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SV2A PET 测定的突触前密度与突触后代谢型谷氨酸受体 5 的可及性密切相关，且与早期认知障碍中的淀粉样蛋白病理学无关。

Presynaptic density determined by SV2A PET is closely associated with postsynaptic metabotropic glutamate receptor 5 availability and independent of amyloid pathology in early cognitive impairment.

机构信息

Department of Nuclear Medicine & PET Center, Huashan Hospital, Fudan University, Shanghai, China.

Institute of Biomedical Engineering, Shenzhen Bay Laboratory, Shenzhen, China.

出版信息

Alzheimers Dement. 2024 Jun;20(6):3876-3888. doi: 10.1002/alz.13817. Epub 2024 Apr 18.

DOI:10.1002/alz.13817
PMID:38634334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11180932/
Abstract

INTRODUCTION

Metabotropic glutamate receptor 5 (mGluR5) is involved in regulating integrative brain function and synaptic transmission. Aberrant mGluR5 signaling and relevant synaptic failure play a key role in the pathophysiological mechanism of Alzheimer's disease (AD).

METHODS

Ten cognitively impaired (CI) individuals and 10 healthy controls (HCs) underwent [F]SynVesT-1 and [F]PSS232 positron emission tomography (PET)/magnetic resonance to assess synaptic density and mGluR5 availability. The associations between mGluR5 availability and synaptic density were examined. A mediation analysis was performed to investigate the possible mediating effects of mGluR5 availability and synaptic loss on the relationship between amyloid deposition and cognition.

RESULTS

CI patients exhibited lower mGluR5 availability and synaptic density in the medial temporal lobe than HCs. Regional synaptic density was closely associated with regional mGluR5 availability. mGluR5 availability and synaptic loss partially mediated the relationship between amyloid deposition and cognition.

CONCLUSIONS

Reductions in mGluR5 availability and synaptic density exhibit similar spatial patterns in AD and are closely linked.

HIGHLIGHTS

Cognitively impaired patients exhibited lower mGluR5 availability and synaptic density in the medial temporal lobe than HCs. Reductions in mGluR5 availability and synaptic density exhibit similar spatial patterns in AD. Regional synaptic density was closely associated with regional mGluR5 availability. mGluR5 availability and synaptic loss partially mediated the relationship between amyloid deposition and global cognition. With further research, modulating mGluR5 availability might be a potential therapeutic strategy for improving synaptic function in AD.

摘要

简介

代谢型谷氨酸受体 5（mGluR5）参与调节大脑的整合功能和突触传递。异常的 mGluR5 信号和相关的突触功能障碍在阿尔茨海默病（AD）的病理生理机制中起着关键作用。

方法

10 名认知障碍（CI）个体和 10 名健康对照（HC）接受 [F]SynVesT-1 和 [F]PSS232 正电子发射断层扫描（PET）/磁共振检查，以评估突触密度和 mGluR5 可及性。研究了 mGluR5 可及性与突触密度之间的相关性。进行中介分析以探讨 mGluR5 可及性和突触丧失对淀粉样蛋白沉积与认知之间关系的可能中介作用。

结果

CI 患者的内侧颞叶 mGluR5 可及性和突触密度均低于 HC。区域突触密度与区域 mGluR5 可及性密切相关。mGluR5 可及性和突触丧失部分介导了淀粉样蛋白沉积与认知之间的关系。

结论

AD 中 mGluR5 可及性和突触密度的降低具有相似的空间模式，并密切相关。

重点

认知障碍患者的内侧颞叶 mGluR5 可及性和突触密度均低于 HC。AD 中 mGluR5 可及性和突触密度的降低具有相似的空间模式。区域突触密度与区域 mGluR5 可及性密切相关。mGluR5 可及性和突触丧失部分介导了淀粉样蛋白沉积与全球认知之间的关系。随着进一步的研究，调节 mGluR5 可及性可能是改善 AD 中突触功能的潜在治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/434342492825/ALZ-20-3876-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/5898a20adfea/ALZ-20-3876-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/174f715807b6/ALZ-20-3876-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/1d9dcd463392/ALZ-20-3876-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/a632b7eb56fe/ALZ-20-3876-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/0347bf2eb9ed/ALZ-20-3876-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/434342492825/ALZ-20-3876-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/5898a20adfea/ALZ-20-3876-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/174f715807b6/ALZ-20-3876-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/1d9dcd463392/ALZ-20-3876-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/a632b7eb56fe/ALZ-20-3876-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/0347bf2eb9ed/ALZ-20-3876-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac6/11180932/434342492825/ALZ-20-3876-g002.jpg

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