Studies
Journal Published
Schizophrenia Bulletin, Volume 44, Issue 2, March 2018, Pages 398–408,
Year Published
2017
Full Article
SystemicZBiomarkersZofZAcceleratedZAgingZinZSchizophrenia.pdf
Hypothesis
This study aims to evaluate evidence for accelerated biological aging in schizophrenia using systemic markers of biological aging.
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Are aging-related biomarkers abnormal in schizophrenia?
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Which biomarkers are specifically involved in aging in schizophrenia?
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What clinical characteristics in schizophrenia are risk vs protective factors for accelerated biological aging?
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Are aging-related biomarkers abnormal in schizophrenia?
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Which biomarkers are specifically involved in aging in schizophrenia?
Background
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Schizophrenia is associated with markedly increased physical comorbidity and mortality.
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Physiological changes seen throughout the body with normal aging occur at an earlier age in people with schizophrenia than in healthy comparison subjects (HCs).
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Younger adults with schizophrenia are prone to diseases associated with aging such as diabetes and cardiovascular disorders
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The average life span of a person with schizophrenia is 15–20 years shorter than that of an unaffected person
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Patients with schizophrenia have 2–12 times higher mortality rate than age-comparable general population.
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Given that lifespans are generally increasing for the population as a whole, understanding alterations in the aging process within schizophrenia is clearly imperative
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Two-thirds of the excess deaths in schizophrenia are not from suicide, but due to “natural causes” such as cardiac and metabolic disorders.
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This has led to a provocative suggestion that schizophrenia is not only a brain disease but rather, a disease of the whole body.
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Prior attempts to address systemic biological defects in schizophrenia failed,at least in part, because of a lack of specific and sensitive systemic biomarkers of aging.
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Several prior reviews have examined accelerated aging in schizophrenia from various perspectives (including metabolic disease cognition, brain structure, telomere length (TL),and oxidative stress, however, no publication, to our knowledge, has provided a comprehensive review of multiple biomarkers relevant to the hypothesis of accelerated biological aging in schizophrenia.
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Although many comparisons and similarities have been drawn between schizophrenia and normal aging, we have a limited understanding as to which biomarkers are most altered with age in schizophrenia.
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The identification of biological factors that underlie alterations in the aging process may permit identification of individuals at high risk for accelerated aging, and potentially open up consideration of new avenues for intervention.
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Though the recent literature has frequently used the term “accelerated biological aging,” no review has synthesized evidence for this claim at system level.
Journal Published
Am J Psychiatry
Year Published
2016
Full Article
AcceleratedZBrainZAgingZinZSchizophrenia.pdf
Hypothesis
Does the progressive brain loss in schizophrenia reflect accelerated aging of the brain, or is it caused by a fundamentally different process?
Background
- Cross-sectional MRI studies have convincingly shown that brain volumesin schizophrenia patients are smaller than those in healthy subjects.
- Some of these abnormalities (such as changes in white matter volume and structure) are present beforeillness onset and aremostlikely of a developmental, possibly genetic, nature and appear to be stable over time.
- In contrast, other brain changes (such as reductionsin gray matter volume) become more pronounced during the course of the illness.
- Although several studies suggest that gray matter volume reductions are related to outcome, psychosis, relapses, medication, cannabis use, and genetic liability, the cause and nature of the progressive loss of gray matter are still unclear.
- Indeed, despite the multitude of longitudinal neuroimaging studies, a basic question on the progressive brain loss in schizophrenia remains unaddressed.
