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dc.contributor.authorFolch J.
dc.contributor.authorEttcheto M.
dc.contributor.authorPetrov D.
dc.contributor.authorAbad S.
dc.contributor.authorPedrós I.
dc.contributor.authorMarin M.
dc.contributor.authorOlloquequi J.
dc.contributor.authorCamins A.
dc.date.accessioned2020-09-02T22:17:54Z
dc.date.available2020-09-02T22:17:54Z
dc.date.issued2018
dc.identifier10.1016/j.nrl.2015.03.012
dc.identifier.citation33, 1, 35-46
dc.identifier.issn02134853
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4491
dc.descriptionIntroduction Alzheimer disease (AD) is a major neurodegenerative disorder which eventually results in total intellectual disability. The high global prevalence and the socioeconomic burden associated with the disease pose major challenges for public health in the 21st century. In this review we focus on both existing treatments and the therapies being developed, which principally target the β-amyloid protein. Discussion The amyloidogenic hypothesis proposes that β-amyloid plays a key role in AD. Several pharmacological approaches aim to reduce the formation of β-amyloid peptides by inhibiting the β-secretase and γ-secretase enzymes. In addition, both passive and active immunotherapies have been developed for the purpose of inhibiting β-amyloid peptide aggregation. Conclusions Progress in identifying the molecular basis of AD may provide better models for understanding the causes of this neurodegenerative disease. The lack of efficacy of solanezumab (a humanised monoclonal antibody that promotes β-amyloid clearance in the brain), demonstrated by 2 recent Phase III clinical trials in patients with mild AD, suggests that the amyloidogenic hypothesis needs to be revised. © 2015 Sociedad Española de Neurología
dc.language.isoen
dc.language.isoes
dc.publisherSpanish Society of Neurology
dc.subjectAlzheimer disease
dc.subjectAmyloid hypotheses
dc.subjectBeta-amyloid
dc.subjectBeta-secretase
dc.subjectGamma-secretase
dc.subjectamyloid beta protein
dc.subjectbeta secretase
dc.subjectgamma secretase
dc.subjectnootropic agent
dc.subjectamyloid beta protein
dc.subjectamyloid precursor protein
dc.subjectAPP protein, human
dc.subjectmonoclonal antibody
dc.subjectsecretase
dc.subjectsolanezumab
dc.subjectactive immunotherapy
dc.subjectAlzheimer disease
dc.subjectenzyme inhibition
dc.subjecthuman
dc.subjectprotein aggregation
dc.subjectprotein targeting
dc.subjectShort Survey
dc.subjectAlzheimer disease
dc.subjectmetabolism
dc.subjectAlzheimer Disease
dc.subjectAmyloid beta-Peptides
dc.subjectAmyloid beta-Protein Precursor
dc.subjectAmyloid Precursor Protein Secretases
dc.subjectAntibodies, Monoclonal, Humanized
dc.subjectHumans
dc.titleReview of the advances in treatment for Alzheimer disease: Strategies for combating β-amyloid protein [Una revisión de los avances en la terapéutica de la enfermedad de Alzheimer: estrategia frente a la proteína β-amiloide]
dc.typeShort Survey


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