Zobrazeno 1 - 8
of 8
pro vyhledávání: '"Karla Salgado-Puga"'
Publikováno v:
Behavioural Neurology, Vol 2015 (2015)
Alzheimer’s disease (AD) is associated with an early hippocampal dysfunction, which is likely induced by an increase in soluble amyloid beta peptide (Aβ). This hippocampal failure contributes to the initial memory deficits observed both in patient
Externí odkaz:
https://doaj.org/article/a94d7a9cd30c415990c471f8f626a9dc
Publikováno v:
PLoS ONE, Vol 8, Iss 9, p e75745 (2013)
Early olfactory dysfunction has been consistently reported in both Alzheimer's disease (AD) and in transgenic mice that reproduce some features of this disease. In AD transgenic mice, alteration in olfaction has been associated with increased levels
Externí odkaz:
https://doaj.org/article/592e942d23e34e21a80198d0c9f561cf
Autor:
Mónica López-Hidalgo, Karla Salgado-Puga, Reynaldo Alvarado-Martínez, Andrea Cristina Medina, Roberto A Prado-Alcalá, Jesús García-Colunga
Publikováno v:
PLoS ONE, Vol 7, Iss 11, p e49998 (2012)
Nicotine enhances synaptic transmission and facilitates long-term memory. Now it is known that bi-directional glia-neuron interactions play important roles in the physiology of the brain. However, the involvement of glial cells in the effects of nico
Externí odkaz:
https://doaj.org/article/5765b86fa55b4abc95062a019a70b789
Autor:
Benjamín Villasana-Salazar, Guadalupe Manrique-Maldonado, Rebeca Hernández-Soto, Benito Ordaz, Fernando Peña-Ortega, Karla Salgado-Puga, María Estefanía Guerrero-Gómez
Publikováno v:
Epilepsy research. 166
Chronic intermittent hypoxia (CIH) is the most distinct feature of obstructive sleep apnea (OSA), a common breathing and sleep disorder that leads to several neuropathological consequences, including alterations in the hippocampal network and in seiz
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::980794974df8482c2d9f476659ebc279
https://pubmed.ncbi.nlm.nih.gov/32745888
https://pubmed.ncbi.nlm.nih.gov/32745888
Publikováno v:
Protein & Peptide Letters. 22:303-321
It has long been known that amyloid s protein (As) plays a key role in Alzheimer's Disease (AD) and in Down Syndrome cognitive decline. Recent findings have shown that soluble forms of As (mostly As oligomers; Aso), rather than insoluble forms (fibri
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7acbf442e2a0981ec361289ed2f578b2
https://doi.org/10.2174/0929866522666150202112154
https://doi.org/10.2174/0929866522666150202112154
Publikováno v:
Journal of Alzheimer's disease : JAD. 57(1)
In addition to coupling cell metabolism and excitability, ATP-sensitive potassium channels (KATP) are involved in neural function and plasticity. Moreover, alterations in KATP activity and expression have been observed in Alzheimer's disease (AD) and
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ef49aab33b183db697376d6873316969
https://pubmed.ncbi.nlm.nih.gov/28222502
https://pubmed.ncbi.nlm.nih.gov/28222502
Publikováno v:
Behavioural Neurology, Vol 2015 (2015)
Behavioural Neurology
Behavioural Neurology
Alzheimer’s disease (AD) is associated with an early hippocampal dysfunction, which is likely induced by an increase in soluble amyloid beta peptide (Aβ). This hippocampal failure contributes to the initial memory deficits observed both in patient
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::978e6c6fda69e15a05f36f8dbd6195f8
Autor:
Jesús García-Colunga, Reynaldo Alvarado-Martínez, Mónica López-Hidalgo, Roberto A. Prado-Alcalá, Andrea C. Medina, Karla Salgado-Puga
Publikováno v:
PLoS ONE, Vol 7, Iss 11, p e49998 (2012)
PLoS ONE
PLoS ONE
Nicotine enhances synaptic transmission and facilitates long-term memory. Now it is known that bi-directional glia-neuron interactions play important roles in the physiology of the brain. However, the involvement of glial cells in the effects of nico
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::134fb25e8774829b1c7796de18082bfb
https://doi.org/10.1371/journal.pone.0049998
https://doi.org/10.1371/journal.pone.0049998