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.accessioned2017-07-05T13:24:08Z
dc.date.available2017-07-05T13:24:08Z
dc.date.issued2017
dc.descriptionARTICULOes_ES
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.es_ES
dc.description.sponsorshipLos autoreses_ES
dc.identifier.urihttp://hdl.handle.net/20.500.11764/643
dc.language.isoenes_ES
dc.publisherAnnals of Neuroscienceses_ES
dc.relation.ispartofseriesAnnals of Neurosciences;
dc.subjectNEUROBIOLOGIAes_ES
dc.subjectENFERMEDAD DE ALZHEIMERes_ES
dc.subjectCOSTA RICAes_ES
dc.titleMolecular Pathogenesis of Alzheimer’s Disease: An Updatees_ES
dc.typeArticlees_ES

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