Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients

Detalhes bibliográficos
Autor(a) principal: Esteves, A. R.
Data de Publicação: 2020
Outros Autores: Cardoso, S. M.
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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spelling 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
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dc.publisher.none.fl_str_mv Springer Nature
publisher.none.fl_str_mv Springer Nature
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