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双相情感障碍中与神经进展相关的生物学通路

Biological Pathways Associated with Neuroprogression in Bipolar Disorder.

作者信息

Wollenhaupt-Aguiar Bianca, Kapczinski Flavio, Pfaffenseller Bianca

机构信息

Department of Psychiatry and Behavioural Neuroscience, McMaster University, Hamilton, ON L8N 3K7, Canada.

Mood Disorders Program, St. Joseph's Healthcare Hamilton, Hamilton, ON L8N 3K7, Canada.

出版信息

Brain Sci. 2021 Feb 12;11(2):228. doi: 10.3390/brainsci11020228.

DOI:10.3390/brainsci11020228
PMID:33673277
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7918818/
Abstract

There is evidence suggesting clinical progression in a subset of patients with bipolar disorder (BD). This progression is associated with worse clinical outcomes and biological changes. Molecular pathways and biological markers of clinical progression have been identified and may explain the progressive changes associated with this disorder. The biological basis for clinical progression in BD is called neuroprogression. We propose that the following intertwined pathways provide the biological basis of neuroprogression: inflammation, oxidative stress, impaired calcium signaling, endoplasmic reticulum and mitochondrial dysfunction, and impaired neuroplasticity and cellular resilience. The nonlinear interaction of these pathways may worsen clinical outcomes, cognition, and functioning. Understanding neuroprogression in BD is crucial for identifying novel therapeutic targets, preventing illness progression, and ultimately promoting better outcomes.

摘要

有证据表明双相情感障碍(BD)患者的一个亚组存在临床进展。这种进展与更差的临床结局和生物学变化相关。临床进展的分子途径和生物学标志物已被确定,可能解释与该疾病相关的渐进性变化。BD临床进展的生物学基础被称为神经进展。我们提出以下相互交织的途径为神经进展提供生物学基础:炎症、氧化应激、钙信号传导受损、内质网和线粒体功能障碍,以及神经可塑性和细胞弹性受损。这些途径的非线性相互作用可能会使临床结局、认知和功能恶化。了解BD中的神经进展对于确定新的治疗靶点、预防疾病进展以及最终促进更好的结局至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be76/7918818/c03e40f87bab/brainsci-11-00228-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be76/7918818/4c5d330a1ab7/brainsci-11-00228-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be76/7918818/c03e40f87bab/brainsci-11-00228-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be76/7918818/4c5d330a1ab7/brainsci-11-00228-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be76/7918818/c03e40f87bab/brainsci-11-00228-g002.jpg

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