ISSN: 2161-0460

Revista de enfermedad de Alzheimer y parkinsonismo

Acceso abierto

Nuestro grupo organiza más de 3000 Series de conferencias Eventos cada año en EE. UU., Europa y América. Asia con el apoyo de 1.000 sociedades científicas más y publica más de 700 Acceso abierto Revistas que contienen más de 50.000 personalidades eminentes, científicos de renombre como miembros del consejo editorial.

Revistas de acceso abierto que ganan más lectores y citas
700 revistas y 15 000 000 de lectores Cada revista obtiene más de 25 000 lectores

Indexado en
  • Índice Copérnico
  • Google Académico
  • sherpa romeo
  • Abrir puerta J
  • Revista GenámicaBuscar
  • Claves Académicas
  • TOC de revistas
  • Infraestructura Nacional del Conocimiento de China (CNKI)
  • Biblioteca de revistas electrónicas
  • Búsqueda de referencia
  • Universidad Hamdard
  • EBSCO AZ
  • OCLC-WorldCat
  • Catálogo en línea SWB
  • Biblioteca Virtual de Biología (vifabio)
  • publones
  • Fundación de Ginebra para la educación y la investigación médicas
  • Pub Europeo
  • ICMJE
Comparte esta página

Abstracto

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.

Descargo de responsabilidad: este resumen se tradujo utilizando herramientas de inteligencia artificial y aún no ha sido revisado ni verificado.