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dc.contributor.advisorHernández Rojas, Edith del Carmen
dc.contributor.advisorForero Rodríguez, Lady Johanna
dc.contributor.authorArias Rodríguez, Natalia
dc.date.accessioned2021-09-09T21:22:07Z
dc.date.available2021-09-09T21:22:07Z
dc.date.issued2021-05-21
dc.identifier.urihttps://repositorio.unicolmayor.edu.co/handle/unicolmayor/2834
dc.description.abstractLa enfermedad de Parkinson es un trastorno neurodegenerativo, que se basa principalmente en el deterioro de la sustancia nigra pars compacta del cerebro y que trae como consecuencia la pérdida de células dopaminérgicas. La alteración de diversos sistemas neuronales son los causales de los síntomas motores y no motores de la enfermedad entre los que se encuentra el estreñimiento, presente en cerca del 80% de pacientes con EP, incluso 20 años antes del diagnóstico. Teniendo de base la comunicación bidireccional entre el cerebro y el intestino y los recientes estudios que reportan alterada composición bacteriana en pacientes vs controles sanos, se vio pertinente evaluar la composición bacteriana fecal de 25 pacientes con EP y 25 controles sanos de Colombia, a través de extracción de ADN, secuenciación del gen 16 's rRNA por Illumina y análisis taxonómico - bioinformático en R Studio. Se identificó que, no había diferencias significativas en la riqueza y abundancia en las muestras a través de la diversidad alfa; mientras que la diversidad beta, con la medida Weight UniFrac Bray Curtis, evidencio diferencias entre pacientes y controles, comprobado por la prueba estadística ANOSIM. Adicionalmente, se destaca una disminución en las familias Lactobacillaceae y Streptococcaceae, y un aumento de Lachnospiraceae, Ruminoccocaceae, Verrucomicrobiaceae y Peptostreptococcaceae, esta última es por primera vez descrita como significativa en los casos de Colombia, la cual está implicada en la síntesis de AGCC, degradación de mucina y fibras vegetales, siendo importantes para el mantenimiento de la barrera intestinal y la neuroprotección.spa
dc.description.tableofcontentsResumen 14 Resumen ejecutivo 16 INTRODUCCIÓN 18 1. ANTECEDENTES 21 2. MARCO TEÓRICO 55 2.1. Enfermedad de Parkinson 55 2.2. Parkinson genético 57 2.2.1. Parkinson clásico 57 2.2.2. Parkinson esporádico o atípico 59 2.3. Parkinson idiopático EPI 59 2.4. Parkinsonismo 60 2.5. Tipos de parkinsonismo 61 2.6. Células dopaminérgicas 62 2.7. Ganglios basales 62 2.8.vías de respuesta motora 64 2.9. Alfa sinucleína 65 2.10. Cuerpos de Lewy 67 2.11. Tratamientos para la enfermedad de Parkinson 69 2.12. Patología de la enfermedad de Parkinson 70 2.13. Vías motoras en la enfermedad de Parkinson 71 2.14. Síntomas de la enfermedad de Parkinson 73 2.14.1. Síntomas motores 73 2.14.2. Síntomas no motores 74 2.15. Microbiota 75 2.16. Microbiota intestinal 76 2.17. Enterotipos 78 2.18. Disbiosis 81 2.19. Metabolitos intestinales e inflamación 83 2.20. Estrés oxidativo en la enfermedad de Parkinson 85 2.21.Interacción alfa sinucleína y metabolitos bacterianos 87 2.22. Disbiosis en la enfermedad de Parkinson 90 2.23. Axis microbiota - intestinal - cerebro 93 2.24. Diversidad de especies 97 2.25. Diversidad alfa 98 2.26. Índices de diversidad 98 2.27. Rarefacción 98 2.28. Diversidad beta 99 2.29. Ordenación de especies 99 2.30. Métodos de ordenación 99 3. DISEÑO METODOLÓGICO 101 3.1. Tipo de investigación 101 3.2. Enfoque, nivel o alcance de la investigación 101 3.3. Hipótesis 101 3.4. Población y muestra 102 3.5. Muestreo 103 3.6. Métodos, técnicas e instrumentos de recolección de datos 103 3.6.1. Antecedentes legales 103 3.7. Variables 108 4. RESULTADOS 115 4.1. Filtros de calidad de secuencias y uso de Qiime 2 112 4.2. Asignación taxonómica de ASV 114 4.3. Rarefacción 114 4.4. Normalización de los datos 115 4.5. Análisis de alfa diversidad 116 4.6. Significancia de la diversidad alfa 118 4.7. Beta diversidad 119 4.7.1. Medidas de distancias, Bray Curtis -NMDS 119 4.7.2. Weight UniFrac 120 4.7.3. Prueba ANOSIM 121 4.7.4. Unweight UniFrac 121 4.7.5. Prueba ANOSIM 122 4.8. Abundancia relativa por familias 123 4.9. Abundancia relativa por filum 125 4.10. Diferencias significativas por bacterias 126 5. DISCUSIÓN 131 6. CONCLUSIONES 140 7. PERSPECTIVAS 143 8. REFERENCIAS BIBLIOGRÁFICAS 144spa
dc.format.extent160p.spa
dc.format.mimetypeapplication/pdfspa
dc.language.isospaspa
dc.publisherUniversidad Colegio Mayor de Cundinamarcaspa
dc.rightsDerechos Reservados - Universidad Colegio Mayor de Cundinamarca, 2021spa
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0/spa
dc.titleCaracterización de la composición bacteriana fecal en pacientes con enfermedad de Parkinson y controles sanos de Colombiaspa
dc.typeTrabajo de grado - Pregradospa
dc.description.degreelevelPregradospa
dc.description.degreenameBacteriólogo(a) y Laboratorista Clínicospa
dc.publisher.facultyFacultad de Ciencias de la Saludspa
dc.publisher.placeBogotá D.Cspa
dc.publisher.programBacteriología y Laboratorio Clínicospa
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dc.rights.accessrightsinfo:eu-repo/semantics/closedAccessspa
dc.rights.creativecommonsAtribución-NoComercial-CompartirIgual 4.0 Internacional (CC BY-NC-SA 4.0)spa
dc.subject.lembComposición bacteriana
dc.subject.lembTrastorno neurodegenerativo
dc.subject.lembCélulas dopaminérgicas
dc.subject.proposalEnfermedad de Parkinsonspa
dc.subject.proposalParkinson idiopáticospa
dc.subject.proposalmicrobiota intestinalspa
dc.subject.proposalDisbiosis intestinalspa
dc.subject.proposalMetabolitos bacterianosspa
dc.subject.proposalNeuroinflamaciónspa
dc.subject.proposalSistema nervioso centralspa
dc.subject.proposalSistema nervioso entéricospa
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