Browsing by Author "Inestrosa Cantín, Nibaldo"
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- ItemA Human Prion Protein Peptide (Prp(59-91)) Protects Against Copper Neurotoxicity(2003) Chacón, Matías F.; García-Huidobro Toro, Juan Pablo; Inestrosa Cantín, Nibaldo
- ItemA Major Portion of Synaptic Basal Lamina Acetylcholinesterase Is Detached by High Salt-And Heparin-Containing Buffers From Rat Diaphragm Muscle and Torpedo Electric Organ(1998) Casanueva, O.; Garrido, Jorge; Inestrosa Cantín, Nibaldo
- ItemA novel function for Wnt signaling modulating neuronal firing activity and the temporal structure of spontaneous oscillation in the entorhinal-hippocampal circuit(2015) Oliva Gutiérrez, Carolina Andrea; Inestrosa Cantín, Nibaldo
- ItemA Structural Motif of Acetylcholinesterase That Promotes Amyloid β-Peptide Fibril Formation(2001) De Ferrari, G.; Inestrosa Cantín, Nibaldo
- ItemAccelerating Alzheimer's research through 'natural' animal models(2015) Braidy, N.; Inestrosa Cantín, Nibaldo
- ItemAcetylcholinesterase (AChE) - Amyloid-β-Peptide Complexes in Alzheimers Disease. The Wnt Signaling Pathway(2004) Inestrosa Cantín, Nibaldo
- ItemAcetylcholinesterase Accelerates Assembly of Amyloid-β-Peptides Into Alzheimer's Fibrils: Possible Role of the Peripheral Site of the Enzyme(1996) Inestrosa Cantín, Nibaldo; Álvarez Rojas, Alejandra; Moreno Mauro, Ricardo D.; Garrido, Jorge
- ItemAcetylcholinesterase Induces Neuronal Cell Loss, Astrocyte Hypertrophy and Behavioral Deficits in Mammalian Hippocampus(2003) Chacón, Matías F.; Inestrosa Cantín, Nibaldo
- ItemAcetylcholinesterase promotes the aggregation of amyloid-β-peptide fragments by forming a complex with the growing fibrils(1997) Álvarez Rojas, Alejandra; Garrido, Jorge; Inestrosa Cantín, Nibaldo
- ItemAcetylcholinesterase, a senile plaque component, affects the fibrillogenesis of amyloid-β-peptides(1995) Álvarez Rojas, Alejandra; Bronfman C., Francisca; Garrido, Jorge; Inestrosa Cantín, Nibaldo
- ItemActivation of Wnt Signaling in Cortical Neurons Enhances Glucose Utilization through Glycolysis(2016) Cisternas, Pedro; Salazar, Paulina; Silva Alvarez, Carmen; Barros, L. Felipe; Inestrosa Cantín, Nibaldo
- ItemAge Progression of Neuropathological Markers in the Brain of the Chilean Rodent Octodon degus, a Natural Model of Alzheimer's Disease(2015) Inestrosa Cantín, Nibaldo; Rios, Juvenal A.; Cisternas, Pedro; Tapia Rojas, Cheril Cecilia; Rivera, Daniela S.; Braidy, Nady; Zolezzi, Juan M.; Godoy, Juan A.; Carvajal Cachaña, Francisco Javier; Ardiles, Alvaro O.
- ItemAlzheimer's Disease-Related Protein Expression in the Retina of Octodon degus(2015) Du, Lucia Y.; Chang, Lily Y-L.; Ardiles, Alvaro O.; Tapia Rojas, Cheril Cecilia; Araya, Joaquin; Inestrosa Cantín, Nibaldo; Palacios, Adrian G.; Acosta, Monica L.
- ItemAlzheimer's disease: relevant molecular and physiopathological events affecting amyloid-beta brain balance and the putative role of PPARs(2014) Santos Alcántara, Manuel; Inestrosa Cantín, Nibaldo
- ItemAmphiphilic Behavior of a Brain Tetrameric Acetylcholinesterase Form Lacking the Plasma Membrane Anchoring Domain(1992) Fuentes, María Elena; Inestrosa Cantín, Nibaldo
- ItemAmyloid Precursor Protein Fragment and Acety Lcholinesterase Increase With Cell Confluence and Differentiation in a Neuronal Cell Line(1996) Bronfman C., Francisca; Inestrosa Cantín, Nibaldo
- ItemAmyloid-B-Acetylcholinesterase complexes potentiate neurodegenerative changes induced by the AB peptide. Implications for the pathogenesis of Alzheimer's disease(2010) Dinamarca Ceballos, Margarita Constanza.; Sagal, Juan P.; Quintanilla Gómez, Rodrigo Arthur; Godoy, Juan A.; Arrázola, Macarena S; Inestrosa Cantín, NibaldoAbstract 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.
- ItemAmyloid-beta Peptide Nitrotyrosination Stabilizes Oligomers and Enhances NMDAR-Mediated Toxicity(2016) Guivernau, Biuse; Bonet, Jaume; Valls Comamala, Victoria; Bosch Morato, Mónica; Godoy, Juan A.; Inestrosa Cantín, Nibaldo
- ItemAmyloid-cholinesterase interactions - Implications for Alzheimer's disease(2008) Inestrosa Cantín, Nibaldo; Dinamarca Ceballos, Margarita Constanza; Álvarez Rojas, Alejandra