| Autor: |
Goldsteins G; A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland., Hakosalo V; A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland., Jaronen M; A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland., Keuters MH; Neuroscience Center, University of Helsinki, 00014 Helsinki, Finland., Lehtonen Š; A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.; Neuroscience Center, University of Helsinki, 00014 Helsinki, Finland., Koistinaho J; A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70211 Kuopio, Finland.; Neuroscience Center, University of Helsinki, 00014 Helsinki, Finland. |
| Abstrakt: |
A single paragraph of about 200 words maximum. Neurodegenerative diseases (ND), such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, pose a global challenge in the aging population due to the lack of treatments for their cure. Despite various disease-specific clinical symptoms, ND have some fundamental common pathological mechanisms involving oxidative stress and neuroinflammation. The present review focuses on the major causes of central nervous system (CNS) redox homeostasis imbalance comprising mitochondrial dysfunction and endoplasmic reticulum (ER) stress. Mitochondrial disturbances, leading to reduced mitochondrial function and elevated reactive oxygen species (ROS) production, are thought to be a major contributor to the pathogenesis of ND. ER dysfunction has been implicated in ND in which protein misfolding evidently causes ER stress. The consequences of ER stress ranges from an increase in ROS production to altered calcium efflux and proinflammatory signaling in glial cells. Both pathological pathways have links to ferroptotic cell death, which has been implicated to play an important role in ND. Pharmacological targeting of these pathological pathways may help alleviate or slow down neurodegeneration. |
