揭示了无氧基因和阿尔茨海默病病原体之间的复杂联系
NyEmma Drakes1,2, Galina Kondrikova1,3, Dariusz Pytel1,4
1Department of Pathology and Laboratory Medicine, Medical University of South Carolina.
The Journal of infectious diseases
|September 10, 2024
概括
微生物失生症,特别是无氧细菌,与阿尔茨海默病 (AD) 有关. 慢性口腔和肠道疾病可能会将厌氧细菌转移到大脑,导致神经退行.
科学领域:
- 神经病理学神经病理学
- 微生物学 微生物学
- 神经退行性疾病 神经退行性疾病
背景情况:
- 微生物失生症与包括阿尔茨海默病 (AD) 在内的全身性疾病有关.
- 导致阿尔茨海默病的微生物失生症的起源尚不清楚.
- 与年龄相关的大脑变化会产生无氧,这可能会促进微生物社区的转变.
研究的目的:
- 探索接近大脑的无氧.
- 为了识别这些利基内的无气生物及其对AD的影响.
- 调查与AD相关的微生物失生症的潜在来源.
主要方法:
- 审查关于无氧和它们与大脑的关联现有的文献.
- 在AD病变发生过程中涉及的无氧细菌的鉴定.
- 对无氧微生物到大脑的潜在转移路线的分析.
主要成果:
- 慢性口腔失生症 (牙口袋) 和肠道微生物群失生症是无氧细菌转移到大脑的主要来源.
- 厌氧物种在血脑屏障上的大脑动脉样硬化斑块中占主导地位.
- 焦点大脑,大脑,和骨髓体代表了大脑外围膜附近的慢性无氧.
结论:
- 在大脑附近的无氧,包括口腔,肠道和大脑病理,是研究的关键领域.
- 了解这些无氧环境及其相关微生物可能会揭示阿尔茨海默病的关键病因因素.
- 对这些无氧的进一步研究可以确定AD的新型治疗点.
相关概念视频
Alzheimer's Disease: Overview
452
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
452
Alzheimer's Disease: Treatment
170
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
170
Amyloid Fibrils
9.3K
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
9.3K


