Amyotrophic lateral sclerosis—Evolutionary and other perspectives
Identifieur interne : 000B67 ( Main/Exploration ); précédent : 000B66; suivant : 000B68Amyotrophic lateral sclerosis—Evolutionary and other perspectives
Auteurs : Andrew Eisen [Canada]Source :
- Muscle & Nerve [ 0148-639X ] ; 2009-08.
English descriptors
- KwdEn :
Abstract
In this study some particular and puzzling aspects of amyotrophic lateral sclerosis (ALS) are discussed, with an emphasis on the role of neocortical evolution. Other issues explored include the nature of the clinical deficit in ALS; anatomical and evolutionary aspects of the neocortex, motor cortex, and corpus callosum; and some discussion as to when ALS begins. In common with other neurodegenerative diseases, ALS may result from dysfunctional neocortical circuitry. It is suggested that the disease starts some years prior to clinical onset, possibly in adolescence, or even earlier, when there is marked alteration of anatomy, physiology, and biochemistry of the neocortex. The failure of naturally occurring animal models of ALS or models that truly replicate the human disease may reflect the unique, continued, and increased neocortical evolution of modern humans. Muscle Nerve 40: 297–304, 2009
Url:
DOI: 10.1002/mus.21404
Affiliations:
Links toward previous steps (curation, corpus...)
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<front><div type="abstract" xml:lang="en">In this study some particular and puzzling aspects of amyotrophic lateral sclerosis (ALS) are discussed, with an emphasis on the role of neocortical evolution. Other issues explored include the nature of the clinical deficit in ALS; anatomical and evolutionary aspects of the neocortex, motor cortex, and corpus callosum; and some discussion as to when ALS begins. In common with other neurodegenerative diseases, ALS may result from dysfunctional neocortical circuitry. It is suggested that the disease starts some years prior to clinical onset, possibly in adolescence, or even earlier, when there is marked alteration of anatomy, physiology, and biochemistry of the neocortex. The failure of naturally occurring animal models of ALS or models that truly replicate the human disease may reflect the unique, continued, and increased neocortical evolution of modern humans. Muscle Nerve 40: 297–304, 2009</div>
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