[Animal models of neurodegenerative diseases].
Identifieur interne : 000C52 ( PubMed/Checkpoint ); précédent : 000C51; suivant : 000C53[Animal models of neurodegenerative diseases].
Auteurs : Dominique Langui [France] ; François Lachapelle ; Charles DuyckaertsSource :
- Medecine sciences : M/S [ 0767-0974 ] ; 2007.
English descriptors
- KwdEn :
- Alzheimer Disease (genetics), Amyloid beta-Peptides (deficiency), Amyloid beta-Peptides (genetics), Amyloid beta-Peptides (physiology), Animals, Animals, Genetically Modified, Ataxia (genetics), Caenorhabditis elegans (genetics), Dementia (genetics), Disease Models, Animal, Drosophila melanogaster (genetics), Gene Targeting, Genes, Recessive, Heredodegenerative Disorders, Nervous System (genetics), Humans, Lewy Body Disease (metabolism), Mice, Mice, Knockout, Mice, Neurologic Mutants, Minisatellite Repeats, Neurodegenerative Diseases (chemically induced), Neurotoxins (toxicity), Parkinsonian Disorders, Prion Diseases (genetics), Species Specificity, alpha-Synuclein (genetics), alpha-Synuclein (metabolism), tau Proteins (deficiency), tau Proteins (genetics), tau Proteins (physiology).
- MESH :
- chemical , deficiency : Amyloid beta-Peptides, tau Proteins.
- chemically induced : Neurodegenerative Diseases.
- genetics : Alzheimer Disease, Amyloid beta-Peptides, Ataxia, Caenorhabditis elegans, Dementia, Drosophila melanogaster, Heredodegenerative Disorders, Nervous System, Prion Diseases, alpha-Synuclein, tau Proteins.
- metabolism : Lewy Body Disease, alpha-Synuclein.
- chemical , physiology : Amyloid beta-Peptides, tau Proteins.
- chemical , toxicity : Neurotoxins.
- Animals, Animals, Genetically Modified, Disease Models, Animal, Gene Targeting, Genes, Recessive, Humans, Mice, Mice, Knockout, Mice, Neurologic Mutants, Minisatellite Repeats, Parkinsonian Disorders, Species Specificity.
Abstract
Numerous evidences indicate that the phenotype of a neurodegenerative disease and its pathogenetic mechanism are only loosely linked. The phenotype is directly related to the topography of the lesions and is reproduced whatever the mechanism as soon as the same neurons are destroyed or deficient: the symptoms of Parkinson disease are mimicked by any destruction of the neurons of the substantia nigra, caused for instance by the toxin MPTP. This does not mean that idiopathic Parkinson disease is due to MPTP. In the same way, mouse lines such as Reeler, Weaver and Staggerer in which ataxia occurs spontaneously does not help to understand human ataxias: now that mutations responsible for these phenotypes have been identified, it appears that one is responsible for lissencephaly (mutation of the reelin gene) and the other two have no equivalent in man. Therapeutic attempts, however, rely on the understanding of the pathogenetic mechanisms. Introducing a mutated human transgene in the genome of an animal has, in many instances, significantly improved this understanding. Transgenic mice have proven useful in reproducing lesions seen in neurodegenerative disease such as the plaques of Alzheimer disease (in the APP mouse which has integrated the mutated gene of the amyloid protein precursor), the tau glial and neuronal accumulation (seen in cases of frontotemporal dementias due to tau mutation), the nuclear inclusions caused by CAG triplet expansion (seen in the mutation of Huntington disease and autosomal dominant spinocerebellar ataxias). These recent advances have fostered numerous therapeutic attempts. Transgenesis in drosophila and in the worm Caenorhabditis elegans have opened new possibilities in the screening of protein partners, modifier genes, and potential therapeutic molecules. However, it is also becoming clear that introducing a human mutated gene in an animal does not necessarily trigger pathogenetic cascades identical to those seen in the human disease. Human diseases have to be studied in parallel with their animal models to ensure that the model mimic at least a few original mechanisms, on which new therapeutics may be tested.
