GABAergic imbalance in Parkinson’s disease–related depression determined with MEGA-PRESS

IF 3.4 2区 医学 Q2 NEUROIMAGING Neuroimage-Clinical Pub Date : 2024-01-01 DOI:10.1016/j.nicl.2024.103641
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Abstract

Objective

The pathogenesis of depression in patients with Parkinson’s disease (PD) is poorly understood. Therefore, this study aimed to explore the changes in γ-aminobutyric acid (GABA) and glutamate plus glutamine (Glx) levels in patients with PD with or without depression determined using MEscher-GArwood Point Resolved Spectroscopy (MEGA-PRESS).

Materials and methods

A total of 83 patients with primary PD and 24 healthy controls were included. Patients with PD were categorized into depressed PD (DPD, n = 19) and nondepressed PD (NDPD, n = 64) based on the 17-item Hamilton Depression Rating Scale. All participants underwent T1-weighted imaging and MEGA-PRESS sequence to acquire GABA+ and Glx values. The MEGA-PRESS sequence was conducted using 18.48 mL voxels in the left thalamus and medial frontal cortex. The GABA+, Glx, and creatine values were quantified using Gannet 3.1 software.

Results

The GABA+ and Glx values were not significantly disparate between patients with PD and controls in the thalamus and medial frontal cortex. However, the levels of N-acetyl aspartate/creatine and choline/creatine in the left thalamus were significantly lower in patients with PD than in controls (P = .031, P = .009). The GABA+/Water and GABA+/Creatine in the medial frontal cortex were higher in DPD than in NDPD (P = .001, P = .004). The effects of depression on Glx or other metabolite levels were not evident, and no significant difference in metabolite values was noted in the left thalamus among all groups (P > .05).

Conclusions

GABA+ levels increased in the medial frontal cortex in DPD, which may be more closely related to depressive pathology. Thus, alterations in GABAergic function in special brain structures may be related to the clinical manifestations of PD symptoms, and hence mediating this function might help in treating depression in PD.

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用 MEGA-PRESS 测定帕金森病相关抑郁症中的加巴能失衡现象
目的 帕金森病(PD)患者抑郁的发病机制尚不清楚。因此,本研究旨在探讨使用 MEscher-GArwood 点分辨光谱仪(MEGA-PRESS)测定伴有或不伴有抑郁的帕金森病患者体内γ-氨基丁酸(GABA)和谷氨酸加谷氨酰胺(Glx)水平的变化。根据汉密尔顿抑郁评定量表(Hamilton Depression Rating Scale)的17个项目,将帕金森病患者分为抑郁性帕金森病(DPD,n = 19)和非抑郁性帕金森病(NDPD,n = 64)。所有参与者都接受了T1加权成像和MEGA-PRESS序列,以获得GABA+和Glx值。MEGA-PRESS 序列使用了左侧丘脑和内侧额叶皮层的 18.48 mL 体素。结果丘脑和内侧额叶皮层的 GABA+ 和 Glx 值在帕金森病患者和对照组之间没有明显差异。然而,PD 患者左丘脑中的 N-乙酰天冬氨酸/肌酸和胆碱/肌酸水平明显低于对照组(P = .031, P = .009)。内侧额叶皮质中的 GABA+/Water 和 GABA+/Creatine 在帕金森病患者中高于非帕金森病患者(P = .001, P = .004)。抑郁症对 Glx 或其他代谢物水平的影响并不明显,所有组间左丘脑的代谢物值无显著差异(P >.05)。因此,特殊脑结构中GABA能功能的改变可能与帕金森病症状的临床表现有关,因此介导这一功能可能有助于帕金森病抑郁症的治疗。
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来源期刊
Neuroimage-Clinical
Neuroimage-Clinical NEUROIMAGING-
CiteScore
7.50
自引率
4.80%
发文量
368
审稿时长
52 days
期刊介绍: NeuroImage: Clinical, a journal of diseases, disorders and syndromes involving the Nervous System, provides a vehicle for communicating important advances in the study of abnormal structure-function relationships of the human nervous system based on imaging. The focus of NeuroImage: Clinical is on defining changes to the brain associated with primary neurologic and psychiatric diseases and disorders of the nervous system as well as behavioral syndromes and developmental conditions. The main criterion for judging papers is the extent of scientific advancement in the understanding of the pathophysiologic mechanisms of diseases and disorders, in identification of functional models that link clinical signs and symptoms with brain function and in the creation of image based tools applicable to a broad range of clinical needs including diagnosis, monitoring and tracking of illness, predicting therapeutic response and development of new treatments. Papers dealing with structure and function in animal models will also be considered if they reveal mechanisms that can be readily translated to human conditions.
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