سامانه همایش های دانشگاه آزاد اسلامی واحد نجف آباد

صفحه اصلی / اولین همایش بین المللی تحول خدمات سلامت: تلفیق مراقبت، درمان، بازتوانی و امیدبخشی

Pathogenesis of Alzheimer’s Disease

نویسندگان :

Zeinab Shakerin¹

1- دانشگاه آزاد اسلامی واحد نجف آباد

کلمات کلیدی :

Alzheimer Disease،Neuroinflammatory،Amyloid-beta،IGF1،Oxidative Stress

چکیده :

Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the common cause of dementia(1). Beta-amyloid plaque deposition, neurofibrillary tangles, and mitochondrial dysfunction are common neuropathological features in Alzheimer's disease(2). In various studies, in addition to the significant role of amyloid beta and tau protein accumulation, various mechanisms, including neuroinflammation (3), oxidative stress, mitochondrial stress(2), impaired insulin-like growth factor (IGF1) (4), vascular disorders, and changes in blood-brain barrier permeability(5) have been identified as important pathological processes in Alzheimer's disease. Method: A literature search was conducted in PubMed, Google Scholar, Scopus and Web of Science to identify articles published in the last 10 years on pathogenesis of Alzheimer’s disease. The search strategy used a combination of Medical Subject Headings (MeSH) terms and keywords, including "Alzheimer's disease," "pathogenesis," "amyloid beta," "tau protein," "neuroinflammation", "oxidative stress". The search was restricted to articles published between 2015 and 2026 to ensure the inclusion of the most recent finding. Only English-language articles were included. Relevant studies were screened by title, abstract, and full text Finding: This study demonstrated that Alzheimer's pathogenesis is a complex, multifactorial process driven by synergistic interactions between amyloid beta, tau-induced neurodegeneration, neuroinflammation, vascular, and metabolic factors. Conclusion: In conclusion, Alzheimer’s disease pathogenesis is a multifactorial and progressive process that requires early and targeted therapeutic approaches.