ISSN: 2161-0460

Jornal da doença de Alzheimer e parkinsonismo

Acesso livre

Nosso grupo organiza mais de 3.000 Séries de conferências Eventos todos os anos nos EUA, Europa e outros países. Ásia com o apoio de mais 1.000 Sociedades e publica mais de 700 Acesso aberto Periódicos que contém mais de 50.000 personalidades eminentes, cientistas de renome como membros do conselho editorial.

Periódicos de acesso aberto ganhando mais leitores e citações
700 periódicos e 15 milhões de leitores Cada periódico está obtendo mais de 25.000 leitores

Indexado em
  • Índice Copérnico
  • Google Scholar
  • Sherpa Romeu
  • Abra o portão J
  • Genâmica JournalSeek
  • Chaves Acadêmicas
  • JornalTOCs
  • Infraestrutura Nacional de Conhecimento da China (CNKI)
  • Biblioteca de Periódicos Eletrônicos
  • RefSeek
  • Universidade Hamdard
  • EBSCO AZ
  • OCLC – WorldCat
  • Catálogo online SWB
  • Biblioteca Virtual de Biologia (vifabio)
  • Publons
  • Fundação de Genebra para Educação e Pesquisa Médica
  • Euro Pub
  • ICMJE
Compartilhe esta página

Abstrato

Preliminary Set Theory-Type Analysis of Proteins Associated With Parkinson's Disease

Paul Whitesman

In an attempt to create a model of Parkinson’s disease (PD) eighty-three proteins were extracted from the Swiss- Prot protein database that had some casual mention of PD. These were split up into various subsets of proteins of which three are focused on here: PARK, made up of proteins that had some indication that polymorphisms in the protein might increase a person’s susceptibility to develop PD; MITOCHOND, proteins which had some association with the mitochondria; and MT-C1D, proteins that were implicated in mitochondrial complex 1 deficiency. The PARK subset had 21 out of 83 proteins (21/83); MITOCHOND 33 out of 83 proteins (33/83); and MT-C1D 17 out of 83 proteins (17/83). The results could be used to build up a basic model of PD creating phenotypes based on sets of proteins. The main phenotypes established here are; non-mitochondrial PD (50/83) and mitochondrial PD (33/83). Further division is possible dependant on whether proteins have polymorphisms which increase susceptibility to develop PD. MT-C1D seems to be independent of the PARK set. This is a very simplistic attempt at trying to model Parkinson’s disease at the proteomic level and will need further work to build up the more complex and realistic PD proteomic disease model.