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西班牙裔老年人中特定及累积接触感染源与认知障碍的关联。

The association of specific and cumulative exposure to infectious agents with cognitive impairment in older Hispanic adults.

作者信息

Rangel Giselle A, Muñoz Berta A, Ramirez Morgan, Wroblewski Kristen, Villarreal Alcibiades E, Oviedo Diana C, Carreira Maria B, McLeod Rima, Britton Gabrielle B

机构信息

Departamento de Neurociencias, Instituto de Investigaciones Científicas y Servicios de Alta Tecnología (INDICASAT-AIP), Ciudad del Saber, Panama City, Panama.

Sistema Nacional de Investigación (SNI), Secretaría Nacional de Ciencia Tecnología e Innovación (SENACYT), Panama City, Panamá.

出版信息

J Alzheimers Dis Rep. 2025 Jul 24;9:25424823251361066. doi: 10.1177/25424823251361066. eCollection 2025 Jan-Dec.

DOI:10.1177/25424823251361066
PMID:40727258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12301615/
Abstract

BACKGROUND

Accumulating evidence implicates infectious pathogens as triggers of immune-inflammatory processes that contribute to neurodegeneration. Inflammation in both the brain and peripheral circulation is recognized as a critical factor in the development and progression of cognitive decline and neurodegenerative disorders, including Alzheimer's disease.

OBJECTIVE

This retrospective case-control study investigated the association between cognitive impairment and presence of serum antibodies to seven pathogens in older adults.

METHODS

One hundred sixty-five participants aged ≥ 65 years from the Panama Aging Research Initiative Health Disparities (PARI-HD) study were evaluated. Presence of IgG antibodies against , Herpes Simplex Virus Type 1 (HSV-1), Human Cytomegalovirus (HCMV), , and was measured. Participant demographics, inflammatory biomarkers and cognitive-functional factors were analyzed for associations with single/multiple pathogen-specific antibodies reactivity using multivariable regression models.

RESULTS

Only seropositivity was significantly different between cognitively unimpaired and impaired groups (p = 0.02) and increasing TNF-α levels were directly associated with C. seropositivity (OR = 2.08, CI 1.0-4.1, p = 0.04). Additionally, cumulative exposure to infectious agents increased the likelihood of cognitive impairment (OR = 1.51, CI 1.01-2.26, p = 0.04) and was associated with slower processing speed as measured by TMT A test (OR = 17.43, CI 2.32-32.53, p = 0.02). Notably, the presence of in multiple pathogen interactions further raised the likelihood of cognitive impairment (OR = 4.07, CI 1.24-13.36, p = 0.03).

CONCLUSIONS

These results enhance our understanding of cognitive impairment in a Hispanic population and underscore the need for further studies on the role of and multi-pathogen infection in Alzheimer's disease.

摘要

背景

越来越多的证据表明,感染性病原体是导致免疫炎症过程的触发因素,而这些过程会促进神经退行性变。大脑和外周循环中的炎症被认为是认知能力下降和神经退行性疾病(包括阿尔茨海默病)发生和发展的关键因素。

目的

这项回顾性病例对照研究调查了老年人认知障碍与血清中七种病原体抗体存在之间的关联。

方法

对来自巴拿马衰老研究倡议健康差异(PARI-HD)研究的165名年龄≥65岁的参与者进行了评估。检测了针对1型单纯疱疹病毒(HSV-1)、人巨细胞病毒(HCMV)等的IgG抗体的存在情况。使用多变量回归模型分析参与者的人口统计学特征、炎症生物标志物和认知功能因素与单一/多种病原体特异性抗体反应性之间的关联。

结果

在认知未受损和受损组之间,仅[病原体名称未明确]血清阳性率存在显著差异(p = 0.02),并且肿瘤坏死因子-α(TNF-α)水平升高与[病原体名称未明确]血清阳性直接相关(比值比[OR]=2.08,置信区间[CI]1.0 - 4.1,p = 0.04)。此外,累积接触感染因子增加了认知障碍的可能性(OR = 1.51,CI 1.01 - 2.26,p = 0.04),并且与通过数字符号替换测验A(TMT A)测量的处理速度减慢相关(OR = 17.43,CI 翻页 2.32 - 32.53,p = 0.02)。值得注意的是,在多种病原体相互作用中存在[病原体名称未明确]进一步增加了认知障碍的可能性(OR = 4.07,CI 1.24 - 13.36,p = 0.03)。

结论

这些结果增进了我们对西班牙裔人群认知障碍的理解,并强调了有必要进一步研究[病原体名称未明确]和多病原体感染在阿尔茨海默病中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/478bf8322e4b/10.1177_25424823251361066-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/44be950c70e9/10.1177_25424823251361066-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/8dc207bff359/10.1177_25424823251361066-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/574873dfba20/10.1177_25424823251361066-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/69acd77f5eef/10.1177_25424823251361066-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/478bf8322e4b/10.1177_25424823251361066-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/44be950c70e9/10.1177_25424823251361066-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/8dc207bff359/10.1177_25424823251361066-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/574873dfba20/10.1177_25424823251361066-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/69acd77f5eef/10.1177_25424823251361066-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49b0/12301615/478bf8322e4b/10.1177_25424823251361066-fig5.jpg

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