An extracellular mechanism that can explain the neurotoxic effects of α-synuclein aggregates in the brain
Identifieur interne : 000377 ( Ncbi/Curation ); précédent : 000376; suivant : 000378An extracellular mechanism that can explain the neurotoxic effects of α-synuclein aggregates in the brain
Auteurs : C Pacheco [Chili] ; L Aguayo [Chili] ; C Opazo [Chili]Source :
- Frontiers in Physiology ; 2012.
Abstract
Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), and Dementia with Lewy bodies (DLB), display an accumulation of proteins including α-synuclein aggregates in cortical and subcortical regions of the brain. PD is a complex, progressive disease which involves damage of motor and cognitive brain regions, as well as autonomic and sensory areas. Since α-synuclein is a neuronal cytosolic protein, it is assumed that pathogenic changes induced by α-synuclein aggregates occur only at the cytoplasmic level. However, recent studies have identified the presence of extracellular α-synuclein, suggesting that the pathogenic action of this protein may also occur in the extracellular milieu through an unknown mechanism. One of the hypotheses is that extracellular α-synuclein aggregates or oligomers may directly disrupt the neuronal membrane by the formation of a pore reminiscent to the ones formed by β-amyloid aggregates. Here, we will review some evidence that support this mechanism, analyzing the interactions of α-synuclein with components of the plasma membrane, the formation of pore/perforated structures, and the implications on ionic dyshomeostasis. Furthermore, we will also discuss how this mechanism can be integrated into a general phenomenon that may explain the synaptotoxicity and neurotoxicity observed in different neurodegenerative diseases.
Url:
DOI: 10.3389/fphys.2012.00297
PubMed: 22934048
PubMed Central: 3429068
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id="aff1"><institution>Laboratory of Neurobiometals, Department of Physiology, University of Concepción</institution><country>Concepción, Chile</country></nlm:aff><country xml:lang="fr">Chili</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Laboratory of Neurophysiology, Department of Physiology, University of Concepción</institution><country>Concepción, Chile</country></nlm:aff><country xml:lang="fr">Chili</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author><author><name sortKey="Aguayo, L G" sort="Aguayo, L G" uniqKey="Aguayo L" first="L" last="Aguayo">L Aguayo</name><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Laboratory of Neurophysiology, Department of Physiology, University of Concepción</institution><country>Concepción, Chile</country></nlm:aff><country xml:lang="fr">Chili</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author><author><name sortKey="Opazo, C" sort="Opazo, C" uniqKey="Opazo C" first="C" last="Opazo">C Opazo</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Laboratory of Neurobiometals, Department of Physiology, University of Concepción</institution><country>Concepción, Chile</country></nlm:aff><country xml:lang="fr">Chili</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Physiology</title><idno type="e-ISSN">1664-042X</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), and Dementia with Lewy bodies (DLB), display an accumulation of proteins including α-synuclein aggregates in cortical and subcortical regions of the brain. PD is a complex, progressive disease which involves damage of motor and cognitive brain regions, as well as autonomic and sensory areas. Since α-synuclein is a neuronal cytosolic protein, it is assumed that pathogenic changes induced by α-synuclein aggregates occur only at the cytoplasmic level. However, recent studies have identified the presence of extracellular α-synuclein, suggesting that the pathogenic action of this protein may also occur in the extracellular milieu through an unknown mechanism. One of the hypotheses is that extracellular α-synuclein aggregates or oligomers may directly disrupt the neuronal membrane by the formation of a pore reminiscent to the ones formed by β-amyloid aggregates. Here, we will review some evidence that support this mechanism, analyzing the interactions of α-synuclein with components of the plasma membrane, the formation of pore/perforated structures, and the implications on ionic dyshomeostasis. Furthermore, we will also discuss how this mechanism can be integrated into a general phenomenon that may explain the synaptotoxicity and neurotoxicity observed in different neurodegenerative diseases.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Aarsland, D" uniqKey="Aarsland D">D. Aarsland</name></author><author><name sortKey="Bronnick, K" uniqKey="Bronnick K">K. Bronnick</name></author><author><name sortKey="Ehrt, U" uniqKey="Ehrt U">U. Ehrt</name></author><author><name sortKey="De Deyn, P P" uniqKey="De Deyn P">P. P. De Deyn</name></author><author><name sortKey="Tekin, S" uniqKey="Tekin S">S. Tekin</name></author><author><name sortKey="Emre, M" uniqKey="Emre M">M. Emre</name></author><author><name sortKey="Cummings, J L" uniqKey="Cummings J">J. L. Cummings</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Abeliovich, A" uniqKey="Abeliovich A">A. 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Lezcano</name></author><author><name sortKey="Ros, R" uniqKey="Ros R">R. Ros</name></author><author><name sortKey="Ampuero, I" uniqKey="Ampuero I">I. Ampuero</name></author><author><name sortKey="Vidal, L" uniqKey="Vidal L">L. Vidal</name></author><author><name sortKey="Hoenicka, J" uniqKey="Hoenicka J">J. Hoenicka</name></author><author><name sortKey="Rodriguez, O" uniqKey="Rodriguez O">O. Rodriguez</name></author><author><name sortKey="Atares, B" uniqKey="Atares B">B. Atares</name></author><author><name sortKey="Llorens, V" uniqKey="Llorens V">V. Llorens</name></author><author><name sortKey="Gomez, Tortosa E" uniqKey="Gomez T">Tortosa E. Gomez</name></author><author><name sortKey="Del Ser, T" uniqKey="Del Ser T">T. Del Ser</name></author><author><name sortKey="Munoz, D G" uniqKey="Munoz D">D. G. Munoz</name></author><author><name sortKey="De Yebenes, J G" uniqKey="De Yebenes J">J. G. 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