Browsing by Author "Palomer, Ernest"

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  • Activation of PKR causes amyloid beta-peptide accumulation via De-Repression of Bace1 expression
    Ill-Raga, Gerard, 1982-; Palomer, Ernest; Wozniak, Matthew A; Ramos Fernández, Eva, 1984-; Bosch Morató, Mònica, 1986-; Tajes Orduña, Marta; Guix Ràfols, Francesc Xavier; Galán, José J; Clarimón Echevarría, Jordi; Antúnez, Carmen; Real, Luis M; Boada, Mercè; Itzhaki, Ruth F; Fandos, César; Muñoz López, Francisco José, 1964- (Public Library of Science (PLoS), 2011)
    BACE1 is a key enzyme involved in the production of amyloid ß-peptide (Aß) in Alzheimer's disease (AD) brains. Normally, its expression is constitutively inhibited due to the presence of the 5′untranslated region (5′UTR) ...
  • CB1 agonist ACEA protects neurons and reduces the cognitive impairment of AβPP/PS1 mice
    Aso Pérez, Ester; Palomer, Ernest; Juvés, Salvador; Maldonado, Rafael, 1961-; Muñoz López, Francisco José, 1964-; Ferrer, Isidre (IOS Press, 2012)
    The present study shows that chronic administration of the cannabinoid receptor type 1 (CB1) receptor agonist arachidonyl-2-chloroethylamide (ACEA) at pre-symptomatic or at early symptomatic stages, at a non-amnesic dose, ...
  • Fibrinogen nitrotyrosination after ischemic stroke impairs thrombolysis and promotes neuronal death
    Ill-Raga, Gerard, 1982-; Palomer, Ernest; Ramos Fernández, Eva, 1984-; Guix Ràfols, Francesc Xavier; Bosch Morató, Mònica, 1986-; Guivernau Almazán, Biuse, 1988-; Tajes Orduña, Marta; Valls Comamala, Victòria, 1987-; Jiménez Conde, Jordi; Ois Santiago, Angel Javier; Gil Gómez, Gabriel; Alameda Quitllet, Francisco; Roquer, Jaume; Valverde, M. A. (Miguel Ángel), 1963-; Muñoz López, Francisco José, 1964- (Elsevier, 2015)
    Ischemic stroke is an acute vascular event that compromises neuronal viability, and identification of the pathophysiological mechanisms is critical for its correct management. Ischemia produces increased nitric oxide ...
  • Nitro-oxidative stress after neuronal ischemia induces protein nitrotyrosination and cell death
    Tajes Orduña, Marta; Ill-Raga, Gerard, 1982-; Palomer, Ernest; Ramos Fernández, Eva, 1984-; Guix Ràfols, Francesc Xavier; Bosch Morató, Mònica, 1986-; Guivernau Almazán, Biuse, 1988-; Jiménez Conde, Jordi; Ois Santiago, Angel Javier; Pérez Asensio, Fernando; Reyes Navarro, Mario; Caballo, Carolina; Galán, Ana M.; Alameda Quitllet, Francisco; Escolar, Ginès; Opazo, Carlos M.; Planas, Anna; Roquer, Jaume; Valverde, M. A. (Miguel Ángel), 1963-; Muñoz López, Francisco José, 1964- (Hindawi, 2013)
    Ischemic stroke is an acute vascular event that obstructs blood supply to the brain, producing irreversible damage that affects neurons but also glial and brain vessel cells. Immediately after the stroke, the ischemic ...
  • PKR and PP1C polymorphisms in alzheimer’s disease risk
    Palomer, Ernest; Ill-Raga, Gerard, 1982-; Tajes Orduña, Marta; Ramos Fernández, Eva, 1984-; Bosch Morató, Mònica, 1986-; Guivernau Almazán, Biuse, 1988-; Galán, José J; Clarimón Echevarría, Jordi; Antúnez, Carmen; Boada, Mercè; Real, Luis M; Fandos, César; Muñoz López, Francisco José, 1964- (Scientific Research Publishing, 2011)
    Alzheimer’s disease (AD) is a neurodegenerative disease characterized by senile plaques and neurofibrillary tangles. Senile plaques are deposits of amyloid ß-peptide (Aß) produced by the cleavage of a transmembrane protein ...
  • Posttranslational nitro-glycative modifications of albumin in Alzheimer's disease: implications in cytotoxicity and amyloid-β peptide aggregation
    Ramos Fernández, Eva, 1984-; Tajes Orduña, Marta; Palomer, Ernest; Ill-Raga, Gerard, 1982-; Bosch Morató, Mònica, 1986-; Guivernau Almazán, Biuse, 1988-; Roman Degano, Irene; Eraso Pichot, Abel; Alcolea, Daniel; Fortea, Juan; Núñez, Laura; Páez, Antonio; Alameda Quitllet, Francisco; Fernàndez Busquets, Xavier; Lleó, Alberto; Elosua Llanos, Roberto; Boada, Mercè; Valverde, M. A. (Miguel Ángel), 1963-; Muñoz López, Francisco José, 1964- (IOS Press, 2014)
    Glycation and nitrotyrosination are pathological posttranslational modifications that make proteins prone to losing their physiological properties. Since both modifications are increased in Alzheimer's disease (AD) due to ...
  • The antigen-binding fragment of human gamma immunoglobulin prevents amyloid β-peptide folding into β-sheet to form oligomers
    Valls Comamala, Victòria, 1987-; Guivernau Almazán, Biuse, 1988-; Bonet Martínez, Jaume, 1982-; Puig, Marta; Perálvarez Marín, Alex; Palomer, Ernest; Fernàndez Busquets, Xavier; Altafaj, Xavier; Tajes Orduña, Marta; Puig Pijoan, Albert; Vicente García, Rubén, 1978-; Oliva Miguel, Baldomero; Muñoz López, Francisco José, 1964- (Impact Journals, 2017)
    The amyloid beta-peptide (Aβ) plays a leading role in Alzheimer's disease (AD) physiopathology. Even though monomeric forms of Aβ are harmless to cells, Aβ can aggregate into β-sheet oligomers and fibrils, which are both ...