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阿尔茨海默病:一种替代方法。

Alzheimer's disease: An alternative approach.

机构信息

Department of Neurology, National Institute of Mental Health and Neurosciences, Bengaluru, India.

出版信息

Indian J Med Res. 2017 Jun;145(6):723-729. doi: 10.4103/ijmr.IJMR_74_17.

DOI:10.4103/ijmr.IJMR_74_17
PMID:29067973
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5674541/
Abstract

Alzheimer's disease (AD) is the most common neurodegenerative cortical dementia. It starts with memory loss, spatial disorientation in people above the age of 65 yr with a preference to females. Its incidence is expected to increase threefold by 2050. It affects almost one out of ten persons above the age of 65 years. Majority of patients are sporadic, but a very small percentage is autosomal dominant. The pathomechanisms postulated include amyloid cascade hypothesis according to which mutation in amyloid precursor protein causes Aβ aggregation. The next hypothesis is signal transducer and activation of transcription 3 (STAT3) causing aberration in intracellular signalling pathways. Senile plaques and neurofibrillary tangles are other important pathological changes reported. It is observed that dementia research has not yielded the expected result world over, and therefore, the pitfalls with reference to known facts about diagnosis, clinical features, pathogenic mechanisms, assessment of progression, biomarkers, treatment and prevention, as well as brief information on our experiments with relatively inexpensive methods of differentiating the most common types of dementia AD and frontotemporal dementia are discussed.

摘要

阿尔茨海默病(AD)是最常见的神经退行性皮质性痴呆。它始于 65 岁以上人群的记忆丧失和空间定向障碍,女性更为常见。预计到 2050 年,其发病率将增加三倍。它影响着近十分之一的 65 岁以上人群。大多数患者为散发性,但一小部分为常染色体显性遗传。推测的发病机制包括淀粉样蛋白级联假说,根据该假说,淀粉样前体蛋白的突变导致 Aβ聚集。下一个假说是信号转导和转录激活因子 3(STAT3),它导致细胞内信号通路的异常。老年斑和神经原纤维缠结是另一个重要的病理变化。观察到痴呆症研究在全球范围内并未产生预期的结果,因此,讨论了与诊断、临床特征、发病机制、进展评估、生物标志物、治疗和预防相关的已知事实的陷阱,以及简要介绍我们用相对便宜的方法区分最常见类型痴呆症(AD 和额颞叶痴呆)的实验。