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遗忘型轻度认知障碍中纵向突触丧失与tau蛋白Braak分期的关系

Longitudinal synaptic loss versus tau Braak staging in amnestic mild cognitive impairment.

作者信息

Vanderlinden Greet, Koole Michel, Michiels Laura, Lemmens Robin, Vandenbulcke Mathieu, Van Laere Koen

机构信息

Nuclear Medicine and Molecular Imaging, Imaging and Pathology, KU Leuven, Leuven, Belgium.

Leuven Brain Institute, KU Leuven, Leuven, Belgium.

出版信息

Alzheimers Dement. 2025 Feb;21(2):e14412. doi: 10.1002/alz.14412. Epub 2024 Dec 28.

DOI:10.1002/alz.14412
PMID:39732507
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11848342/
Abstract

INTRODUCTION

The longitudinal progression of synaptic loss in Alzheimer's disease (AD) and how it is affected by tau pathology remains poorly understood.

METHODS

Thirty patients with amnestic mild cognitive impairment (aMCI) and 26 healthy controls underwent cognitive evaluations and tau, synaptic vesicle protein 2A (SV2A), and amyloid positron emission tomography. Twenty-one aMCI underwent 2-year follow-up (FU) investigations.

RESULTS

Tau levels in aMCI increased longitudinally in Braak regions III through VI but not in Braak regions I and II. SV2A decreased longitudinally in all Braak regions in aMCI. Baseline tau was negatively associated with longitudinal SV2A loss in early Braak regions and with SV2A at FU across regions. Baseline tau and longitudinal change in SV2A were associated with longitudinal cognitive decline.

DISCUSSION

Tau accumulation reaches a plateau in early Braak regions already in the aMCI stage of AD. In early Braak regions, the association between baseline tau and longitudinal SV2A loss might reflect synaptic dysfunction caused by tau pathology.

HIGHLIGHTS

Tau accumulation reached a plateau in early Braak regions in amnestic mild cognitive impairment (aMCI) patients. aMCI patients show widespread longitudinal decrease in synaptic vesicle protein 2A (SV2A) over 2 years. Baseline tau was predictive for longitudinal SV2A loss. The tau-SV2A relation showed individual variability and was negative across patients. Baseline tau and longitudinal SV2A change were associated with change in cognition.

摘要

引言

阿尔茨海默病（AD）中突触损失的纵向进展以及它如何受tau病理影响仍知之甚少。

方法

30例遗忘型轻度认知障碍（aMCI）患者和26名健康对照者接受了认知评估以及tau、突触囊泡蛋白2A（SV2A）和淀粉样蛋白正电子发射断层扫描。21例aMCI患者接受了为期2年的随访（FU）调查。

结果

aMCI患者的tau水平在Braak III至VI区纵向升高，但在Braak I和II区没有升高。aMCI患者所有Braak区的SV2A均纵向降低。基线tau与早期Braak区的纵向SV2A损失以及各区域随访时的SV2A呈负相关。基线tau和SV2A的纵向变化与纵向认知衰退相关。

讨论

在AD的aMCI阶段，tau积累在早期Braak区已达到平台期。在早期Braak区，基线tau与纵向SV2A损失之间的关联可能反映了tau病理导致的突触功能障碍。

要点

遗忘型轻度认知障碍（aMCI）患者的tau积累在早期Braak区达到平台期。aMCI患者在2年期间突触囊泡蛋白2A（SV2A）普遍出现纵向下降。基线tau可预测纵向SV2A损失。tau与SV2A的关系存在个体差异且在患者中呈负相关。基线tau和纵向SV2A变化与认知变化相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/3ea191f4bf62/ALZ-21-e14412-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/7534fa580066/ALZ-21-e14412-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/3c7e7e177958/ALZ-21-e14412-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/e51b6c167efc/ALZ-21-e14412-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/de87ab2a0352/ALZ-21-e14412-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/3ea191f4bf62/ALZ-21-e14412-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/7534fa580066/ALZ-21-e14412-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/3c7e7e177958/ALZ-21-e14412-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/e51b6c167efc/ALZ-21-e14412-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/de87ab2a0352/ALZ-21-e14412-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac4/11848342/3ea191f4bf62/ALZ-21-e14412-g001.jpg

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