期刊
EXPERT REVIEW OF NEUROTHERAPEUTICS
卷 11, 期 7, 页码 1017-1028出版社
TAYLOR & FRANCIS LTD
DOI: 10.1586/ERN.10.185
关键词
allostatic load; bipolar disorder; cognition; cytokines; early life stress; general medical comorbidities; HPA; insulin; neuroplasticity; oxidative stress
资金
- Stanley Medical Research Institute
- National Alliance for Research on Schizophrenia and Depression (NARSAD)
- Eli Lilly
- Janssen-Ortho
- Shire
- AstraZeneca
- Pfizer
- Bristol-Myers Squibb
Bipolar disorder (BD) is associated with substantial morbidity, as well as premature mortality. Available evidence indicates that 'stress-sensitive' chronic medical disorders, such as cardiovascular disease, obesity and Type 2 diabetes mellitus, are critical mediators and/or moderators of BD. Changes in physiologic systems implicated in allostasis have been proposed to impact brain structures and neurocognition, as well as medical comorbidity in this population. For example, abnormalities in insulin physiology, for example, insulin resistance, hyperinsulinemia and central insulinopenia, are implicated as effectors of allostatic load in BD. Insulin's critical role in CNS physiological (e.g., neurotrophism and synaptic plasticity) and pathophysiological (e.g., neurocognitive deficits, pro-apoptosis and amyloid deposition) processes is amply documented. This article introduces the concept that insulin is a mediator of allostatic load in the BD and possibly a therapeutic target.
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