Pathophysiological Correlation between Cigarette Smoking and Amyotrophic Lateral Sclerosis

Menounos, S; Hansbro, PM; Diwan, AD; Das, A

Pathophysiological Correlation between Cigarette Smoking and Amyotrophic Lateral Sclerosis

Menounos, S Hansbro, PM Diwan, AD Das, A

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Publisher:: Elsevier
Publication Type:: Journal Article
Citation:: Neuroscience, 2021, 2, (2), pp. 120-134
Issue Date:: 2021-04-20

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Field	Value	Language
dc.contributor.author	Menounos, S
dc.contributor.author	Hansbro, PM
dc.contributor.author	Diwan, AD
dc.contributor.author	Das, A
dc.date.accessioned	2022-02-12T23:56:50Z
dc.date.available	2022-02-12T23:56:50Z
dc.date.issued	2021-04-20
dc.identifier.citation	Neuroscience, 2021, 2, (2), pp. 120-134
dc.identifier.issn	0306-4522
dc.identifier.issn	2673-4087
dc.identifier.uri	http://hdl.handle.net/10453/154445
dc.description.abstract	Cigarette smoke (CS) has been consistently demonstrated to be an environmental risk factor for amyotrophic lateral sclerosis (ALS), although the molecular pathogenic mechanisms involved are yet to be elucidated. Here, we propose different mechanisms by which CS exposure can cause sporadic ALS pathogenesis. Oxidative stress and neuroinflammation are widely implicated in ALS pathogenesis, with blood–spinal cord barrier disruption also recognised to be involved in the disease process. In addition, immunometabolic, epigenetic and microbiome alterations have been implicated in ALS recently. Identification of the underlying pathophysiological mechanisms that underpin CS-associated ALS will drive future research to be conducted into new targets for treatment.
dc.language	en
dc.publisher	Elsevier
dc.relation.ispartof	Neuroscience
dc.relation.isbasedon	10.3390/neurosci2020008
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	1109 Neurosciences, 1701 Psychology, 1702 Cognitive Sciences
dc.subject.classification	Neurology & Neurosurgery
dc.title	Pathophysiological Correlation between Cigarette Smoking and Amyotrophic Lateral Sclerosis
dc.type	Journal Article
utslib.citation.volume	2
utslib.for	1109 Neurosciences
utslib.for	1701 Psychology
utslib.for	1702 Cognitive Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
utslib.copyright.status	open_access	*
pubs.consider-herdc	false
dc.date.updated	2022-02-12T23:56:48Z
pubs.issue	2
pubs.publication-status	Published
pubs.volume	2
utslib.citation.issue	2

Abstract:

Cigarette smoke (CS) has been consistently demonstrated to be an environmental risk factor for amyotrophic lateral sclerosis (ALS), although the molecular pathogenic mechanisms involved are yet to be elucidated. Here, we propose different mechanisms by which CS exposure can cause sporadic ALS pathogenesis. Oxidative stress and neuroinflammation are widely implicated in ALS pathogenesis, with blood–spinal cord barrier disruption also recognised to be involved in the disease process. In addition, immunometabolic, epigenetic and microbiome alterations have been implicated in ALS recently. Identification of the underlying pathophysiological mechanisms that underpin CS-associated ALS will drive future research to be conducted into new targets for treatment.

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http://hdl.handle.net/10453/154445