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Article: Relationships between mitochondrial dysfunction and neurotransmission failure in Alzheimer’s disease

TitleRelationships between mitochondrial dysfunction and neurotransmission failure in Alzheimer’s disease
Authors
KeywordsAlzheimer’s disease
mitochondrial dysfunction
monoaminergic
neurotransmission
dysfunction
Issue Date2020
PublisherBuck Institute for Age Research. The Journal's web site is located at http://www.aginganddisease.org
Citation
Aging and Disease, 2020, Epub 2020-10-01, v. 11 n. 5 How to Cite?
AbstractBesides extracellular deposition of amyloid beta and formation of phosphorylated tau in the brains of patients with Alzheimer's disease (AD), the pathogenesis of AD is also thought to involve mitochondrial dysfunctions and altered neurotransmission systems. However, none of these components can describe the diverse cognitive, behavioural, and psychiatric symptoms of AD without the pathologies interacting with one another. The purpose of this review is to understand the relationships between mitochondrial and neurotransmission dysfunctions in terms of (1) how mitochondrial alterations affect cholinergic and monoaminergic systems via disruption of energy metabolism, oxidative stress, and apoptosis; and (2) how different neurotransmission systems drive mitochondrial dysfunction via increasing amyloid beta internalisation, oxidative stress, disruption of mitochondrial permeabilisation, and mitochondrial trafficking. All these interactions are separately discussed in terms of neurotransmission systems. The association of mitochondrial dysfunctions with alterations in dopamine, norepinephrine, and histamine is the prospective goal in this research field. By unfolding the complex interactions surrounding mitochondrial dysfunction in AD, we can better develop potential treatments to delay, prevent, or cure this devastating disease.
Persistent Identifierhttp://hdl.handle.net/10722/281209
ISSN
2019 Impact Factor: 5.402
2015 SCImago Journal Rankings: 1.542

 

DC FieldValueLanguage
dc.contributor.authorWong, KY-
dc.contributor.authorROY, J-
dc.contributor.authorFung, ML-
dc.contributor.authorHeng, BC-
dc.contributor.authorZhang, C-
dc.contributor.authorLim, LW-
dc.date.accessioned2020-03-09T09:51:35Z-
dc.date.available2020-03-09T09:51:35Z-
dc.date.issued2020-
dc.identifier.citationAging and Disease, 2020, Epub 2020-10-01, v. 11 n. 5-
dc.identifier.issn2152-5250-
dc.identifier.urihttp://hdl.handle.net/10722/281209-
dc.description.abstractBesides extracellular deposition of amyloid beta and formation of phosphorylated tau in the brains of patients with Alzheimer's disease (AD), the pathogenesis of AD is also thought to involve mitochondrial dysfunctions and altered neurotransmission systems. However, none of these components can describe the diverse cognitive, behavioural, and psychiatric symptoms of AD without the pathologies interacting with one another. The purpose of this review is to understand the relationships between mitochondrial and neurotransmission dysfunctions in terms of (1) how mitochondrial alterations affect cholinergic and monoaminergic systems via disruption of energy metabolism, oxidative stress, and apoptosis; and (2) how different neurotransmission systems drive mitochondrial dysfunction via increasing amyloid beta internalisation, oxidative stress, disruption of mitochondrial permeabilisation, and mitochondrial trafficking. All these interactions are separately discussed in terms of neurotransmission systems. The association of mitochondrial dysfunctions with alterations in dopamine, norepinephrine, and histamine is the prospective goal in this research field. By unfolding the complex interactions surrounding mitochondrial dysfunction in AD, we can better develop potential treatments to delay, prevent, or cure this devastating disease.-
dc.languageeng-
dc.publisherBuck Institute for Age Research. The Journal's web site is located at http://www.aginganddisease.org-
dc.relation.ispartofAging and Disease-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAlzheimer’s disease-
dc.subjectmitochondrial dysfunction-
dc.subjectmonoaminergic-
dc.subjectneurotransmission-
dc.subjectdysfunction-
dc.titleRelationships between mitochondrial dysfunction and neurotransmission failure in Alzheimer’s disease-
dc.typeArticle-
dc.identifier.emailFung, ML: fungml@hku.hk-
dc.identifier.emailZhang, C: zhangcf@hku.hk-
dc.identifier.emailLim, LW: limlw@hku.hk-
dc.identifier.authorityFung, ML=rp00433-
dc.identifier.authorityZhang, C=rp01408-
dc.identifier.authorityLim, LW=rp02088-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.14336/AD.2019.1125-
dc.identifier.hkuros309287-
dc.identifier.volumeEpub 2020-10-01, v. 11 n. 5-
dc.publisher.placeUnited States-

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