关键词: cognitive impairment magnetic resonance spectroscopy neuromyelitis optica spectrum disorder neurotransmitter imbalances

Mesh : Humans Gyrus Cinguli / metabolism diagnostic imaging Female Adult Neuromyelitis Optica / metabolism diagnostic imaging Male Glutamic Acid / metabolism Magnetic Resonance Spectroscopy / methods Middle Aged gamma-Aminobutyric Acid / metabolism Glutathione / metabolism Young Adult Neurotransmitter Agents / metabolism Cognitive Dysfunction / metabolism diagnostic imaging

来  源:   DOI:10.1093/cercor/bhae304   PDF(Pubmed)

Abstract:
Cognitive impairment affects 29-67% of patients with neuromyelitis optica spectrum disorder. Previous studies have reported glutamate homeostasis disruptions in astrocytes, leading to imbalances in gamma-aminobutyric acid levels. However, the association between these neurotransmitter changes and cognitive deficits remains inadequately elucidated. Point RESolved Spectroscopy and Hadamard Encoding and Reconstruction of MEGA-Edited Spectroscopy techniques were utilized to evaluate gamma-aminobutyric acid, glutamate, glutathione levels, and excitation/inhibition balance in the anterior cingulate cortex, posterior cingulate cortex, and occipital cortex of 39 neuromyelitis optica spectrum disorder patients and 41 healthy controls. Cognitive function was assessed using neurocognitive scales. Results showed decreased gamma-aminobutyric acid levels alongside increased glutamate, glutathione, and excitation/inhibition ratio in the anterior cingulate cortex and posterior cingulate cortex of neuromyelitis optica spectrum disorder patients. Specifically, within the posterior cingulate cortex of neuromyelitis optica spectrum disorder patients, decreased gamma-aminobutyric acid levels and increased excitation/inhibition ratio correlated significantly with anxiety scores, whereas glutathione levels predicted diminished executive function. The results suggest that neuromyelitis optica spectrum disorder patients exhibit dysregulation in the GABAergic and glutamatergic systems in their brains, where the excitation/inhibition imbalance potentially acts as a neuronal metabolic factor contributing to emotional disorders. Additionally, glutathione levels in the posterior cingulate cortex region may serve as predictors of cognitive decline, highlighting the potential benefits of reducing oxidative stress to safeguard cognitive function in neuromyelitis optica spectrum disorder patients.
摘要:
认知障碍影响29-67%的视神经脊髓炎谱系障碍患者。以前的研究报道了星形胶质细胞中谷氨酸稳态的破坏,导致γ-氨基丁酸水平失衡。然而,这些神经递质变化与认知缺陷之间的关联仍未得到充分阐明.点求解光谱和哈达玛编码和MEGA编辑光谱技术的重建被用来评估γ-氨基丁酸,谷氨酸,谷胱甘肽水平,和前扣带皮质的兴奋/抑制平衡,后扣带皮质,39例视神经脊髓炎谱系障碍患者和41例健康对照者的枕皮质。使用神经认知量表评估认知功能。结果显示γ-氨基丁酸水平下降,谷氨酸增加,谷胱甘肽,视神经脊髓炎谱系障碍患者的前扣带皮质和后扣带皮质的兴奋/抑制比。具体来说,视神经脊髓炎谱系障碍患者的后扣带皮质内,降低的γ-氨基丁酸水平和增加的兴奋/抑制率与焦虑评分显著相关,而谷胱甘肽水平预测执行功能减弱。结果表明,视神经脊髓炎谱系障碍患者表现出大脑中GABA能和谷氨酸能系统的失调,其中兴奋/抑制失衡可能是导致情绪障碍的神经元代谢因素。此外,后扣带皮质区域的谷胱甘肽水平可以作为认知衰退的预测因子,强调减少氧化应激保护视神经脊髓炎谱系障碍患者认知功能的潜在益处。
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