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主观听力损失与载脂蛋白 E ε4 等位基因对阿尔茨海默病神经退行性变的影响。

Association of Subjective Hearing Loss and Apolipoprotein E ε4 Allele on Alzheimer's Disease Neurodegeneration.

机构信息

Department of Otolaryngology-Head and Neck Surgery, University of Kentucky College of Medicine.

Department of Neurology.

出版信息

Otol Neurotol. 2021 Jan;42(1):e15-e21. doi: 10.1097/MAO.0000000000002855.

DOI:10.1097/MAO.0000000000002855
PMID:33301284
Abstract

OBJECTIVE

Hearing loss (HL) and apolipoprotein E ε4 (ApoE4) allele are both dementia risk factors. No research has investigated the association of these variables regarding dementia, specifically Alzheimer's disease. Our goal was to evaluate HL and ApoE4 allele positivity toward degree of Alzheimer's neurodegeneration.

STUDY DESIGN

Retrospective.

SETTING

Academic.

PATIENTS

Alzheimer's neuropathology obtained from brain tissue databank. Documented demographics, subjective hearing status, cognition, and ApoE4. Subjects divided into four groups based on hearing status and ApoE4 positivity.

MAIN OUTCOME MEASURES

Differences in cognition (clinical dementia rating, mini mental state examination (MMSE), geriatric depression score) and Alzheimer's neuropathology staging (Braak, CERAD) between groups.

RESULTS

Two-hundred and fifty-nine subjects. No significant difference between groups, with regard to hearing status or ApoE4 positivity, in premorbid cognition, including scores for clinical dementia rating and MMSE (p = 0.2332). HL subjects had less severe neuropathology, as compared with normal hearing subjects. For example, high grade Braak stage was present in 27.1 and 51.0% of HL and normal hearing subjects, respectively (p = 0.0263). This finding was in context of equivocal clinical cognition between groups. ApoE4+ individuals had more severe neurodegeneration; for example, 65.7 and 33.5% with high grade Braak stage for ApoE4+ and ApoE4- subjects, respectively (p < 0.0001).

CONCLUSION

Subjective HL subjects had less severe neuropathology with no difference in cognition, suggesting an additive effect of HL to cognitive burden of Alzheimer's neuropathology. HL appeared to increase cognitive burden, but wasn't manifested by greater neurodegeneration. This is clinically relevant in that treating HL could slow Alzheimer's disease progression.

摘要

目的

听力损失(HL)和载脂蛋白 E ε4(ApoE4)等位基因都是痴呆的危险因素。没有研究调查这些变量与痴呆症(特别是阿尔茨海默病)的关联。我们的目标是评估 HL 和 ApoE4 等位基因阳性与阿尔茨海默病神经退行性变的程度。

研究设计

回顾性。

地点

学术。

患者

从脑组织数据库获得阿尔茨海默病神经病理学。记录人口统计学、主观听力状况、认知和 ApoE4。根据听力状况和 ApoE4 阳性将受试者分为四组。

主要观察指标

各组之间认知(临床痴呆评定、简易精神状态检查(MMSE)、老年抑郁评分)和阿尔茨海默病神经病理学分期(Braak、CERAD)的差异。

结果

259 例患者。在认知(临床痴呆评定和 MMSE)方面,无论听力状况或 ApoE4 阳性,HL 组与正常听力组之间无显著差异(p=0.2332)。与正常听力受试者相比,HL 受试者的神经病理学表现较轻。例如,高级 Braak 分期分别见于 27.1%和 51.0%的 HL 和正常听力受试者(p=0.0263)。这一发现与两组之间不确定的临床认知有关。ApoE4+个体的神经退行性变更严重;例如,ApoE4+和 ApoE4-受试者的高级 Braak 分期分别为 65.7%和 33.5%(p<0.0001)。

结论

主观 HL 受试者的神经病理学表现较轻,认知无差异,提示 HL 对阿尔茨海默病神经病理学的认知负担有叠加作用。HL 似乎增加了认知负担,但没有表现出更多的神经退行性变。这在临床上具有重要意义,因为治疗 HL 可能会减缓阿尔茨海默病的进展。

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