SARS-CoV-2感染和α-synucleinopathies:潜在的联系和潜在的机制
Joanna Agata Motyl1, Grażyna Gromadzka2, Grzegorz Arkadiusz Czapski3
1Department of Hybrid Microbiosystems Engineering, Nalecz Institute of Biocybernetics and Biomedical Engineering, Polish Academy of Sciences, Ks. Trojdena 4 St., 02-109 Warsaw, Poland.
International journal of molecular sciences
|November 27, 2024
概括
SARS-CoV-2 病毒可能会触发或恶化α-synuclein 聚合,导致像帕金森氏症这样的神经退行性疾病. 这篇评论探讨了COVID-19和α-synucleinopathies之间的联系.
科学领域:
- 神经科学是一个神经科学.
- 病毒学 病毒学
- 病理学 病理学 病理学
背景情况:
- 阿尔法-同核素 (α-syn) 对大脑功能至关重要,但可以错误折叠和聚合,导致神经退行.
- 包括帕金森病在内的α-syn核蛋白病变与α-syn聚合和神经炎症有关.
- SARS-CoV-2 感染影响神经系统,促使人们对其在神经退行性疾病中的作用进行调查.
研究的目的:
- 为了调查SARS-CoV-2是否作为α-synucleinopathies的环境触发因素.
- 审查SARS-CoV-2在调节α-syn功能中的作用的证据.
- 讨论SARS-CoV-2和帕金森症样症状之间的潜在因果关系.
主要方法:
- 文献综述侧重于SARS-CoV-2和α-synuclein. 这是一篇关于SARS-CoV-2和α-synuclein.
- 对神经炎症和病毒对神经系统的影响现有证据的分析.
- 检查将COVID-19与神经症状和α-syn聚合联系在一起的研究.
主要成果:
- SARS-CoV-2 感染与神经系统症状和神经炎症有关.
- 有证据表明,SARS-CoV-2可能会影响α-syn错误折叠和聚合.
- 在SARS-CoV-2和帕金森症类似症状的发展之间存在潜在的因果关系.
结论:
- SARS-CoV-2可能会导致α-synucleinopathies的发病或进展.
- 需要进一步的研究才能充分理解将SARS-CoV-2与α-syn聚合和神经退行相关联的机制.
- COVID-19可能是帕金森病和相关疾病的新型环境风险因素.
相关概念视频
Amyloid Fibrils
9.2K
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,...
9.2K
Neural Regulation
39.1K
Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
39.1K
Parkinson's Disease: Overview
482
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
482
Lysosomal Hydrolases
3.8K
Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
3.8K
Single Nucleotide Polymorphisms-SNPs
14.0K
A single nucleotide polymorphism or SNP is a single nucleotide variation at a specific genomic position in a large population. It is the most prevalent type of sequence variation found in the human genome. Point mutations that occur in more than 1% of the population qualify as SNPs. These are present once every 1000 nucleotides on an average in the human genome. Replacement of a purine with another purine (A/G) or a pyrimidine with another pyrimidine (C/T) is known as a transition. In contrast,...
14.0K
Alzheimer's Disease: Overview
448
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...
448


