Bibliografía (Bases genéticas y moleculares)

- I. Tasset, F. Sánchez, I. Túnez. Bases moleculares de la enfermedad de Huntington: papel del estrés oxidativo . [REV NEUROL 2009; 49: 424-9]. Available from: http://www.neurologia.com/pdf/Web/4908/bc080424.pdf

- A. Benítez-Burraco. Enfermedad de Huntington: fundamentos moleculares e implicaciones para una caracterización de los mecanismos neuronales responsables del procesamiento lingüístico. [REV NEUROL 2009; 48: 75-84]. Available from: http://www.unioviedo.es/biolang/pdf/Huntington%26lenguaje.pdf

- Vijayvargia R, Epand R, Leitner A, Jung T, Shin B, Jung R et al. Huntingtin’s spherical solenoid structure enables polyglutamine tract-dependent modulation of its structure and function. eLife. 2016;5. Available from: http://elifesciences.org/content/5/e11184v2

- Shi-Hua Li, Xiao-Jiang Li. Huntingtin–protein interactions and the pathogenesis of Huntington's disease [Internet]. Sciencedirect.com. March 2004; 20(3): 146-154. [cited 27 April 2016]. Available from: http://www.sciencedirect.com/science/article/pii/S016895250400023X

- Menzies FM e. Calpain inhibition mediates autophagy-dependent protection against polyglutamine toxicity. - PubMed - NCBI [Internet]. Ncbi.nlm.nih.gov. 2016 [cited 27 April 2016]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/25257175

- López del Val, Burguera Hernández. Enfermedad de Huntington. Claves y respuestas para un desafío singular. Edición 2010.

- Keum J, Shin A, Gillis T, Mysore J, Abu Elneel K, Lucente D et al. The HTT CAG-Expansion Mutation Determines Age at Death but Not Disease Duration in Huntington Disease. The American Journal of Human Genetics. 2016;98(2):287-298. Available from: http://www.cell.com/ajhg/abstract/S0002-9297%2815%2900513-3

- Jang-Ho J Cha . Transcriptional dysregulation in Huntington’s disease. Trends in neurosciences: cell press. September 2000; 23(9): 387-392. Available from: http://0-www.sciencedirect.com.cisne.sim.ucm.es/science/article/pii/S016622360001609X

- Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington's disease [Internet]. Sciencedirect.com. 2016 [cited 27 April 2016]. Available from: http://www.sciencedirect.com/science/article/pii/S096999611200040X

- Thomas E, Coppola G, Desplats P, Tang B, Soragni E, Burnett R et al. The HDAC inhibitor 4b ameliorates the disease phenotype and transcriptional abnormalities in Huntington's disease transgenic mice. Proceedings of the National Academy of Sciences. 2008;105(40):15564-15569. [cited 27 April 2016]. Available from: http://www.pnas.org/content/105/40/15564.short

- Sadri-Vakili, GCha J. Mechanisms of Disease: histone modifications in Huntington's disease. Nature Clinical Practice Neurology. 2006;2(6):330-338. Available from: http://www.nature.com/nrneurol/journal/v2/n6/full/ncpneuro0199.html

- Deisy Guirettia, Ana Sempereb, Jose P. Lopez-Atalayaa, Antonio Ferrer-Montielb, Angel Barcoa, Luis M. Valora. Specific promoter deacetylation of histone H3 is conserved across mouse models of Huntington's disease in the absence of bulk changes. Neurobiology of Disease. May 2015; 89: 190-201. Available from: http://www.sciencedirect.com/science/article/pii/S0969996116300250

- Valcárcel-Ocete L e. Exploring Genetic Factors Involved in Huntington Disease Age of Onset: E2F2 as a New Potential Modifier Gene. - PubMed - NCBI [Internet]. Ncbi.nlm.nih.gov. 2016 [cited 27 April 2016]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26148071

- Riechers SP e. Interactome network analysis identifies multiple caspase-6 interactors involved in the pathogenesis of HD. - PubMed - NCBI [Internet]. Ncbi.nlm.nih.gov. 2016 [cited 27 April 2016]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26908611

- Wong BK e. Partial rescue of some features of Huntington Disease in the genetic absence of caspase-6 in YAC128 mice. - PubMed - NCBI [Internet]. Ncbi.nlm.nih.gov. 2016 [cited 27 April 2016]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/25583186

- Hensman Moss D, Poulter M, Beck J, Hehir J, Polke J, Campbell T et al. C9orf72 expansions are the most common genetic cause of Huntington disease phenocopies. Neurology. 2013;82(4):292-299. Available from : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929197/

- BR S. The clinical and genetic features of Huntington disease. - PubMed - NCBI [Internet]. Ncbi.nlm.nih.gov. 2016 [cited 27 April 2016]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20923757

- Jorge Michel Rodríguez Pupo, Yuna Viviana Díaz Rojas, Yesenia Rojas Rodríguez, Yordanis Rodríguez Batista, Enriqueta Núñez Arias. ARTÍCULO DE REVISIÓN: Actualización en enfermedad de Huntington (Update on Huntington Disease). sCielo. 2013; 17(1). Available from : http://scielo.sld.cu/scielo.php?script=sci_arttext&pid=S1560-43812013000500003