Neurodegenerative Diseases: Neurotoxins as Sufficient Etiologic Agents?
Identifieur interne : 002452 ( Main/Exploration ); précédent : 002451; suivant : 002453Neurodegenerative Diseases: Neurotoxins as Sufficient Etiologic Agents?
Auteurs : Christopher A. Shaw ; Günter U. HöglingerSource :
- Neuromolecular medicine [ 1535-1084 ] ; 2007.
English descriptors
- KwdEn :
- Amyotrophic Lateral Sclerosis (chemically induced), Amyotrophic Lateral Sclerosis (epidemiology), Animals, Dementia (chemically induced), Dementia (epidemiology), Guadeloupe (epidemiology), Guam (epidemiology), Humans, MPTP Poisoning (epidemiology), MPTP Poisoning (etiology), Neurodegenerative Diseases (chemically induced), Neurodegenerative Diseases (epidemiology), Neurodegenerative Diseases (genetics), Neurotoxins (toxicity), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (epidemiology), Parkinsonian Disorders (chemically induced), Parkinsonian Disorders (epidemiology), Toxins, Biological (toxicity).
- MESH :
- chemical , toxicity : Neurotoxins, Toxins, Biological.
- geographic , epidemiology : Guadeloupe, Guam.
- chemically induced : Amyotrophic Lateral Sclerosis, Dementia, Neurodegenerative Diseases, Parkinson Disease, Secondary, Parkinsonian Disorders.
- epidemiology : Amyotrophic Lateral Sclerosis, Dementia, MPTP Poisoning, Neurodegenerative Diseases, Parkinson Disease, Secondary, Parkinsonian Disorders.
- etiology : MPTP Poisoning.
- genetics : Neurodegenerative Diseases.
- Animals, Humans.
Abstract
A dominant paradigm in neurological disease research is that the primary etiological factors for diseases such as Alzheimer’s (AD), Parkinson’s (PD), and amyotrophic lateral sclerosis (ALS) are genetic. Opposed to this perspective are the clear observations from epidemiology that purely genetic casual factors account for a relatively small fraction of all cases. Many who support a genetic etiology for neurological disease take the view that while the percentages may be relatively small, these numbers will rise in the future with the inevitable discoveries of additional genetic mutations. The follow up argument is that even if the last is not true, the events triggered by the aberrant genes identified so far will be shown to impact the same neuronal cell death pathways as those activated by environmental factors that trigger most sporadic disease cases. In this article we present a countervailing view that environmental neurotoxins may be the sole sufficient factor in at least three neurological disease clusters. For each, neurotoxins have been isolated and characterized that, at least in animal models, faithfully reproduce each disorder without the need for genetic co-factors. Based on these data, we will propose a set of principles that would enable any potential toxin to be evaluated as an etiological factor in a given neurodegenerative disease. Finally, we will attempt to put environmental toxins into the context of possible genetically-determined susceptibility.
Url:
DOI: 10.1007/s12017-007-8016-8
PubMed: 17985252
PubMed Central: 2814816
Affiliations:
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Le document en format XML
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Shaw</name></author><author><name sortKey="Hoglinger, Gunter U" sort="Hoglinger, Gunter U" uniqKey="Hoglinger G" first="Günter U." last="Höglinger">Günter U. Höglinger</name></author></analytic><series><title level="j">Neuromolecular medicine</title><idno type="ISSN">1535-1084</idno><idno type="eISSN">1559-1174</idno><imprint><date when="2007">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amyotrophic Lateral Sclerosis (chemically induced)</term><term>Amyotrophic Lateral Sclerosis (epidemiology)</term><term>Animals</term><term>Dementia (chemically induced)</term><term>Dementia (epidemiology)</term><term>Guadeloupe (epidemiology)</term><term>Guam (epidemiology)</term><term>Humans</term><term>MPTP Poisoning (epidemiology)</term><term>MPTP Poisoning (etiology)</term><term>Neurodegenerative Diseases (chemically induced)</term><term>Neurodegenerative Diseases (epidemiology)</term><term>Neurodegenerative Diseases (genetics)</term><term>Neurotoxins (toxicity)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (epidemiology)</term><term>Parkinsonian Disorders (chemically induced)</term><term>Parkinsonian Disorders (epidemiology)</term><term>Toxins, Biological (toxicity)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Neurotoxins</term><term>Toxins, Biological</term></keywords><keywords scheme="MESH" type="geographic" qualifier="epidemiology" xml:lang="en"><term>Guadeloupe</term><term>Guam</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Dementia</term><term>Neurodegenerative Diseases</term><term>Parkinson Disease, Secondary</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Dementia</term><term>MPTP Poisoning</term><term>Neurodegenerative Diseases</term><term>Parkinson Disease, Secondary</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>MPTP Poisoning</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Neurodegenerative Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P2">A dominant paradigm in neurological disease research is that the primary etiological factors for diseases such as Alzheimer’s (AD), Parkinson’s (PD), and amyotrophic lateral sclerosis (ALS) are genetic. Opposed to this perspective are the clear observations from epidemiology that purely genetic casual factors account for a relatively small fraction of all cases. Many who support a genetic etiology for neurological disease take the view that while the percentages may be relatively small, these numbers will rise in the future with the inevitable discoveries of additional genetic mutations. The follow up argument is that even if the last is not true, the events triggered by the aberrant genes identified so far will be shown to impact the same neuronal cell death pathways as those activated by environmental factors that trigger most sporadic disease cases. In this article we present a countervailing view that environmental neurotoxins may be the sole sufficient factor in at least three neurological disease clusters. For each, neurotoxins have been isolated and characterized that, at least in animal models, faithfully reproduce each disorder without the need for genetic co-factors. Based on these data, we will propose a set of principles that would enable any potential toxin to be evaluated as an etiological factor in a given neurodegenerative disease. Finally, we will attempt to put environmental toxins into the context of possible genetically-determined susceptibility.</p></div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Hoglinger, Gunter U" sort="Hoglinger, Gunter U" uniqKey="Hoglinger G" first="Günter U." last="Höglinger">Günter U. Höglinger</name><name sortKey="Shaw, Christopher A" sort="Shaw, Christopher A" uniqKey="Shaw C" first="Christopher A." last="Shaw">Christopher A. Shaw</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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