Affiliations: [a] Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal | [b] Faculty of Medicine, Institute of Physiology, University of Coimbra, Coimbra, Portugal | [c] Faculty of Sciences and Technology, Department of Zoology, University of Coimbra, Coimbra, Portugal | [d] Faculty of Medicine, Institute of Biochemistry, University of Coimbra, Coimbra, Portugal
Correspondence:
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Corresponding author: Catarina R. Oliveira, Center for Neuroscience and Cell Biology, Institute of Biochemistry, Faculty of Medicine, University of Coimbra, 3004-517 Coimbra, Portugal. E-mail: catarina@cnc.cj.uc.pt or catarina.n.oliveira@gmail.com.
Note: [1] Both authors contributed equally to this work.
Abstract: The processes underlying the pathogenesis of Alzheimer's disease involve several factors including impaired glucose/energy metabolism, mitochondrial dysfunction, oxidative stress and altered insulin-signaling pathways. This review is mainly devoted to discuss evidence supporting the notion that mitochondrial dysfunction and oxidative stress are interconnected and intimately associated with the development and progression of Alzheimer's disease. Furthermore, the review explores the role of insulin signaling in the pathophysiology of the disease. Indeed, several studies have begun to find links between insulin and mechanisms with clear pathogenic implications for this disorder. Understanding the key mechanisms involved in the etiopathogenesis of Alzheimer's disease may provide opportunities for the design of efficacious preventive and therapeutic strategies.
