Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/106701
Title: Differential protein expression in diverse brain areas of Parkinson's and Alzheimer's disease patients
Authors: Esteves, A. R. 
Cardoso, S. M. 
Issue Date: 4-Aug-2020
Publisher: Springer Nature
Project: This work was funded by Santa Casa da Misericórdia de Lisboa, Portugal through Mantero Belard Neurosciences Prize 2016 (MB-40-2016); by the European Regional Development Fund (ERDF), through the Centro 2020 Regional Operational Programme under project CENTRO-01-0145-FEDER-000012 (HealthyAging2020) and through the COMPETE 2020—Operational Programme for Competitiveness and Internationalisation and Portuguese national funds via FCT—Fundação para a Ciência e a Tecnologia, under project POCI01-0145- FEDER-030712. We are indebted to the IDIBAPS Biobank and to Professor I Ferrer Abizanda, Bellvitge Hospital Universitari, Institut Català de la Salut, Barcelona, Spain for sample and data procurement. The mass spectrometry technique was performed at the i3S Proteomics Scientific Platform with the assistance of Hugo Osório, supported from the Portuguese Mass Spectrometry Network, integrated in the National Roadmap of Research Infrastructures of Strategic Relevance (ROTEIRO/0028/2013; LISBOA-01-0145-FEDER-022125). 
Serial title, monograph or event: Scientific Reports
Volume: 10
Issue: 1
Abstract: 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.
URI: https://hdl.handle.net/10316/106701
ISSN: 2045-2322
DOI: 10.1038/s41598-020-70174-z
Rights: openAccess
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais
I&D CIBB - Artigos em Revistas Internacionais
FMUC Medicina - Artigos em Revistas Internacionais

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