在中度与中度严重的阿尔茨海默病中对认知刺激的不同反应
Susana I Justo-Henriques1, Rosa C Gomes Silva2, Janessa O Carvalho3
1Department of Education, Social and Behavioral Sciences, Polytechnic Institute of Beja.
概括
个人认知刺激 (iCS) 在中度阿尔茨海默病 (AD) 中改善了记忆力,但在严重的AD中没有. 疾病的严重程度会影响阿尔茨海默病患者认知干预措施的有效性.
科学领域:
- 神经科学是一个神经科学.
- 老年学是一门学科.
- 临床心理学 临床心理学
背景情况:
- 阿尔茨海默病 (AD) 显著影响认知功能,特别是记忆和执行功能.
- 认知刺激疗法是一种潜在的非药物干预,用于AD.
- 了解基于疾病严重程度的干预效果对于个性化护理至关重要.
研究的目的:
- 评估个人认知刺激 (iCS) 计划在中度至中度严重阿尔茨海默病的老年人中的有效性.
- 为了确定AD的严重程度是否影响认知刺激治疗的结果.
主要方法:
- 一个多中心随机对照试验,涉及80名葡萄牙老年人患有AD.
- 参与者被分配到ICS或通常的治疗中.
- 用迷你精神状态检查来评估阿尔茨海默病的严重程度,将参与者分为中度 (15-20) 和中度严重 (10-14) 组.
主要成果:
- iCS显著改善了记忆结果 (记忆评估测试),并显示了对中度AD参与者的全球认知改善的趋势.
- 在患有中度严重AD的参与者中没有观察到显著的认知益处.
- 分析证实,ICS在中度AD患者中显著更有效,而不是中度AD患者中 (p < .001).
结论:
- 在中度阿尔茨海默病患者中,个人认知刺激有效提高记忆力和潜在的全球认知能力.
- 随着阿尔茨海默氏症的严重程度的增加,对ICS的响应性会减少,这表明对中度严重损伤患者的益处有限.
- 疾病严重程度是决定对阿尔茨海默病认知刺激干预措施有效性的关键因素.
相关概念视频
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
926
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
926
Alzheimer's Disease: Overview
1.7K
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...
1.7K
Alzheimer's Disease: Treatment
1.3K
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...
1.3K
Cognitive Development During Adulthood
1.4K
Cognitive development continues throughout adulthood, undergoing significant shifts across early, middle, and late stages. Individual transition occurs from adolescent idealism to pragmatic and adaptable thinking in early adulthood. During this period, individuals learn to integrate personal beliefs with the recognition that other perspectives are equally valid. Exposure to the complexities of modern society, diverse experiences, and higher education contribute to this adaptive thought process,...
1.4K
Alzheimer Disease l: Introduction
21
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...
21
Alzheimer Disease ll: Pathophysiology
35
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...
35


