{"title":"Impact of Diabetes Mellitus Type 2 on the Development of Alzheimer’s Disease","authors":"Maria Isabel Gomez-Coral","doi":"10.19080/oajnn.2024.19.556004","DOIUrl":null,"url":null,"abstract":"Diabetes Mellitus Type 2 (T2DM) and Alzheimer's Disease (AD) are prevalent chronic conditions in the aging population. T2DM is characterized by insulin resistance and chronic hyperglycemia, leading to long-term complications. AD, the most common form of dementia, is marked by progressive cognitive decline, amyloid-beta plaques, and neurofibrillary tangles. Epidemiological evidence suggests a significant correlation between T2DM and an increased risk of AD. This review explores the shared pathophysiological mechanisms linking T2DM and AD, including insulin resistance, oxidative stress, and inflammation. Insulin signaling in the brain is crucial for neuronal survival and cognitive function, and its disruption in T2DM contributes to AD pathology. Chronic hyperglycemia in T2DM induces oxidative stress and the formation of advanced glycation end products (AGEs), exacerbating neuronal damage and cognitive decline. Vascular complications in diabetes further impair cerebral blood flow, promoting neurodegeneration. Clinical implications highlight the necessity for integrated management strategies. Glycemic control, achieved through medications such as metformin and lifestyle interventions, can mitigate cognitive decline. Emerging therapies, including GLP-1 receptor agonists and intranasal insulin, show promise in addressing both metabolic and neurodegenerative aspects. Preventive measures, such as a balanced diet and regular physical activity, are crucial in reducing the risk of T2DM and AD. Future research should focus on understanding the precise mechanisms linking these diseases, optimizing therapeutic approaches, and exploring personalized medicine. This integrated perspective is essential for reducing the combined burden of T2DM and AD, ultimately improving patient outcomes.","PeriodicalId":317103,"journal":{"name":"Open Access Journal of Neurology & Neurosurgery","volume":" 39","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Open Access Journal of Neurology & Neurosurgery","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.19080/oajnn.2024.19.556004","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Diabetes Mellitus Type 2 (T2DM) and Alzheimer's Disease (AD) are prevalent chronic conditions in the aging population. T2DM is characterized by insulin resistance and chronic hyperglycemia, leading to long-term complications. AD, the most common form of dementia, is marked by progressive cognitive decline, amyloid-beta plaques, and neurofibrillary tangles. Epidemiological evidence suggests a significant correlation between T2DM and an increased risk of AD. This review explores the shared pathophysiological mechanisms linking T2DM and AD, including insulin resistance, oxidative stress, and inflammation. Insulin signaling in the brain is crucial for neuronal survival and cognitive function, and its disruption in T2DM contributes to AD pathology. Chronic hyperglycemia in T2DM induces oxidative stress and the formation of advanced glycation end products (AGEs), exacerbating neuronal damage and cognitive decline. Vascular complications in diabetes further impair cerebral blood flow, promoting neurodegeneration. Clinical implications highlight the necessity for integrated management strategies. Glycemic control, achieved through medications such as metformin and lifestyle interventions, can mitigate cognitive decline. Emerging therapies, including GLP-1 receptor agonists and intranasal insulin, show promise in addressing both metabolic and neurodegenerative aspects. Preventive measures, such as a balanced diet and regular physical activity, are crucial in reducing the risk of T2DM and AD. Future research should focus on understanding the precise mechanisms linking these diseases, optimizing therapeutic approaches, and exploring personalized medicine. This integrated perspective is essential for reducing the combined burden of T2DM and AD, ultimately improving patient outcomes.
2 型糖尿病(T2DM)和阿尔茨海默病(AD)是老龄人口中普遍存在的慢性疾病。2 型糖尿病的特点是胰岛素抵抗和长期高血糖,会导致长期并发症。老年痴呆症(AD)是最常见的痴呆症,主要表现为认知能力逐渐下降、淀粉样蛋白-β斑块和神经纤维缠结。流行病学证据表明,T2DM 与 AD 风险增加之间存在显著相关性。本综述探讨了连接 T2DM 和 AD 的共同病理生理机制,包括胰岛素抵抗、氧化应激和炎症。大脑中的胰岛素信号传导对神经元的存活和认知功能至关重要,T2DM 中的胰岛素信号传导紊乱会导致 AD 病变。T2DM 中的慢性高血糖会诱发氧化应激和高级糖化终产物(AGEs)的形成,加剧神经元损伤和认知能力下降。糖尿病血管并发症会进一步损害脑血流,促进神经退行性变。对临床的影响凸显了综合管理策略的必要性。通过二甲双胍等药物和生活方式干预来控制血糖,可以缓解认知能力下降。包括 GLP-1 受体激动剂和鼻内胰岛素在内的新兴疗法有望同时解决代谢和神经退行性病变问题。均衡饮食和定期体育锻炼等预防措施对于降低 T2DM 和 AD 的风险至关重要。未来的研究应侧重于了解这些疾病的确切关联机制、优化治疗方法和探索个性化医疗。这种综合视角对于减轻 T2DM 和 AD 的综合负担,最终改善患者预后至关重要。