Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients
Autor(a) principal: | |
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Data de Publicação: | 2020 |
Outros Autores: | |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10316/106701 https://doi.org/10.1038/s41598-020-70174-z |
Resumo: | Many hypotheses have been postulated to define the etiology of sporadic Parkinson's and Alzheimer's disorders (PD and AD) but there is no consensus on what causes these devastating age-related diseases. Braak staging of both pathologies helped researchers to better understand the progression and to identify their prodromal and symptomatic phases. Indeed, it is well accepted that Lewy body pathology and neurofibrillary tangles appearance correlates with disease progression and severity of symptoms in PD and AD, respectively. Additionally, several studies in PD and AD models try to disclose which cellular mechanisms are defaulted and trigger the neurodegenerative process that culminates with neuronal death causing PD and AD classical symptomatology. Herein, we determined expression levels of proteins involved in microtubule assembly, autophagic-lysosomal pathway and unfolded protein response in the cortex, hippocampus and SNpc of PD and AD patients, vascular dementia patients and aged-match controls. The differential expression allowed us to determine which pathways are determinant to synaptic dysfunction and to establish a time line for disease progression. Our results allow us to challenge the hypothesis that both PD and AD pathologies are caused by α-synuclein or Aβ pathology propagation throughout the brain in a prion-like manner. |
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Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patientsAgedAged, 80 and overAlzheimer DiseaseCerebral CortexFemaleHippocampusHumansMaleNerve Tissue ProteinsParkinson DiseaseGene Expression RegulationUnfolded Protein ResponseMany hypotheses have been postulated to define the etiology of sporadic Parkinson's and Alzheimer's disorders (PD and AD) but there is no consensus on what causes these devastating age-related diseases. Braak staging of both pathologies helped researchers to better understand the progression and to identify their prodromal and symptomatic phases. Indeed, it is well accepted that Lewy body pathology and neurofibrillary tangles appearance correlates with disease progression and severity of symptoms in PD and AD, respectively. Additionally, several studies in PD and AD models try to disclose which cellular mechanisms are defaulted and trigger the neurodegenerative process that culminates with neuronal death causing PD and AD classical symptomatology. Herein, we determined expression levels of proteins involved in microtubule assembly, autophagic-lysosomal pathway and unfolded protein response in the cortex, hippocampus and SNpc of PD and AD patients, vascular dementia patients and aged-match controls. The differential expression allowed us to determine which pathways are determinant to synaptic dysfunction and to establish a time line for disease progression. Our results allow us to challenge the hypothesis that both PD and AD pathologies are caused by α-synuclein or Aβ pathology propagation throughout the brain in a prion-like manner.Springer Nature2020-08-04info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/106701http://hdl.handle.net/10316/106701https://doi.org/10.1038/s41598-020-70174-zeng2045-2322Esteves, A. R.Cardoso, S. M.info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-04-18T07:46:23Zoai:estudogeral.uc.pt:10316/106701Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T21:23:07.060251Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients |
title |
Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients |
spellingShingle |
Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients Esteves, A. R. Aged Aged, 80 and over Alzheimer Disease Cerebral Cortex Female Hippocampus Humans Male Nerve Tissue Proteins Parkinson Disease Gene Expression Regulation Unfolded Protein Response |
title_short |
Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients |
title_full |
Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients |
title_fullStr |
Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients |
title_full_unstemmed |
Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients |
title_sort |
Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients |
author |
Esteves, A. R. |
author_facet |
Esteves, A. R. Cardoso, S. M. |
author_role |
author |
author2 |
Cardoso, S. M. |
author2_role |
author |
dc.contributor.author.fl_str_mv |
Esteves, A. R. Cardoso, S. M. |
dc.subject.por.fl_str_mv |
Aged Aged, 80 and over Alzheimer Disease Cerebral Cortex Female Hippocampus Humans Male Nerve Tissue Proteins Parkinson Disease Gene Expression Regulation Unfolded Protein Response |
topic |
Aged Aged, 80 and over Alzheimer Disease Cerebral Cortex Female Hippocampus Humans Male Nerve Tissue Proteins Parkinson Disease Gene Expression Regulation Unfolded Protein Response |
description |
Many hypotheses have been postulated to define the etiology of sporadic Parkinson's and Alzheimer's disorders (PD and AD) but there is no consensus on what causes these devastating age-related diseases. Braak staging of both pathologies helped researchers to better understand the progression and to identify their prodromal and symptomatic phases. Indeed, it is well accepted that Lewy body pathology and neurofibrillary tangles appearance correlates with disease progression and severity of symptoms in PD and AD, respectively. Additionally, several studies in PD and AD models try to disclose which cellular mechanisms are defaulted and trigger the neurodegenerative process that culminates with neuronal death causing PD and AD classical symptomatology. Herein, we determined expression levels of proteins involved in microtubule assembly, autophagic-lysosomal pathway and unfolded protein response in the cortex, hippocampus and SNpc of PD and AD patients, vascular dementia patients and aged-match controls. The differential expression allowed us to determine which pathways are determinant to synaptic dysfunction and to establish a time line for disease progression. Our results allow us to challenge the hypothesis that both PD and AD pathologies are caused by α-synuclein or Aβ pathology propagation throughout the brain in a prion-like manner. |
publishDate |
2020 |
dc.date.none.fl_str_mv |
2020-08-04 |
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://hdl.handle.net/10316/106701 http://hdl.handle.net/10316/106701 https://doi.org/10.1038/s41598-020-70174-z |
url |
http://hdl.handle.net/10316/106701 https://doi.org/10.1038/s41598-020-70174-z |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
2045-2322 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.publisher.none.fl_str_mv |
Springer Nature |
publisher.none.fl_str_mv |
Springer Nature |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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RCAAP |
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RCAAP |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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