Correlation between abnormal cellular immune and changes of magnetic resonance spectroscopy in patients with Alzheimer's disease

Hongmei Zeng; Qifang Zhang; Lijie Liu; Feifei Deng; Huabo Han; Fuxue Meng; Hua Bai

doi:10.1016/j.neuint.2024.105737

Correlation between abnormal cellular immune and changes of magnetic resonance spectroscopy in patients with Alzheimer's disease

Neurochem Int. 2024 Apr 9:176:105737. doi: 10.1016/j.neuint.2024.105737. Online ahead of print.

Authors

Hongmei Zeng¹, Qifang Zhang², Lijie Liu³, Feifei Deng⁴, Huabo Han⁵, Fuxue Meng⁶, Hua Bai⁷

Affiliations

¹ Department of Neurology, The Third Affiliated Hospital of Guizhou Medical University, Duyun, 558099, China; Department of Neurology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.
² Key Laboratory of Endemic and Ethnic Diseases, Ministry of Education, Guizhou Medical University, Guiyang, 550004, China; Key Laboratory of Medical Molecular Biology, Guizhou Medical University, Guiyang, 550004, China.
³ Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050004, China.
⁴ Department of Neurology, The Third Affiliated Hospital of Guizhou Medical University, Duyun, 558099, China.
⁵ Department of Radiology, The Third Affiliated Hospital of Guizhou Medical University, Duyun, 558099, China.
⁶ Medical Laboratory Center, Third Affiliated Hospital of Guizhou Medical University, Duyun, 558099, China.
⁷ Department of Neurology, The Third Affiliated Hospital of Guizhou Medical University, Duyun, 558099, China; Department of Neurology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China; Medical Laboratory Center, Third Affiliated Hospital of Guizhou Medical University, Duyun, 558099, China. Electronic address: baih2020@gmc.edu.cn.

PMID: 38599243
DOI: 10.1016/j.neuint.2024.105737

Abstract

Background: Evidence from previous studies indicates that neuroinflammation contributes to the onset of Alzheimer's Disease (AD). Moreover, cellular dysfunction is induced by impaired signaling of neurotransmitters. This study aimed to explore the correlation between cellular immune dysfunction and neurotransmitter changes through cranial Magnetic Resonance Spectroscopy (MRS) in AD patients.

Methods: Here, 32 AD, 40 Vascular Dementia (VD), and 35 Non-Dementia Elderly Control (NDE) cases were enrolled. Flow cytometry was performed to characterize lymphocyte subsets in plasma samples. The IL-1β and Caspase-1 levels were detected by ELISA. The NLRP3 expression level was measured by Western Blot (WB). The equivalence of N-acetylaspartate (NAA), Creatine (Cr), Choline (Cho), and Inositol (MI) in bilateral hippocampi of patients was examined by MRS. The association of NAA/Cr or MI/Cr ratios with the proportion of T lymphocyte subsets or NK cell subsets was determined through single-factor correlation analysis.

Results: The proportion of T lymphocyte subsets was significantly lower in the AD group than in the NDE group (P < 0.01). On the other hand, the Caspase-1, NLRP3, and IL-1β protein expression levels were significantly higher in the AD group than in the other groups. Further analysis showed that the NAA/Cr ratio was lower in the AD group than in the NDE group. Additionally, a significant positive correlation was found between the NAA/Cr ratio and the MMSE score (r = 0.81, P < 0.01). Moreover, a significant positive correlation was observed between the NAA/Cr and T lymphocyte ratios. The NAA/Cr ratio was significantly negatively correlated with the proportion of NK cells in the blood (r = －0.83, P < 0.01). A significant negative correlation was also recorded between the MI/Cr and T cell ratios in blood samples.

Conclusions: Impaired cellular immune dysfunction in AD patients was significantly correlated with abnormal MRS. Neuroimmune dysfunction may contribute to the pathogenesis of AD and alter the metabolism of neurotransmitters such as aspartic acid and MI in the brains of AD patients.

Trial registration: Not applicable.

Keywords: Alzheimer’s disease; Caspase-1; Inflammasome; Interleukin-1 beta; Magnetic resonance spectroscopy; Nucleotide-binding oligomerization domain-like receptor protein 3.