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Hugo Balleza-Tapia

Researcher at Karolinska Institutet

Publications -  13
Citations -  290

Hugo Balleza-Tapia is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: Hippocampal formation & Amyloid beta. The author has an hindex of 7, co-authored 12 publications receiving 211 citations. Previous affiliations of Hugo Balleza-Tapia include CINVESTAV.

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Journal ArticleDOI

Beta-amyloid protein (25-35) disrupts hippocampal network activity: role of Fyn-kinase.

TL;DR: The data suggest that βAP acutely affects proper hippocampal function through a Fyn‐dependent mechanism, and proposes that such alteration might be related to the cognitive impairment observed, at least, during the early phases of Alzheimer's disease.
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TrpV1 receptor activation rescues neuronal function and network gamma oscillations from Aβ-induced impairment in mouse hippocampus in vitro.

TL;DR: It is found that the TrpV1-receptor agonist capsaicin rescues Aβ-induced degradation of hippocampal gamma oscillations by reversing both the desynchronization of AP firing in CA3 pyramidal cells and the shift in excitatory/inhibitory current balance.
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Beta-like hippocampal network activity is differentially affected by amyloid beta peptides.

TL;DR: The results support the idea that different amyloid peptides might alter specific cellular mechanisms related to the generation of specific neuronal network activities, instead of a generalized inhibitory effect of Abeta peptides on neuronal network function.
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Impaired spike-gamma coupling of area CA3 fast-spiking interneurons as the earliest functional impairment in the AppNL-G-F mouse model of Alzheimer's disease.

TL;DR: In Alzheimer's disease, the accumulation of amyloid-β (Aβ) correlates with degradation of cognition-relevant gamma oscillations as discussed by the authors, and the degradation correlates with increased Aβ1-42 concentration in the brain.
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Amyloid beta 1-42 inhibits entorhinal cortex activity in the beta-gamma range: role of GSK-3.

TL;DR: The results suggest that amyloid beta-induced inhibition of entorhinal cortex beta-gamma activity involves GSK-3 activation, which may provide a molecular mechanism for amyloidsbeta-induced neural network disruption and support the use of GSK3 inhibitors to treat Alzheimer Disease.