表观遗传衰老和帕金森病的风险
Xiaojing Peng1, Mario H Flores-Torres2, Marianna Cortese2
1Department of Epidemiology, Harvard T H Chan School of Public Health, Boston, Massachusetts, USA xpeng@hsph.harvard.edu.
Journal of neurology, neurosurgery, and psychiatry
|December 30, 2025
概括
在一项大型前性研究中,表观遗传年龄加速,即生物衰老的衡量标准,无法可靠地预测帕金森病 (PD) 的风险或发病率. 这些发现表明表观遗传时钟可能不是适合用于早期PD检测的生物标志物.
科学领域:
- 神经科学是一个神经科学.
- 遗传学 遗传学 是一个
- 生物标志物 生物标志物
背景情况:
- 像帕金森病 (PD) 这样的神经系统疾病的风险随着年龄的增长而增加.
- 表观遗传钟是与年龄有关的疾病的有希望的生物标志物.
- 这项研究调查了与PD相关的表观遗传年龄加速.
研究的目的:
- 为了前性地评估表观遗传年龄加速是否预测PD风险.
- 为了确定表观遗传年龄加速是否预测PD发病时的年龄.
- 评估表观遗传年龄加速是否预测了PD转变的时间.
主要方法:
- 在护士健康研究中进行的一项前性,嵌套的病例控制研究.
- 分析了患有PD的个体的DNA甲基化概况,PD特征和年龄匹配的对照.
- 使用六种不同的表观遗传时钟估计表观遗传年龄加速,并评估与PD结果的关联.
主要成果:
- 表观遗传年龄加速与更高的PD风险没有一致的关联,即使是在诊断前几年.
- 在调整生活方式因素 (吸烟,饮食,BMI等) 后,结果保持一致. ) 的情况.
- 表观遗传年龄加速与PD发病时的早期年龄或转化现象的时间无关.
结论:
- 基于表观遗传时钟的生物标志物不能可靠地预测PD风险.
- 这些生物标志物对于预测PD发病时的年龄并不有效.
- 目前,表观遗传时钟对于预测PD变异的时间是不可靠的.
更多相关视频
08:09Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
Published on: January 7, 2014
7.9K
13:47Lentiviral Vector Platform for the Efficient Delivery of Epigenome-editing Tools into Human Induced Pluripotent Stem Cell-derived Disease Models
Published on: March 29, 2019
10.2K
相关概念视频
Parkinson's Disease: Overview
1.7K
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...
1.7K
Neural Regulation
43.0K
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.
43.0K
Parkinson's Disease: Treatment
933
Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
933
Human Genetics
1.4K
Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...
The complex relationship between genetics and psychology is observable through common biological components such...
1.4K
Aging
561
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...
561
Pharmacodynamics in Geriatric Patients: Effects of Age
174
Age-related pharmacokinetic changes are extensively documented, but understanding age-related pharmacodynamic alterations is relatively limited. This knowledge gap can be partly attributed to the complexity of developing appropriate measures of drug responses compared to bioanalytical methods for determining drug concentrations.Most information regarding age-related differences in human pharmacodynamics originates from cross-sectional studies. However, these studies assume that observed mean...
174
