Amyloid-B-Acetylcholinesterase complexes potentiate neurodegenerative changes induced by the AB peptide. Implications for the pathogenesis of Alzheimer's disease

Simple item page
dc.contributor.authorDinamarca Ceballos, Margarita Constanza.
dc.contributor.authorSagal, Juan P.
dc.contributor.authorQuintanilla Gómez, Rodrigo Arthur
dc.contributor.authorGodoy, Juan A.
dc.contributor.authorArrázola, Macarena S
dc.contributor.authorInestrosa Cantín, Nibaldo
dc.date.accessioned2019-10-17T14:28:12Z
dc.date.available2019-10-17T14:28:12Z
dc.date.issued2010
dc.date.updated2019-10-14T18:52:39Z
dc.description.abstractAbstract The presence of amyloid-β (Aβ) deposits in selected brain regions is a hallmark of Alzheimer's disease (AD). The amyloid deposits have "chaperone molecules" which play critical roles in amyloid formation and toxicity. We report here that treatment of rat hippocampal neurons with Aβ-acetylcholinesterase (Aβ-AChE) complexes induced neurite network dystrophia and apoptosis. Moreover, the Aβ-AChE complexes induced a sustained increase in intracellular Ca2+ as well as a loss of mitochondrial membrane potential. The Aβ-AChE oligomers complex also induced higher alteration of Ca2+ homeostasis compared with Aβ-AChE fibrillar complexes. These alterations in calcium homeostasis were reversed when the neurons were treated previously with lithium, a GSK-3β inhibitor; Wnt-7a ligand, an activator for Wnt Pathway; and an N-methyl-D-aspartate (NMDA) receptor antagonist (MK-801), demonstrating protective roles for activation of the Wnt signaling pathway as well as for NMDA-receptor inhibition. Our results indicate that the Aβ-AChE complexes enhance Aβ-dependent deregulation of intracellular Ca2+ as well as mitochondrial dysfunction in hippocampal neurons, triggering an enhanced damage than Aβ alone. From a therapeutic point of view, activation of the Wnt signaling pathway, as well as NMDAR inhibition may be important factors to protect neurons under Aβ-AChE attack.
dc.fuente.origenBiomed Central
dc.identifier.citationMolecular Neurodegeneration. 2010 Jan 18;5(1):4
dc.identifier.doi10.1186/1750-1326-5-4
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/26698
dc.identifier.urihttps://doi.org/10.1186/1750-1326-5-4
dc.issue.numeroNo. 4
dc.language.isoen
dc.nota.accesoContenido completo
dc.pagina.final15
dc.pagina.inicio1
dc.revistaMolecular Neurodegenerationes_ES
dc.rightsacceso abierto
dc.rights.holderDinamarca et al; licensee BioMed Central Ltd.
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.otherVía de señalización Wntes_ES
dc.subject.otherHipocampo (Cerebro)es_ES
dc.subject.otherPéptido beta-Amiloidees_ES
dc.subject.otherEnfermedad de Alzheimeres_ES
dc.titleAmyloid-B-Acetylcholinesterase complexes potentiate neurodegenerative changes induced by the AB peptide. Implications for the pathogenesis of Alzheimer's diseasees_ES
dc.typeartículo
dc.volumenVol. 5
sipa.codpersvinculados1010409
sipa.codpersvinculados102372
sipa.codpersvinculados99331
Files
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
13024_2009_Article_122.pdf
Size:
5.17 MB
Format:
Adobe Portable Document Format
Description:
Download
License bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
license.txt
Size:
0 B
Format:
Item-specific license agreed upon to submission
Description:
Download
Collections
Artículos de revistas