在衰老和神经退行症的故事中,天体细胞蛋白质稳定
Felipe Cabral-Miranda1, Isadora Matias1, Flávia Carvalho Alcantara Gomes1
1Institute of Biomedical Sciences, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Ageing research reviews
|November 18, 2024
概括
星球细胞中的蛋白质稳态 (蛋白质稳态) 对大脑健康和衰老至关重要. 天体细胞蛋白质稳定中的功能障碍有助于神经退行性疾病和衰老,提供了新的治疗点.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 衰老研究研究 衰老研究
背景情况:
- 蛋白质平衡 (proteostasis) 对于细胞功能至关重要,并与神经退行和大脑衰老有关.
- 神经蛋白质稳定性得到了充分的研究,但天体细胞蛋白质稳定性的作用仍然不太清楚.
- 星球细胞,关键的质细胞,越来越多地被认为对大脑健康和疾病的参与.
研究的目的:
- 审查当前关于天体细胞中蛋白质稳定功能障碍的知识.
- 探索星球细胞蛋白质稳定在神经退行性疾病和衰老中的影响.
- 突出星体细胞作为潜在的治疗目标,用于治疗大脑疾病和衰老.
主要方法:
- 对最近关于天体细胞蛋白质稳定性研究的文献综述.
- 分析星球细胞内的不同蛋白质稳定路径.
- 综合数据将天体细胞蛋白质稳定与神经退行和衰老联系起来.
主要成果:
- 天体细胞中的蛋白质稳定功能障碍与神经退行性病理有关.
- 特定的天体细胞蛋白质稳定节点和途径有助于大脑功能和与年龄有关的疾病.
- 星球细胞在维持大脑健康方面发挥着重要的,但被低估的作用.
结论:
- 天体细胞蛋白质稳定是神经元生理学和与年龄相关的功能衰退的关键因素.
- 了解天体细胞蛋白质稳定为神经退行性疾病提供了新的干预策略.
- 这项研究为老龄化和大脑疾病的生物学提供了关键的见解.
相关概念视频
Aging
37
Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
37
The Proteasome
815
Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. This involves participation of a series of enzymes including— E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. This involves participation of a series of enzymes including— E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...
815
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
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
Neurogenesis and Regeneration of Nervous Tissue
728
In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
728
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


