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1. Cell-Type-Specific Gene Expression Profiling in Adult Mouse Brain Reveals Normal and Disease-State Signatures

2. Huntingtin Aggregation Impairs Autophagy, Leading to Argonaute-2 Accumulation and Global MicroRNA Dysregulation.

3. The Self-Inactivating KamiCas9 System for the Editing of CNS Disease Genes.

4. Coupling of D2R Short but not D2R Long receptor isoform to the Rho/ ROCK signaling pathway renders striatal neurons vulnerable to mutant huntingtin.

5. Viral-mediated overexpression of mutant huntingtin to model HD in various species

6. Diminished hippocalcin expression in Huntington’s disease brain does not account for increased striatal neuron vulnerability as assessed in primary neurons.

7. Dysregulation of Gene Expression in Primary Neuron Models of Huntington's Disease Shows That Polyglutamine-Related Effects on the Striatal Transcriptome May Not Be Dependent on Brain Circuitry.

8. Diminished hippocalcin expression in Huntington's disease brain does not account for increased striatal neuron vulnerability as assessed in primary neurons

9. Limitations of Dual-Single Guide RNA CRISPR Strategies for the Treatment of Central Nervous System Genetic Disorders.

10. Mitochondria in Huntington's disease

11. Therapeutic efficacy of regulable GDNF expression for Huntington's and Parkinson's disease by a high-induction, background-free “GeneSwitch” vector.

12. Haloperidol protects striatal neurons from dysfunction induced by mutated huntingtin in vivo

13. Minocycline in phenotypic models of Huntington's disease.

14. Long-term lentiviral-mediated expression of ciliary neurotrophic factor in the striatum of Huntington's disease transgenic mice

15. Altering protein folding, intracellular signaling, or the post-transcriptional program as potential therapeutic strategies to counteract Huntington's disease

16. Capucin does not modify the toxicity of a mutant Huntingtin fragment in vivo

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