Eduardo J. Fernández-Pérez

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A major characteristic of Alzheimer's disease is the presence of amyloid beta (Aβ) oligomers and aggregates in the brain. Aβ oligomers interact with the neuronal membrane inducing perforations, causing an influx of calcium ions and increasing the release of synaptic vesicles that leads to a delayed synaptic failure by vesicle depletion. Here, we identified(More)
Ethanol increased the frequency of miniature glycinergic currents [miniature inhibitory postsynaptic currents (mIPSCs)] in cultured spinal neurons. This effect was dependent on intracellular calcium augmentation, since preincubation with BAPTA (an intracellular calcium chelator) or thapsigargin [a sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) pump(More)
It is well accepted that cortical and hippocampal synaptic densities are reduced in Alzheimer's disease (AD). These alterations in neuronal networking occur at the very onset of AD and may lead to the neuronal loss displayed in later stages of the disease, which is characterized by severe cognitive and behavioral impairments. Many studies suggest that(More)
The ability of beta-amyloid peptide (Aβ) to disrupt the plasma membrane through formation of pores and membrane breakage has been previously described. However, the molecular determinants for these effects are largely unknown. In this study, we examined if the association and subsequent membrane perforation induced by Aβ was dependent on GM1 levels.(More)
Alzheimer's disease is a neurodegenerative disorder that affects mostly the elderly. The main histopathological markers are the senile plaques formed by amyloid-β peptide (Aβ) aggregates that can perforate the plasma membrane of cells, increasing the intracellular calcium levels and releasing synaptic vesicles that finally lead to a delayed synaptic(More)
20 Ethanol increased the frequency of miniature glycinergic currents (mIPSCs) in 21 cultured spinal neurons. This effect was dependent on intracellular calcium 22 augmentation since pre incubation with BAPTA (an intracellular calcium chelator) or 23 thapsigargin (a SERCA pump inhibitor) significantly attenuated this effect. Similarly, 24 U73122 (a(More)
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