New Zebrafish Models of Neurodegeneration

Current Neurology and Neuroscience Reports

Volumn 15, Issue 6, 2015, Pages

  Martín Jiménez, Rebeca ^a   Campanella, Michelangelo ^a,b   Russell, Claire ^a  

^a ROYAL VETERINARY COLLEGE   (United Kingdom)

^b UNIVERSITY COLLEGE LONDON   (United Kingdom)

Author keywords

Danio rerio; Disease model; Drug testing; Mechanism; Neurodegenerative; Therapeutic testing

Indexed keywords

AMYOTROPHIC LATERAL SCLEROSIS; ANIMAL MODEL; CLINICAL FEATURE; CLN2 DISEASE; DIFFUSE LEWY BODY DISEASE; DISEASE MODEL; HUMAN; NERVE DEGENERATION; NONHUMAN; PARKINSON DISEASE; PONTOCEREBELLAR HYPOPLASIA; REVIEW; ZEBRA FISH; ANIMAL; DEGENERATIVE DISEASE; PRECLINICAL STUDY;

ANIMALS; DISEASE MODELS, ANIMAL; DRUG EVALUATION, PRECLINICAL; HUMANS; NEURODEGENERATIVE DISEASES; ZEBRAFISH;

EID: 84928675098     PISSN: 15284042     EISSN: 15346293     Source Type: Journal    
DOI: 10.1007/s11910-015-0555-z     Document Type: Review

References (28)

1. Stewart AM et al. Zebrafish models for translational neuroscience research: from tank to bedside. Trends Neurosci. 2014;37(5):264–78.
2. Rennekamp AJ, Peterson RT. 15 years of zebrafish chemical screening. Curr Opin Chem Biol. 2014;24C:58–70.
3. Phillips JB, Westerfield M. Zebrafish models in translational research: tipping the scales toward advancements in human health. Dis Models Mech. 2014;7(7):739–43.
4. Schmid B, Haass C. Genomic editing opens new avenues for zebrafish as a model for neurodegeneration. J Neurochem. 2013;127(4):461–70.
5. Ivanes F et al. The compound BTB06584 is an IF1-dependent selective inhibitor of the mitochondrial F1 Fo-ATPase. Br J Pharmacol. 2014;171(18):4193–206.
6. Cunliffe VT et al. Epilepsy research methods update: understanding the causes of epileptic seizures and identifying new treatments using non-mammalian model organisms. Seizure. 2014;24:44–51.
7. Shah DI et al. Mitochondrial Atpif1 regulates haem synthesis in developing erythroblasts. Nature. 2012;491(7425):608–12.
8. Wager K, Russell C. Mitophagy and neurodegeneration: the zebrafish model system. Autophagy. 2013;9(11):1693–709.
9. Wager K, Mahmood F, Russell C. Modelling inborn errors of metabolism in zebrafish. J Inherit Metab Dis. 2014;37(4):483–95.
10. Caramillo EM et al. Modeling PTSD in the zebrafish: are we there yet? Behav Brain Res. 2015;276:151–60.
11. Nguyen M, Stewart AM, Kalueff AV. Aquatic blues: modeling depression and antidepressant action in zebrafish. Prog Neuro-Psychopharmacol Biol Psychiatry. 2014;55:26–39.
12. Nasevicius A, Ekker SC. Effective targeted gene ‘knockdown’ in zebrafish. Nat Genet. 2000;26(2):216–20.
13. Auer TO, Del Bene F. CRISPR/Cas9 and TALEN-mediated knock-in approaches in zebrafish. Methods. 2014;69(2):142–50. Auer et al. review the use and application of genome editing approaches that are relatively novel to zebrafish.
14. Kasher PR et al. Impairment of the tRNA-splicing endonuclease subunit 54 (tsen54) gene causes neurological abnormalities and larval death in zebrafish models of pontocerebellar hypoplasia. Hum Mol Genet. 2011;20(8):1574–84.
15. Schaffer AE et al. CLP1 founder mutation links tRNA splicing and maturation to cerebellar development and neurodegeneration. Cell. 2014;157(3):651–63. Schaffer et al. use zebrafish to confirm CLP1 mutations as causing pontocerebellar hypoplasia.
16. Mahmood F et al. A zebrafish model of CLN2 disease is deficient in tripeptidyl peptidase 1 and displays progressive neurodegeneration accompanied by a reduction in proliferation. Brain. 2013;136(Pt 5):1488–507. Mahmood et al. show that locomotion assays can be used to show different movement phenotypes developing over time.
17. O' Donnell KC et al. Axon degeneration and PGC-1α-mediated protection in a zebrafish model of α-synuclein toxicity. Dis Models Mech. 2014;7(5):571–82. O' Donnell et al. demonstrate elegantly that PGC-1a protects against a-syn toxicity.
18. Donnell KC, Vargas ME, Sagasti A. WldS and PGC-1α regulate mitochondrial transport and oxidation state after axonal injury. J Neurosci: Off J Soc Neurosci. 2013;33(37):14778–90. This article demonstrates the power of zebrafish for live analysis of cellular and sub-cellular phenotypes.
19. Namavar Y et al. Classification, diagnosis and potential mechanisms in pontocerebellar hypoplasia. Orphanet J Rare Dis. 2011;6:50.
20. Mink JW et al. Classification and natural history of the neuronal ceroid lipofuscinoses. J Child Neurol. 2013;28(9):1101–5.
21. Bond M et al. Use of model organisms for the study of neuronal ceroid lipofuscinosis. Biochim Biophys Acta. 2013;1832(11):1842–65.
22. Cerveny KL et al. The zebrafish flotte lotte mutant reveals that the local retinal environment promotes the differentiation of proliferating precursors emerging from their stem cell niche. Development. 2010;137(13):2107–15.
23. Lin MK, Farrer MJ. Genetics and genomics of Parkinson’s disease. Genome Med. 2014;6(6):48.
24. Ajroud-Driss S, Siddique T. Sporadic and hereditary amyotrophic lateral sclerosis (ALS). Biochim Biophys Acta. 2014;1852(4):679–84.
25. Vaccaro A et al. Methylene blue protects against TDP-43 and FUS neuronal toxicity in C. elegans and D. rerio. PLoS One. 2012;7(7):e42117. In this paper, methylene blue is shown to be protective for zebrafish models of ALS.
26. Vaccaro A et al. Pharmacological reduction of ER stress protects against TDP-43 neuronal toxicity in vivo. Neurobiol Dis. 2013;55:64–75. Vaccaro et al. demonstrate mechanistic insight derived from pharmacological treatment of a zebrafish ALS model.
27. Jiang HQ et al. Guanabenz delays the onset of disease symptoms, extends lifespan, improves motor performance and attenuates motor neuron loss in the SOD1 G93A mouse model of amyotrophic lateral sclerosis. Neuroscience. 2014;277:132–8.
28. Wang L et al. Guanabenz, which enhances the unfolded protein response, ameliorates mutant SOD1-induced amyotrophic lateral sclerosis. Neurobiol Dis. 2014;71:317–24.