confidence: 99%

“…Several meta-analyses have been published on TL in schizophrenia leading to different conclusions (Lin, 2015;Omidpanah et al, 2019;Polho et al, 2015;Rao et al, 2016;Russo et al, 2018). Three of them conclude that TL is decreased in schizophrenia while, two others (Li et al, 2015;Omidpanah et al, 2019) do not. To explain, these discrepant results, the most recent meta-analysis (Omidpanah et al, 2019) suggests that different subtypes of schizophrenia could have specific relationship with TL, while in the studies used for meta-analyses, patients were not categorized according to disease sub-types.…”

Section: Introductionmentioning

confidence: 99%

No alteration of leukocyte telomere length in first episode psychosis

Schürhoff

Corfdir

Pignon

et al. 2021

Psychiatry Research

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Both shorter telomeres and schizophrenia have been associated with a decrease in life expectancy. Furthermore, several studies found a shorter telomere length (TL) in schizophrenia.Understanding whether or not telomere shortening is directly related to pathophysiology of schizophrenia or is a consequence of a cumulative exposure to chronic stress is of major importance. Comparing the TL of subjects at the very beginning of the disease (FEP) and control subjects could help to decide between these two hypotheses. The aim of the present study was to compare TL between FEP subjects (N=91) and controls (N=137). After accounting for multiple potential confounders, no significant association was observed between FEP and TL.Our result is consistent with the hypothesis that psycho-social stress / adversities and stressful situations in people with schizophrenia affect TL rather than that telomere erosion contributes to the development of this disorder.

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