چاپ صفحه |  صفحه نخست سامانه |  نویسندگان |  اطلاعات تفضیلی |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| نویسنده | نفر چندم مقاله |
|---|---|
| مرتضی عبدی قزلجه | اول |
| عنوان | متن |
|---|---|
| کلمات کلیدی | Oxidative Stress, Neural Cell Death, Neurodegenerative Diseases, Antioxidant Therapy |
| خلاصه مقاله | : Oxidative stress is a major contributor to neural cell death in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS). This review explores the mechanisms by which oxidative stress drives neuronal loss and discusses potential therapeutic strategies aimed at mitigating its harmful effects. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body's ability to detoxify them through antioxidant defenses. Neurons, due to their high metabolic activity and limited capacity for regeneration, are particularly vulnerable to ROS-induced damage. Mitochondria, the primary source of ROS, play a crucial role in this process. Mitochondrial dysfunction not only increases ROS production but also exacerbates oxidative damage to cellular components, such as lipids, proteins, and DNA. This damage disrupts cellular integrity and activates apoptotic and necrotic pathways, leading to progressive neuronal death and contributing to the progression of neurodegenerative diseases. The body’s natural antioxidant systems, including enzymes like superoxide dismutase (SOD) and glutathione peroxidase (GPx), are designed to neutralize ROS and protect cells from oxidative damage. However, in the context of neurodegenerative diseases, these systems are often overwhelmed, allowing oxidative stress to accumulate and promote neural cell death. Given the central role of oxidative stress in neural degeneration, therapeutic approaches targeting this process have gained attention. Antioxidants, such as vitamin E, coenzyme Q10, and Nacetylcysteine (NAC), have been investigated for their potential to reduce ROS levels and protect neurons. Additionally, emerging therapies aimed at preserving mitochondrial function are showing promise in reducing oxidative stress. Advances in nanotechnology have further opened new avenues for targeted antioxidant delivery. Nanoparticle-based systems capable of crossing the blood-brain barrier are being developed to enhance the precision of antioxidant treatments, offering more effective protection against neural cell death. In conclusion, oxidative stress is a key factor in neural cell death and neurodegenerative disease progression. Therapeutic strategies targeting oxidative damage, including antioxidants and mitochondrial protection, hold promise for slowing or preventing neuronal loss and improving patient outcomes. |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| govahi 2.pdf | 1403/11/22 | 237487 | دانلود |
| govahi hozor.pdf | 1403/11/22 | 219749 | دانلود |
| Screenshot (30).png | 1403/11/22 | 205554 | دانلود |
| 565.jpg | 1403/11/22 | 1761830 | دانلود |
