在前性痴呆症的发展中逆元素的作用
1Department of Medical Genetics and Fundamental Medicine, Bashkir State Medical University, 450008 Ufa, Russia.
Frontiers in bioscience (Scholar edition)
|March 28, 2025
概括
前性痴呆症 (FTD) 涉及具有TDP-43,tau和FUS蛋白质的蛋白质病变,这些蛋白质通常会抑制可转移元素. 它们的功能障碍激活了这些元素,创建了一个反循环,驱动FTD进展.
科学领域:
- 神经科学是一个神经科学.
- 遗传学 是一个遗传学.
- 分子生物学分子生物学
背景情况:
- 前性痴呆 (FTD) 与涉及TDP-43,tau和FUS蛋白质的蛋白质病变有关.
- 这些蛋白质具有抗病毒性质,并抑制可移植元素,这些元素可能会被病毒或衰老激活.
- FTD与含有可转移元素基因的监管区域中的SNP有关.
研究的目的:
- 研究可移植元素和遗传倾向在FTD病原发生中的作用.
- 探索从可转移元素衍生的microRNAs作为FTD治疗策略的潜力.
主要方法:
- 关于FTD,蛋白质病变,可移植元素和遗传关联的科学文献的综述.
- 对涉及TDP-43,tau,FUS和反向元件激活的拟议反循环的分析.
- 识别潜在的治疗性微RNAs.
主要成果:
- 遗传倾向可能会影响反元素与TDP-43,tau和FUS蛋白之间的相互作用.
- 蛋白质聚合物的形成导致反元素的抑制丧失,导致它们的激活.
- 建立了一个负反循环,增强蛋白质表达和聚合物积累.
结论:
- 使用可移植元素衍生的微RNA来抑制激活逆元的表观遗传抑制是一种潜在的FTD治疗方法.
- 确定了13种特定的microRNA作为FTD的潜在治疗方法.
更多相关视频
08:33Characterizing Histone Post-translational Modification Alterations in Yeast Neurodegenerative Proteinopathy Models
Published on: March 24, 2019
7.0K
10:59Generation and Characterization of Human Induced Pluripotent Stem Cell-derived Astrocytes Lacking Fragile X Messenger Ribonucleoprotein
Published on: June 6, 2025
1.1K
相关概念视频
Retroviruses
12.2K
Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...
12.2K
LTR Retrotransposons
18.1K
LTR retrotransposons are class I transposable elements with long terminal repeats flanking an internal coding region. These elements are less abundant in mammals compared to other class I transposable elements. About 8 percent of human genomic DNA comprises LTR retrotransposons. Some of the common examples of LTR retrotransposons are Ty elements in yeast and Copia elements in Drosophila.
The internal coding region of LTR retrotransposons and their mechanism of transposition closely resembles a...
The internal coding region of LTR retrotransposons and their mechanism of transposition closely resembles a...
18.1K
Non-LTR Retrotransposons
12.5K
As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
12.5K
Alzheimer Disease l: Introduction
29
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
29
Alzheimer Disease ll: Pathophysiology
42
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
42
Dementia l: Introduction
35
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
35
