کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6263095 1613822 2015 20 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
ReviewAbnormal immune system development and function in schizophrenia helps reconcile diverse findings and suggests new treatment and prevention strategies
ترجمه فارسی عنوان
بررسی عملکرد سیستم عصبی سیستم ایمنی بدن در اسکیزوفرنی کمک می کند تا یافته های مختلف را آشتی کند و راهبردهای جدید درمان و پیشگیری را پیشنهاد کند
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
چکیده انگلیسی


- We present a hypothesis of abnormal immune system development in schizophrenia.
- The hypothesis uniquely helps unify diverse findings in the field.
- We review evidence on 10 key sets of findings explained by the hypothesis.
- We propose several experimental tests of the hypothesis.
- Novel strategies for the treatment and prevention of schizophrenia are outlined.

Extensive research implicates disturbed immune function and development in the etiology and pathology of schizophrenia. In addition to reviewing evidence for immunological factors in schizophrenia, this paper discusses how an emerging model of atypical immune function and development helps explain a wide variety of well-established - but puzzling - findings about schizophrenia. A number of theorists have presented hypotheses that early immune system programming, disrupted by pre- and perinatal adversity, often combines with abnormal brain development to produce schizophrenia. The present paper focuses on the hypothesis that disruption of early immune system development produces a latent immune vulnerability that manifests more fully after puberty, when changes in immune function and the thymus leave individuals more susceptible to infections and immune dysfunctions that contribute to schizophrenia. Complementing neurodevelopmental models, this hypothesis integrates findings on many contributing factors to schizophrenia, including prenatal adversity, genes, climate, migration, infections, and stress, among others. It helps explain, for example, why (a) schizophrenia onset is typically delayed until years after prenatal adversity, (b) individual risk factors alone often do not lead to schizophrenia, and (c) schizophrenia prevalence rates actually tend to be higher in economically advantaged countries. Here we discuss how the hypothesis explains 10 key findings, and suggests new, potentially highly cost-effective, strategies for treatment and prevention of schizophrenia. Moreover, while most human research linking immune factors to schizophrenia has been correlational, these strategies provide ethical ways to experimentally test in humans theories about immune function and schizophrenia.This article is part of a Special Issue entitled SI: Neuroimmunology in Health And Disease.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1617, 18 August 2015, Pages 93-112
نویسندگان
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