Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease of unknown origin. Higher incidences for ALS in certain population subgroups have raised questions about feasible causes and led to controverse discussions, though without providing a real explanation for over 90% of sporadic ALS cases so far. Although speculative to this date however, a combined view on recent data obtained in different scientific fields might offer reasonable explanations for the origin of ALS. Here it is discussed, whether enhanced activation of the sympathetic nervous system (SNS) in concert with raised uncoupling of the mitochondrial respiratory chain in muscle tissue might be a potential key factor that could initiate the onset of ALS. The aim of this document is to show a possible link between mitochondrial uncoupling and the degeneration of motor neurons, primarily to evoke further discussions in this important area.
Highlights
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease of unknown origin
Whether enhanced activation of the sympathetic nervous system (SNS) in concert with raised uncoupling of the mitochondrial respiratory chain in muscle tissue might be a potential key factor that could initiate the onset of ALS
The aim of this document is to show a possible link between mitochondrial uncoupling and the degeneration of motor neurons, primarily to evoke further discussions in this important area
Summary
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease of unknown origin. Whether enhanced activation of the sympathetic nervous system (SNS) in concert with raised uncoupling of the mitochondrial respiratory chain in muscle tissue might be a potential key factor that could initiate the onset of ALS. The first observation that tentatively connect certain activity of muscles to ALS has been published in 2003, and describes upregulation of uncoupling proteins (UCPs) in muscle tissues of ALS models [1].
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