Molecular Pathogenesis of Alzheimer’s Disease: An Update

dc.contributor.authorSanabria Castro, Alfredo
dc.contributor.authorAlvarado-Echeverría, Ileana
dc.contributor.authorMonge-Bonilla, Cecilia
dc.date.accessioned2025-07-14T14:31:48Z
dc.date.available2025-07-14T14:31:48Z
dc.date.issued2017
dc.descriptionARTICULO
dc.description.abstractDementia is a chronic or progressive syndrome, characterized by impaired cognitive capacity beyond what could be considered a consequence of normal aging. It affects the memory, thinking process, Orientation, comprehension, calculation, learning ability, language, and judgment; although awareness is usually unaffected. Alzheimer’s disease (AD) is the most common form of dementia; symptoms include memory loss, difficulty solving problems, disorientation in time and space, among others. The disease was first described in 1906 at a conference in Tubingen, Germany by Alois Alzheimer. One hundred and ten years since its first documentation, many aspects of the pathophysiology of AD have been discovered and understood, however gaps of knowledge continue to exist. This literature review summarizes the main underlying neurobiological mechanisms in AD, including the theory with emphasis on amyloid peptide, cholinergic hypothesis, glutamatergic neurotransmission, the role of tau protein, and the involvement of oxidative stress and calcium
dc.description.sponsorshipLos autores
dc.identifier.otherDOI: 10.1159/000464422
dc.identifier.urihttp://hdl.handle.net/20.500.11764/4908
dc.language.isoen
dc.publisherLos autores
dc.relation.ispartofseriesAnn Neurosci; v.24:46–54 2017
dc.subjectAMILOIDE
dc.subjectENFERMEDAD DE ALZHEIMER
dc.subjectNEUROBIOLOGIA
dc.titleMolecular Pathogenesis of Alzheimer’s Disease: An Update
dc.typeArticle

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