解开团:探索边缘在阿尔茨海默氏症病理生理学上的影响 - - 原因还是后果?
Gamze Sönmez1, Yiğit Yazarkan2, Özlem Erden Aki3
1Department of Medical Biochemistry, Hacettepe University Faculty of Medicine, Ankara, Türkiye.
The Eurasian journal of medicine
|May 16, 2025
概括
阿尔茨海默病 (AD) 不仅仅是大脑疾病,而且是一种全身性疾病. 针对大脑和身体的新型多式疗法为减缓AD进展提供了希望.
科学领域:
- 神经科学是一个神经科学.
- 老年学是一门学科.
- 系统生理学 系统生理学
背景情况:
- 阿尔茨海默病 (AD) 仍然是一个重大挑战,难以捉摸的有效药物治疗.
- 传统上对β-粉样斑块和团的关注显示治疗成功有限.
- 新出现的证据表明,AD涉及复杂的大脑与身体的相互作用,挑战以大脑为中心的观点.
研究的目的:
- 批判性地审查当前对阿尔茨海默氏症病理学的理解.
- 强调外周系统参与的作用及其与大脑的相互作用.
- 探索针对阿尔茨海默病的新型治疗策略.
主要方法:
- 关于阿尔茨海默病研究的文献综述.
- 对阿尔茨海默病理学的系统性因素研究的分析.
- 评估新兴的治疗方法.
主要成果:
- 阿尔茨海默病表现出超出大脑的系统性影响.
- 周围的过程可能有助于或受到AD病理的影响.
- 针对中央和外围方面的多模式疗法显示出有前途.
结论:
- 将AD视为一种具有系统影响的异质性疾病,开辟了新的治疗途径.
- 针对中部和外围阿尔茨海默病理对于有效治疗至关重要.
- 跨学科的合作对于推动AD研究和开发治疗方法至关重要.
更多相关视频
相关概念视频
Alzheimer's Disease: Overview
350
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...
350
Alzheimer's Disease: Treatment
133
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...
133
Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders
302
Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within...
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within...
302
Parkinson's Disease: Overview
353
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...
353
Dementia
76
Dementia is a collective term for cognitive disorders primarily affecting memory, thinking, and reasoning. It is not a specific disease but a syndrome, with Alzheimer's disease being the most common cause, accounting for approximately 60-80% of cases. Other types include vascular dementia, Lewy body dementia, and frontotemporal dementia. Dementia affects millions worldwide, particularly older adults, though it is not a normal part of aging.
The progression of dementia is generally gradual....
The progression of dementia is generally gradual....
76
Amyloid Fibrils
9.1K
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,...
9.1K


