Cognitive Decline in Atherosclerotic Diseases: Mechanisms and Potential Solutions.

IF 3
Japleen Kaur, Ram Agrawal, Chidurala Rahul, Shreya R Kethiri, Kritika Pathak, Neil Patel, Yashendra Sethi, Nirja Kaka, Mohammad Amjad Kamal
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Abstract

Atherosclerosis has been increasingly recognized as a contributor to cognitive decline through mechanisms such as cerebral hypoperfusion, oxidative stress, and chronic inflammation. These mechanisms include cerebral hypoperfusion, which limits oxygen and nutrient supply to the brain; microvascular damage, which impairs small vessel function and blood-brain barrier integrity; chronic inflammation, which promotes neurodegeneration through sustained immune activation; and oxidative stress, which accelerates neuronal aging via mitochondrial dysfunction. This narrative review synthesizes findings from epidemiological studies, mechanistic research, and clinical trials to examine the interplay between atherosclerotic diseases and cognitive impairment. Shared risk factors, including hypertension, diabetes, hyperlipidemia, and smoking, accelerate neurovascular dysfunction and increase susceptibility to dementia. Advances in neuroimaging and biomarker research offer improved diagnostic precision, facilitating early detection and intervention. Preventive strategies, including lifestyle modifications, pharmacological therapies such as statins and antihypertensives, and cognitive rehabilitation, have the potential to mitigate cognitive deterioration associated with atherosclerosis. Despite accumulating evidence, vascular contributions to dementia remain underdiagnosed in clinical settings, highlighting the need for a multidisciplinary approach that integrates cardiovascular and neurological care. A comprehensive strategy encompassing risk stratification, early therapeutic intervention, and long-term monitoring is essential for improving cognitive outcomes in at-risk populations. Future research should focus on refining diagnostic methodologies, optimizing prevention and treatment protocols, and identifying high-risk individuals for targeted interventions. Given the rising global burden of both cardiovascular disease and dementia, a proactive approach addressing modifiable risk factors is critical to reducing morbidity and enhancing quality of life.

动脉粥样硬化性疾病的认知能力下降:机制和潜在的解决方案。
动脉粥样硬化越来越被认为是通过脑灌注不足、氧化应激和慢性炎症等机制导致认知能力下降的一个因素。这些机制包括脑灌注不足,这限制了大脑的氧气和营养供应;微血管损伤,损害小血管功能和血脑屏障完整性;慢性炎症,通过持续的免疫激活促进神经变性;氧化应激通过线粒体功能障碍加速神经元衰老。本文综合了流行病学研究、机制研究和临床试验的结果,以检验动脉粥样硬化性疾病和认知障碍之间的相互作用。共同的危险因素,包括高血压、糖尿病、高脂血症和吸烟,会加速神经血管功能障碍,增加对痴呆的易感性。神经影像学和生物标志物研究的进步提高了诊断精度,促进了早期发现和干预。预防策略,包括改变生活方式,药物治疗,如他汀类药物和抗高血压药物,以及认知康复,有可能减轻与动脉粥样硬化相关的认知退化。尽管有越来越多的证据,但在临床环境中,血管对痴呆的影响仍未得到充分诊断,这凸显了将心血管和神经保健结合起来的多学科方法的必要性。一个包括风险分层、早期治疗干预和长期监测的综合策略对于改善高危人群的认知结果至关重要。未来的研究应侧重于改进诊断方法,优化预防和治疗方案,并确定高危人群进行有针对性的干预。鉴于心血管疾病和痴呆症的全球负担不断增加,采取积极主动的方法处理可改变的风险因素对于降低发病率和提高生活质量至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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