New treatment strategies for Alzheimer's disease: is there a hope?

Detalhes bibliográficos
Autor(a) principal: Aprahamian, Ivan
Data de Publicação: 2013
Outros Autores: Stella, Florindo [UNESP], Forlenza, Orestes V.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://www.ijmr.org.in/article.asp?issn=0971-5916;year=2013;volume=138;issue=4;spage=449;epage=460;aulast=Aprahamian;type=0
http://hdl.handle.net/11449/111277
Resumo: Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease, and corresponds to the most common cause of dementia worldwide. Although not fully understood, the pathophysiology of AD is largely represented by the neurotoxic events triggered by the beta-amyloid cascade and by cytoskeletal abnormalities subsequent to the hyperphosphorylation of microtubule-associated Tau protein in neurons. These processes lead respectively to the formation of neuritic plaques and neurofibrillary tangles, which are the pathological hallmarks of the disease. Clinical benefits of the available pharmacological treatment for AD with antidementia drugs (namely cholinesterase inhibitors and memantine) are unquestionable, although limited to a temporary, symptomatic support to cognitive and related functions. Over the past decade, substantial funding and research have been dedicated to the search and development of new pharmaceutical compounds with disease-modifying properties. The rationale of such approach is that by tackling key pathological processes in AD it may be possible to attenuate or even change its natural history. In the present review, we summarize the available evidence on the new therapeutic approaches that target amyloid and Tau pathology in AD, focusing on pharmaceutical compounds undergoing phase 2 and phase 3 randomized controlled trials.
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spelling New treatment strategies for Alzheimer's disease: is there a hope?Alzheimer's diseaseantidementia drugbeta-amyloidcognitive impairmentTautreatmentAlzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease, and corresponds to the most common cause of dementia worldwide. Although not fully understood, the pathophysiology of AD is largely represented by the neurotoxic events triggered by the beta-amyloid cascade and by cytoskeletal abnormalities subsequent to the hyperphosphorylation of microtubule-associated Tau protein in neurons. These processes lead respectively to the formation of neuritic plaques and neurofibrillary tangles, which are the pathological hallmarks of the disease. Clinical benefits of the available pharmacological treatment for AD with antidementia drugs (namely cholinesterase inhibitors and memantine) are unquestionable, although limited to a temporary, symptomatic support to cognitive and related functions. Over the past decade, substantial funding and research have been dedicated to the search and development of new pharmaceutical compounds with disease-modifying properties. The rationale of such approach is that by tackling key pathological processes in AD it may be possible to attenuate or even change its natural history. In the present review, we summarize the available evidence on the new therapeutic approaches that target amyloid and Tau pathology in AD, focusing on pharmaceutical compounds undergoing phase 2 and phase 3 randomized controlled trials.Univ Sao Paulo, Fac Med, Dept & Inst Psychiat, Lab Neurosci LIM 27, BR-05403010 Sao Paulo, BrazilUNESP, Biosci Inst, Campus Of Rio Claro, SP, BrazilUNESP, Biosci Inst, Campus Of Rio Claro, SP, BrazilIndian Council Medical ResUniversidade de São Paulo (USP)Universidade Estadual Paulista (Unesp)Aprahamian, IvanStella, Florindo [UNESP]Forlenza, Orestes V.2014-12-03T13:07:08Z2014-12-03T13:07:08Z2013-10-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article449-460application/pdfhttp://www.ijmr.org.in/article.asp?issn=0971-5916;year=2013;volume=138;issue=4;spage=449;epage=460;aulast=Aprahamian;type=0Indian Journal of Medical Research. New Delhi: Indian Council Medical Res, v. 138, p. 449-460, 2013.0971-5916http://hdl.handle.net/11449/111277WOS:000330872300004WOS000330872300004.pdf7964386240653380Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengIndian Journal Of Medical Research1.5080,656info:eu-repo/semantics/openAccess2023-12-07T06:18:10Zoai:repositorio.unesp.br:11449/111277Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T19:42:32.867150Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv New treatment strategies for Alzheimer's disease: is there a hope?
title New treatment strategies for Alzheimer's disease: is there a hope?
spellingShingle New treatment strategies for Alzheimer's disease: is there a hope?