DOI: 10.1051/medsci/2007232180
PubMed: 17291428
Affiliations:
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pubmed:17291428Le document en format XML
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<term>Amyloid beta-Peptides (physiology)</term>
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<term>Dementia (genetics)</term>
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<front><div type="abstract" xml:lang="en">Numerous evidences indicate that the phenotype of a neurodegenerative disease and its pathogenetic mechanism are only loosely linked. The phenotype is directly related to the topography of the lesions and is reproduced whatever the mechanism as soon as the same neurons are destroyed or deficient: the symptoms of Parkinson disease are mimicked by any destruction of the neurons of the substantia nigra, caused for instance by the toxin MPTP. This does not mean that idiopathic Parkinson disease is due to MPTP. In the same way, mouse lines such as Reeler, Weaver and Staggerer in which ataxia occurs spontaneously does not help to understand human ataxias: now that mutations responsible for these phenotypes have been identified, it appears that one is responsible for lissencephaly (mutation of the reelin gene) and the other two have no equivalent in man. Therapeutic attempts, however, rely on the understanding of the pathogenetic mechanisms. Introducing a mutated human transgene in the genome of an animal has, in many instances, significantly improved this understanding. Transgenic mice have proven useful in reproducing lesions seen in neurodegenerative disease such as the plaques of Alzheimer disease (in the APP mouse which has integrated the mutated gene of the amyloid protein precursor), the tau glial and neuronal accumulation (seen in cases of frontotemporal dementias due to tau mutation), the nuclear inclusions caused by CAG triplet expansion (seen in the mutation of Huntington disease and autosomal dominant spinocerebellar ataxias). These recent advances have fostered numerous therapeutic attempts. Transgenesis in drosophila and in the worm Caenorhabditis elegans have opened new possibilities in the screening of protein partners, modifier genes, and potential therapeutic molecules. However, it is also becoming clear that introducing a human mutated gene in an animal does not necessarily trigger pathogenetic cascades identical to those seen in the human disease. Human diseases have to be studied in parallel with their animal models to ensure that the model mimic at least a few original mechanisms, on which new therapeutics may be tested.</div>
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<Abstract><AbstractText>Numerous evidences indicate that the phenotype of a neurodegenerative disease and its pathogenetic mechanism are only loosely linked. The phenotype is directly related to the topography of the lesions and is reproduced whatever the mechanism as soon as the same neurons are destroyed or deficient: the symptoms of Parkinson disease are mimicked by any destruction of the neurons of the substantia nigra, caused for instance by the toxin MPTP. This does not mean that idiopathic Parkinson disease is due to MPTP. In the same way, mouse lines such as Reeler, Weaver and Staggerer in which ataxia occurs spontaneously does not help to understand human ataxias: now that mutations responsible for these phenotypes have been identified, it appears that one is responsible for lissencephaly (mutation of the reelin gene) and the other two have no equivalent in man. Therapeutic attempts, however, rely on the understanding of the pathogenetic mechanisms. Introducing a mutated human transgene in the genome of an animal has, in many instances, significantly improved this understanding. Transgenic mice have proven useful in reproducing lesions seen in neurodegenerative disease such as the plaques of Alzheimer disease (in the APP mouse which has integrated the mutated gene of the amyloid protein precursor), the tau glial and neuronal accumulation (seen in cases of frontotemporal dementias due to tau mutation), the nuclear inclusions caused by CAG triplet expansion (seen in the mutation of Huntington disease and autosomal dominant spinocerebellar ataxias). These recent advances have fostered numerous therapeutic attempts. Transgenesis in drosophila and in the worm Caenorhabditis elegans have opened new possibilities in the screening of protein partners, modifier genes, and potential therapeutic molecules. However, it is also becoming clear that introducing a human mutated gene in an animal does not necessarily trigger pathogenetic cascades identical to those seen in the human disease. Human diseases have to be studied in parallel with their animal models to ensure that the model mimic at least a few original mechanisms, on which new therapeutics may be tested.</AbstractText>
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