身体活动对血管痴呆的实验模型的影响:系统性审查和元分析
Ifechukwude J Biose1, Wesley H Chastain2, Rebecca J Solch-Ottaiano3
1Department of Pharmacology and Experimental Therapeutics, Cardiovascular Center of Excellence, LSU Health Sciences Center, New Orleans, LA, USA.
Annals of neurosciences
|August 19, 2024
概括
在血管痴呆症 (VaD) 模型中,运动有益于认知功能和大脑健康. 然而,它可能会增加焦虑和神经炎症,强调需要在这个研究领域仔细设计研究.
科学领域:
- 神经科学是一个神经科学.
- 运动生理学 运动生理学
- 痴呆症研究 痴呆症研究
背景情况:
- 身体活动与人类大脑健康和认知能力的增强有关.
- 在实验性血管痴呆症 (VaD) 模型中,对运动益处的证据需要评估.
- 系统性审查和元分析,以评估运动对VaD模型的影响.
研究的目的:
- 在VaD模型中评估运动对认知和大脑形态学的益处.
- 确定VAD运动干预措施的证据的有效性,范围和质量.
- 提供对运动对VaD影响的公正评估.
主要方法:
- 2021年12月完成了对三个数据库的系统搜索.
- 包括25项用于审查的研究和21项用于元分析.
- 在大鼠,小鼠和猪的VaD模型中分析了对认知功能和大脑形态的影响.
主要成果:
- 在VaD模型中,运动表明认知功能和一些大脑形态标志物的改善.
- 运动干预与增加的焦虑和神经炎症信号有关.
- 识别了报告异常,包括缺乏盲目化和随机化.
结论:
- 运动在VaD模型中显示了提高认知能力的潜力,但有警告.
- 增加的焦虑和神经炎症需要进一步调查.
- 改进的实验设计对于炼干预措施在VaD研究中的转化影响至关重要.
相关概念视频
Alzheimer's Disease: Overview
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 and tau...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer's Disease: Treatment
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...
Pharmacodynamics in Geriatric Patients: Effects of Age
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...
Alzheimer Disease ll: Pathophysiology
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 microglia. Abnormal...
Parkinson Disease ll: Pathophysiology
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
Dementia l: Introduction
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...


