Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Joseph W Goodliffe"'
Autor:
Joseph W Goodliffe, Hanbing Song, Anastasia Rubakovic, Wayne Chang, Maria Medalla, Christina M Weaver, Jennifer I Luebke
Publikováno v:
PLoS ONE, Vol 13, Iss 8, p e0200626 (2018)
Huntington's Disease (HD) is an autosomal dominant, progressive neurodegenerative disorder caused by deleterious expansion of CAG repeats in the Huntingtin gene and production of neurotoxic mutant Huntingtin protein (mHTT). The key pathological featu
Externí odkaz:
https://doaj.org/article/c178b9412fe648b4b86435fb870688df
Autor:
Veronica Go, Maria Medalla, Samantha M. Calderazzo, Diego De Alba, Tara L. Moore, Wayne Chang, Joseph W. Goodliffe, Alexandra Tsolias, Douglas L. Rosene, Dhruba Pathak, Benjamin Buller, Monica A. Pessina
Publikováno v:
J Neurosci
Functional recovery after cortical injury, such as stroke, is associated with neural circuit reorganization, but the underlying mechanisms and efficacy of therapeutic interventions promoting neural plasticity in primates are not well understood. Bone
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dda6b71bcdb814e27bd4fdf2d3be3097
https://doi.org/10.1523/jneurosci.2226-19.2020
https://doi.org/10.1523/jneurosci.2226-19.2020
Publikováno v:
PLoS ONE, Vol 15, Iss 6, p e0234394 (2020)
PLoS ONE
PLoS ONE
In the BACHD mouse model of Huntington's disease (HD), deletion of the N17 domain of the Huntingtin gene (BACHDΔN17, Q97) has been reported to lead to nuclear accumulation of mHTT and exacerbation of motor deficits, neuroinflammation and striatal at
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9cacf048489609ed6efb77facd899748
https://doaj.org/article/80ca1b4c605c4ea6935ee9a4a3a9ab7b
https://doaj.org/article/80ca1b4c605c4ea6935ee9a4a3a9ab7b
Autor:
Tarik F. Haydar, Jose Luis Olmos-Serrano, Joseph W. Goodliffe, Nadine M. Aziz, Diana W. Bianchi, Faycal Guedj, Jeroen L. A. Pennings
Publikováno v:
The Journal of Neuroscience. 36:2926-2944
Studies in humans with Down syndrome (DS) show that alterations in fetal brain development are followed by postnatal deficits in neuronal numbers, synaptic plasticity, and cognitive and motor function. This same progression is replicated in several m
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c0cc4b0a8d4faab5619df8f5ec9afc62
https://doi.org/10.1523/jneurosci.2513-15.2016
https://doi.org/10.1523/jneurosci.2513-15.2016
Autor:
Alan Peters, Claire Sethares, Feng Cheng, William A. Tyler, John Silbereis, Zygmunt Galdzicki, Hyo Jung Kang, Joseph W. Goodliffe, Nathan P. Cramer, Tarik F. Haydar, Jeffrey A. Golden, Ying Zhu, Nenad Sestan, Ivana Delalle, Jose Luis Olmos-Serrano, Mihovil Pletikos, Lucija Jankovic-Rapan
Publikováno v:
Neuron. 89(6)
Trisomy 21, or Down syndrome (DS), is the most common genetic cause of developmental delay and intellectual disability. To gain insight into the underlying molecular and cellular pathogenesis, we conducted a multi-region transcriptome analysis of DS
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::469813841ca6e4eb3a4bfdf117fcd73f
https://pubmed.ncbi.nlm.nih.gov/26924435
https://pubmed.ncbi.nlm.nih.gov/26924435