期刊
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
卷 133, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neubiorev.2021.12.020
关键词
Anterior cingulate cortex; Prefrontal cortex; Mood disorders; Depression; Anxiety; Cognition; Gut inflammation; Neuroinflammation; Microglia; Astrocytes; Inflammatory bowel disease; Ulcerative colitis; Irritable bowel syndrome; Celiac disease; Functional dyspepsia diabetes; Fibromyalgia; Rheumatoid arthritis; Brain fog; Antidepressants; Anti-Inflammatory; vagus stimulation; Microbiota; Autonomic nervous system; Sympathetic nervous system; Peripheral nervous system; Negative schemas; Memory; Crohn's disease
资金
- Alberta Innovates Health Solutions PDF
- NSERC
Most gastrointestinal diseases and disorders (GIDD) are associated with depression, anxiety, and cognitive dysfunction. The anterior cingulate cortex (ACC) is identified as a primary target affected by chronic pain and inflammation in GIDD. The theory proposes that peripheral-triggered neuroinflammation signals injury/illness to ACC, leading to altered mental function and increased pain sensitivity. Chronic peripheral inflammation causes ACC structural remodeling and excessive threat signaling, resulting in anxiodepressive phenotypes and further gut pathology.
Most gastrointestinal diseases and disorders (GIDD) are associated with depression, anxiety, and cognitive dysfunction. This suggests that shared features of GIDD, particularly chronic pain and inflammation, affect specific neural targets. The critical review of clinical and animal research presented here reveals that anterior cingulate cortex (ACC) is a primary target. It is particularly sensitive to neuroinflammation, and its function accounts for altered mental function emergent in GIDD. We propose that peripherally-triggered neuroinflammation normally signals injury/illness to ACC, which increases threat assessment and pain sensitivity to cope with increased vulnerability. Chronic peripheral inflammation over-drives this process, leading to long-term ACC structural remodeling, and excessive threat signaling. This evokes anxiodepressive phenotypes even without direct evidence of threats because ACC utilizes schemas to infer affective outcomes (e.g. pain) based on complex contextual information. This activates the autonomic nervous system, exacerbates immune dysfunction, and promotes further gut pathology. This theory provides a mechanistic account of bidirectional interactions among gastrointestinal, immunological, and neural systems in GIDD, and is likely applicable to other chronic inflammatory conditions.
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