{"title":"[导致痴呆症的神经病理学]。","authors":"Kenji Sakai, Masahito Yamada","doi":"10.11477/mf.1416202610","DOIUrl":null,"url":null,"abstract":"<p><p>Dementia is characterized by acquired cognitive dysfunction caused by various neurological disorders. Many neurological conditions can cause dementia, including neurodegenerative diseases, vascular disorders, infections, inflammation, demyelination, intoxication, metabolic disorders, tumors, and head trauma. Despite recent developments in biomarkers and imaging techniques, neuropathological examination is necessary for the final diagnosis. Moreover, approximately 11% of the patients with dementia have dual or triple pathological conditions. The coexistence of neurological diseases makes it difficult for neurologists to diagnose patients accurately. Degenerative diseases are characterized by neuronal loss with gliosis in distinct parts of the brain, the presence of neuronal or glial inclusions, and abnormal protein accumulation. Senile plaques and neurofibrillary tangles are neuropathological hallmarks of Alzheimer's disease. These findings are characterized by the presence of amyloid β protein (Aβ) and phosphorylated tau protein, respectively. Although vascular dementia is common, it may be difficult to identify the relationship between vascular lesions and cognitive impairment. The incidence of sporadic Aβ-type cerebral amyloid angiopathy (CAA) tends to increase with age and causes dementia due to vascular dysfunction and leukoencephalopathy. Furthermore, patients with CAA can develop inflammation. Clinical neurologists should possess a neuropathological perspective for the appropriate diagnosis and management of patients with dementia.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":"76 4","pages":"333-342"},"PeriodicalIF":0.0000,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Neuropathology of Disorders Leading to Dementia].\",\"authors\":\"Kenji Sakai, Masahito Yamada\",\"doi\":\"10.11477/mf.1416202610\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Dementia is characterized by acquired cognitive dysfunction caused by various neurological disorders. Many neurological conditions can cause dementia, including neurodegenerative diseases, vascular disorders, infections, inflammation, demyelination, intoxication, metabolic disorders, tumors, and head trauma. Despite recent developments in biomarkers and imaging techniques, neuropathological examination is necessary for the final diagnosis. Moreover, approximately 11% of the patients with dementia have dual or triple pathological conditions. The coexistence of neurological diseases makes it difficult for neurologists to diagnose patients accurately. Degenerative diseases are characterized by neuronal loss with gliosis in distinct parts of the brain, the presence of neuronal or glial inclusions, and abnormal protein accumulation. Senile plaques and neurofibrillary tangles are neuropathological hallmarks of Alzheimer's disease. These findings are characterized by the presence of amyloid β protein (Aβ) and phosphorylated tau protein, respectively. Although vascular dementia is common, it may be difficult to identify the relationship between vascular lesions and cognitive impairment. The incidence of sporadic Aβ-type cerebral amyloid angiopathy (CAA) tends to increase with age and causes dementia due to vascular dysfunction and leukoencephalopathy. Furthermore, patients with CAA can develop inflammation. Clinical neurologists should possess a neuropathological perspective for the appropriate diagnosis and management of patients with dementia.</p>\",\"PeriodicalId\":52507,\"journal\":{\"name\":\"Brain and Nerve\",\"volume\":\"76 4\",\"pages\":\"333-342\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Brain and Nerve\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.11477/mf.1416202610\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain and Nerve","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.11477/mf.1416202610","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
摘要
痴呆症的特征是由各种神经系统疾病引起的获得性认知功能障碍。许多神经系统疾病都可导致痴呆,包括神经退行性疾病、血管疾病、感染、炎症、脱髓鞘、中毒、代谢紊乱、肿瘤和头部创伤。尽管生物标志物和成像技术取得了最新进展,但神经病理学检查仍是最终诊断的必要条件。此外,约有 11% 的痴呆症患者有双重或三重病理状况。神经系统疾病的并存给神经科医生准确诊断患者带来了困难。退行性疾病的特征是大脑不同部位的神经元缺失和胶质细胞增生、神经元或胶质细胞内含物的存在以及蛋白质的异常堆积。老年斑和神经纤维缠结是阿尔茨海默病的神经病理学特征。这些结果分别以淀粉样 β 蛋白(Aβ)和磷酸化 tau 蛋白的存在为特征。虽然血管性痴呆很常见,但可能很难确定血管病变与认知障碍之间的关系。散发性Aβ型脑淀粉样血管病(CAA)的发病率往往随着年龄的增长而增加,并因血管功能障碍和白质脑病而导致痴呆。此外,CAA 患者还会出现炎症。临床神经科医生应从神经病理学的角度出发,对痴呆症患者进行适当的诊断和治疗。
[Neuropathology of Disorders Leading to Dementia].
Dementia is characterized by acquired cognitive dysfunction caused by various neurological disorders. Many neurological conditions can cause dementia, including neurodegenerative diseases, vascular disorders, infections, inflammation, demyelination, intoxication, metabolic disorders, tumors, and head trauma. Despite recent developments in biomarkers and imaging techniques, neuropathological examination is necessary for the final diagnosis. Moreover, approximately 11% of the patients with dementia have dual or triple pathological conditions. The coexistence of neurological diseases makes it difficult for neurologists to diagnose patients accurately. Degenerative diseases are characterized by neuronal loss with gliosis in distinct parts of the brain, the presence of neuronal or glial inclusions, and abnormal protein accumulation. Senile plaques and neurofibrillary tangles are neuropathological hallmarks of Alzheimer's disease. These findings are characterized by the presence of amyloid β protein (Aβ) and phosphorylated tau protein, respectively. Although vascular dementia is common, it may be difficult to identify the relationship between vascular lesions and cognitive impairment. The incidence of sporadic Aβ-type cerebral amyloid angiopathy (CAA) tends to increase with age and causes dementia due to vascular dysfunction and leukoencephalopathy. Furthermore, patients with CAA can develop inflammation. Clinical neurologists should possess a neuropathological perspective for the appropriate diagnosis and management of patients with dementia.