Hypothesis on ontogenesis and pathophysiology of Alzheimer’s disease

• Autor(a) principal: Schwab,Eduarda Dal Pisol
• Data de Publicação: 2022
• Outros Autores: Queiroz,Ruliam, Fiebrantz,Anne Karine Bosetto, Bastos,Murilo, Bonini,Juliana Sartori, Silva,Weber Cláudio Francisco Nunes da
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Einstein (São Paulo)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082022000100409
• topic: Alzheimer disease; Oxidative stress; Amyloid beta-peptides; Tau proteins; Apolipoprotein E4; Glycogen synthase kinase 3; Cyclic AMP response element-binding protein; Diabetes mellitus type 3; Endocannabinoids; Insulin resistance

Abstract Alzheimer’s disease is a neurodegenerative condition that causes changes in memory and cognition, in addition to behavioral disorders, and most commonly affects the elderly. Several studies in the literature have presented therapeutic measures in an attempt to interfere with the pathogenic mechanisms of the disease and to mitigate its clinical manifestations. Some factors, such as excitotoxicity, cholinergic dysfunctions, oxidative stress, tau protein hyperphosphorylation, changes in amyloid-beta peptide metabolism, herpes viruses, apolipoprotein E, glycogen synthase kinase 3, insulin resistance, and the endocannabinoid system seem to be related to pathophysiology of Alzheimer’s disease. Given this, a literature review was carried out to address the molecular mechanisms associated with the pathophysiological hypotheses previously mentioned, aiming to better understanding their underlying causes and contributing to possible pharmacological strategies about treatment of the disease.