Literature DB >> 11511401

Transgenic invertebrate models of age-associated neurodegenerative diseases.

C D Link1.   

Abstract

Transgenic Drosophila melanogaster and Caenorhabditis elegans strains have been engineered to express human proteins associated with neurodegenerative diseases. These model systems include transgenic animals expressing beta-amyloid peptide (Alzheimer's disease), polyglutamine repeat proteins (Huntington's disease, Spinocerebellar ataxia), and alpha-synuclein (Parkinson's disease). In most of these invertebrate models, some aspects of the human diseases are reproduced. Although expression of all these proteins in transgenic mice has been instructive, the invertebrate models offer experimental advantages (e.g. forward genetic screens) that can potentially address some of the outstanding questions regarding the cellular processes underlying these diseases. This review considers what has been learned from these invertebrate models, and speculates what further insight may be gained from them.

Entities:  

Mesh:

Year:  2001        PMID: 11511401     DOI: 10.1016/s0047-6374(01)00291-3

Source DB:  PubMed          Journal:  Mech Ageing Dev        ISSN: 0047-6374            Impact factor:   5.432


  20 in total

Review 1.  Modeling human neurodegenerative diseases in transgenic systems.

Authors:  Miguel A Gama Sosa; Rita De Gasperi; Gregory A Elder
Journal:  Hum Genet       Date:  2011-12-14       Impact factor: 4.132

2.  Prediction of S-glutathionylated proteins progression in Alzheimer's transgenic mouse model using principle component analysis.

Authors:  Cheng Zhang; Ching-Chang Kuo; Alan W L Chiu; June Feng
Journal:  J Alzheimers Dis       Date:  2012       Impact factor: 4.472

3.  Fluoxetine protects against amyloid-beta toxicity, in part via daf-16 mediated cell signaling pathway, in Caenorhabditis elegans.

Authors:  Roongpetch Keowkase; Marwa Aboukhatwa; Yuan Luo
Journal:  Neuropharmacology       Date:  2010-04-24       Impact factor: 5.250

4.  Dietary restriction suppresses proteotoxicity and enhances longevity by an hsf-1-dependent mechanism in Caenorhabditis elegans.

Authors:  Katherine A Steinkraus; Erica D Smith; Christina Davis; Daniel Carr; William R Pendergrass; George L Sutphin; Brian K Kennedy; Matt Kaeberlein
Journal:  Aging Cell       Date:  2008-03-10       Impact factor: 9.304

5.  A single point mutation in ecdysone receptor leads to increased ligand specificity: implications for gene switch applications.

Authors:  M B Kumar; T Fujimoto; D W Potter; Q Deng; S R Palli
Journal:  Proc Natl Acad Sci U S A       Date:  2002-10-31       Impact factor: 11.205

6.  The aggregation-prone intracellular serpin SRP-2 fails to transit the ER in Caenorhabditis elegans.

Authors:  Richard M Silverman; Erin E Cummings; Linda P O'Reilly; Mark T Miedel; Gary A Silverman; Cliff J Luke; David H Perlmutter; Stephen C Pak
Journal:  Genetics       Date:  2015-03-18       Impact factor: 4.562

7.  A new role for laminins as modulators of protein toxicity in Caenorhabditis elegans.

Authors:  Louise T Jensen; Tine H Møller; Simon A Larsen; Helle Jakobsen; Anders Olsen
Journal:  Aging Cell       Date:  2011-12-11       Impact factor: 9.304

8.  alpha -Synucleinopathy and selective dopaminergic neuron loss in a rat lentiviral-based model of Parkinson's disease.

Authors:  C Lo Bianco; J-L Ridet; B L Schneider; N Deglon; P Aebischer
Journal:  Proc Natl Acad Sci U S A       Date:  2002-07-16       Impact factor: 11.205

Review 9.  Invertebrate models of neurologic disease: insights into pathogenesis and therapy.

Authors:  Leslie Michels Thompson; J Lawrence Marsh
Journal:  Curr Neurol Neurosci Rep       Date:  2003-09       Impact factor: 5.081

10.  The Caenorhabditis elegans A beta 1-42 model of Alzheimer disease predominantly expresses A beta 3-42.

Authors:  Gawain McColl; Blaine R Roberts; Adam P Gunn; Keyla A Perez; Deborah J Tew; Colin L Masters; Kevin J Barnham; Robert A Cherny; Ashley I Bush
Journal:  J Biol Chem       Date:  2009-07-02       Impact factor: 5.157

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.