New treatment strategies for Alzheimer's disease: is there a hope?
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | , |
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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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 |
|
_version_ |
1808129108681424896 |