Aprahamian, Ivan
Alzheimer's disease
antidementia drug
beta-amyloid
cognitive impairment
Tau
treatment
title_short New treatment strategies for Alzheimer's disease: is there a hope?
title_full New treatment strategies for Alzheimer's disease: is there a hope?
title_fullStr New treatment strategies for Alzheimer's disease: is there a hope?
title_full_unstemmed New treatment strategies for Alzheimer's disease: is there a hope?
title_sort New treatment strategies for Alzheimer's disease: is there a hope?
author Aprahamian, Ivan
author_facet Aprahamian, Ivan
Stella, Florindo [UNESP]
Forlenza, Orestes V.
author_role author
author2 Stella, Florindo [UNESP]
Forlenza, Orestes V.
author2_role author
author
dc.contributor.none.fl_str_mv Universidade de São Paulo (USP)
Universidade Estadual Paulista (Unesp)
dc.contributor.author.fl_str_mv Aprahamian, Ivan
Stella, Florindo [UNESP]
Forlenza, Orestes V.
dc.subject.por.fl_str_mv Alzheimer's disease
antidementia drug
beta-amyloid
cognitive impairment
Tau
treatment
topic Alzheimer's disease
antidementia drug
beta-amyloid
cognitive impairment
Tau
treatment
description Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease, and corresponds to the most common cause of dementia worldwide. Although not fully understood, the pathophysiology of AD is largely represented by the neurotoxic events triggered by the beta-amyloid cascade and by cytoskeletal abnormalities subsequent to the hyperphosphorylation of microtubule-associated Tau protein in neurons. These processes lead respectively to the formation of neuritic plaques and neurofibrillary tangles, which are the pathological hallmarks of the disease. Clinical benefits of the available pharmacological treatment for AD with antidementia drugs (namely cholinesterase inhibitors and memantine) are unquestionable, although limited to a temporary, symptomatic support to cognitive and related functions. Over the past decade, substantial funding and research have been dedicated to the search and development of new pharmaceutical compounds with disease-modifying properties. The rationale of such approach is that by tackling key pathological processes in AD it may be possible to attenuate or even change its natural history. In the present review, we summarize the available evidence on the new therapeutic approaches that target amyloid and Tau pathology in AD, focusing on pharmaceutical compounds undergoing phase 2 and phase 3 randomized controlled trials.
publishDate 2013
dc.date.none.fl_str_mv 2013-10-01
2014-12-03T13:07:08Z
2014-12-03T13:07:08Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://www.ijmr.org.in/article.asp?issn=0971-5916;year=2013;volume=138;issue=4;spage=449;epage=460;aulast=Aprahamian;type=0
Indian Journal of Medical Research. New Delhi: Indian Council Medical Res, v. 138, p. 449-460, 2013.
0971-5916
http://hdl.handle.net/11449/111277
WOS:000330872300004
WOS000330872300004.pdf
7964386240653380
url http://www.ijmr.org.in/article.asp?issn=0971-5916;year=2013;volume=138;issue=4;spage=449;epage=460;aulast=Aprahamian;type=0
http://hdl.handle.net/11449/111277
identifier_str_mv Indian Journal of Medical Research. New Delhi: Indian Council Medical Res, v. 138, p. 449-460, 2013.
0971-5916
WOS:000330872300004
WOS000330872300004.pdf
7964386240653380
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Indian Journal Of Medical Research
1.508
0,656
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 449-460
application/pdf
dc.publisher.none.fl_str_mv Indian Council Medical Res
publisher.none.fl_str_mv Indian Council Medical Res
dc.source.none.fl_str_mv Web of Science
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv
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