{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kocerha J"],"funding":["NIA NIH HHS","NCRR NIH HHS","NINDS NIH HHS","NIH HHS"],"pagination":["88"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3751855"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14"],"pubmed_abstract":["<h4>Background</h4>Huntington's Disease (HD) is a progressive neurodegenerative disorder caused by an expansion in the polyglutamine (polyQ) region of the Huntingtin (HTT) gene. The clinical features of HD are characterized by cognitive, psychological, and motor deficits. Molecular instability, a core component in neurological disease progression, can be comprehensively evaluated through longitudinal transcriptomic profiling. Development of animal models amenable to longitudinal examination enables distinct disease-associated mechanisms to be identified.<h4>Results</h4>Here we report the first longitudinal study of transgenic monkeys with genomic integration of various lengths of the human HTT gene and a range of polyQ repeats. With this unique group of transgenic HD nonhuman primates (HD "],"journal":["BMC neuroscience"],"pubmed_title":["Longitudinal transcriptomic dysregulation in the peripheral blood of transgenic Huntington's disease monkeys."],"pmcid":["PMC3751855"],"funding_grant_id":["R01 AG019206","R01 NS036232","RR01882","P51OD11132","R24 OD010930","R01 NS041669"],"pubmed_authors":["Banta H","Chan AW","Kocerha J","Li SH","Neumann A","Li XJ","Nelson K","Moran S","Larkin K","Liu Y","Yang JJ","Benito J","Chi T","Willoughby D","Chidamparam K","Engelhardt H","Yang SH","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"Longitudinal transcriptomic dysregulation in the peripheral blood of transgenic Huntington's disease monkeys.","description":"<h4>Background</h4>Huntington's Disease (HD) is a progressive neurodegenerative disorder caused by an expansion in the polyglutamine (polyQ) region of the Huntingtin (HTT) gene. The clinical features of HD are characterized by cognitive, psychological, and motor deficits. Molecular instability, a core component in neurological disease progression, can be comprehensively evaluated through longitudinal transcriptomic profiling. Development of animal models amenable to longitudinal examination enables distinct disease-associated mechanisms to be identified.<h4>Results</h4>Here we report the first longitudinal study of transgenic monkeys with genomic integration of various lengths of the human HTT gene and a range of polyQ repeats. With this unique group of transgenic HD nonhuman primates (HD ","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Aug","modification":"2026-05-30T14:02:54.033Z","creation":"2026-04-08T07:24:52.033Z"},"accession":"S-EPMC3751855","cross_references":{"pubmed":["23957861"],"doi":["10.1186/1471-2202-14-88"]}}