RESULTS and PUBLICATIONS
Abada, Y.S., R. Schreiber, and B. Ellenbroek, Motor, emotional and cognitive deficits in adult BACHD mice: A model for Huntington's disease. Behav Brain Res, 2012. 238C: p. 243-251.
Baldo, B., et al., TR-FRET-based duplex immunoassay reveals an inverse correlation of soluble and aggregated mutant huntingtin in huntington's disease. Chem Biol, 2012. 19(2): p. 264-75.
Iderberg, H., V. Francardo, and E.Y. Pioli, Animal models of L-DOPA-induced dyskinesia: an update on the current options. Neuroscience, 2012. 211: p. 13-27.
A Model of GDNF Gene Therapy in Mice with 6 Hydroxydopamine Lesions: Time Course of Neurorestorative Effects and ERK1/2 Activation. Niklas Lindgren, Veronica Francardo, Luis Quintino, Cecilia Lundberg and M. Angela Cenci. Journal of Parkinson’s Disease 2 (2012) 333–348. DOI 10.3233/JPD-012146.
Automated behavioral phenotyping reveals presymptomatic alterations in a SCA3 genetrap mouse model. Hübener J, Casadei N, Teismann P, Seeliger MW, Björkqvist M, von Hörsten S, Riess O, Nguyen HP. J Genet Genomics. 2012 Jun 20;39(6):287-99. doi: 10.1016/j.jgg.2012.04.009. Epub 2012 May 15.
SIRT2 Ablation has no effect on tubulin Acetylation in brain, cholesterol biosynthesis or the progreesion of Huntington's disease phenotypes in vivo. (Bobrowska et al. PLoS ONE 7(4): e34805. doi: 10.1371/journal.pone.0034805. Pub. 2012 Apr 12.)
A screen for enhancers of clearance identifies huntingtin as a heat shock protein 90 (Hsp90) client protein. (Baldo et al. The Journal of Biological Chemistry Vol. 287, No.2, pp. 1406-1414, Jan 6, 2012.)
Oliveras Salvá, M., Van Rompuy, A., Heeman, B., Van Den Haute, C., Baekelandt, V.(2011). Loss-of-function rodent models for Parkin and PINK1. Journal of Parkinson's Disease, 1(3), 229-251.
Induction of autophagy with catalytic mTOR inhibitors reduces huntingtin aggregates in a neuronal cell model. (Roscic et al. J Neurochem. 2011 Oct;119(2):398-407. doi: 10.1111/j.1471-4159.2011.07435.x. Epub 2011 Sep 20.)
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Differential molecular and behavioural responses to L-DOPA in mice injected with 6-hydroxidopamine in the striatum or in the medial forebrain bundle. (Francardo et al. Poster presented at SFN 09 in Washington)
Vascular endothelial growth factor is upregulated by L-dopa in the parkinsonian brain: implications for the development of dyskenesia (Ohlin et al. Brain. 2011 Aug;134(Pt 8):2339-57. Epub 2011 Jul 19.)
Hdac6 Knock-out increases Tubulin Acetylation but does not modify disease progression in the R6/2 Mouse Model of Huntington's Disease. Bobrowska et al. PLoS. 2011. 6(6): p. e20696.
Inhibition of Ras-guanine nucleotide-releasing factor1 (Ras-GRF1) signaling in the striatum reverts motorsymptoms associated with L-dopa–induced dyskinesia. Fasano et al. Proc Natl Acad Sci U S A, 2010. 107(50): p. 21824-9.
Transgenic overexpression of the alpha-synuclein interacting protein synphilin-1 leads to behavioral and neuropathological alterations in mice. Nuber S, Franck T, Wolburg H, Schumann U, Casadei N, Fischer K, Calaminus C, Pichler BJ, Chanarat S, Teismann P, Schulz JB, Luft AR, Tomiuk J, Wilbertz J, Bornemann A, Krüger R, Riess O. Neurogenetics. 2010 Feb;11(1):107-20.
Impact of the lesion procedure on the profiles of motor impairment and molecular responsiveness to L-DOPA in the 6-hydroxydopamine mouse model of Parkinson’s disease. Francardo et al.: Neurobiol. Dis 2011. 42(3): p. 327-40.
Investigating the role of protein modification in Huntington’s disease: the importance of Htt and Hsp90 interaction in protein clearance and stability (Baldo et al.: Poster presented on the HDF Conference Boston, 2010.)
Casadei N et al: Alpha-Synuclein Detection and Quantification in a Genetic-triggered PD Mouse Model; Poster presented at the GEOPD Meeting 2009, Tuebingen