Doctora en Química Biológica, Universidade Federal do Rio de Janeiro, 2007, Brasil

acpaulalima@gmail.com

 

Líneas de Investigación

Mecanismos moleculares de la enfermedad de Alzheimer.

Neurobiología, estrés oxidativo e inflamación.

Publicaciones Recientes

Osorio C., Cavalla F., Paula-Lima A.C., Díaz-Araya G., Vernal R., Ahumada P., Gamonal J., Hernández M. 2015. “H2O2 activates Matrix Metalloproteinases through Nuclear Factor Kappa B Pathway and Ca2+ signals in human Periodontal Fibroblasts”.Journal of Periodontal Research. In press. ISSN: 0022-3484.IF: 2.466.

 

 

Adasme T., Paula-Lima A.C., Hidalgo C. 2015. “Inhibitory ryanodine prevents ryanodine receptor-mediated Ca2+ release without affecting endoplasmic reticulum Ca2+ content in primary hippocampal neurons”.Biochem Biophys Res Commun. 458(1):57-62.ISSN: 0006-291X. IF: 2.297.

 

 

Sanmartín C.D.*, Paula-Lima A.C.*, García A., Barattini, P., Hartel S., Núñez M.T., Hidalgo C. 2014. “Ryanodine receptor-mediated Ca2+ release underlies iron-induced mitochondrial fission and stimulates mitochondrial Ca(2+) uptake in primary hippocampal neurons”.Frontiers in Molecular Neuroscience. 11:7-13. *These authors contributed equally to this work. ISSN: 1662-5099.IF: 4.100.

 

 

Paula-Lima A.C., Adasme T., Hidalgo C. 2014. “Contribution of Ca2+ release channels to hippocampal synaptic plasticity and spatial memory”. Potential redox modulation. Antioxidants and Redox Signaling. 21(6):892-914. ISSN 1523-0864.IF: 7.407.

 

 

Paula-Lima A.C., Hidalgo C. 2013. “Amyloid β-peptide oligomers, ryanodine receptor-mediated Ca2+ release, and Wnt-5a/Ca2+ signaling: opposing roles in neuronal mitochondrial dynamics? Frontiers in Cellular Neuroscience. 7:120. ISSN:1662-5102. IF: 4.300.

 

 

Paula-Lima A.C., Brito-Moreira J., Ferreira S.T. 2013. “Dysregulation of glutamatergic neurotransmission in Alzheimer’s disease”. Review. The Journal of Neurochemistry. 126:191–202. ISSN: 1471-4159. IF: 4.281.

 

 

San Martin C.D., Paula-Lima A.C., Hidalgo C., Nuñez T. 2012. “Sub-lethal levels of amyloid β-peptide oligomers decrease non-transferrin-bound iron uptake and do not potentiate iron toxicity in primary hippocampal neurons”. BioMetals. 25(4)805-13. ISSN: 0966-0844. IF: 2.689.

 

 

San Martin C.D., Adasme T., Hidalgo C., Paula-Lima A.C. 2012. “The antioxidant N-Acetyl-Cysteine prevents the mitochondrial fragmentation induced by soluble Amyloid-β peptide oligomers. Neurodegenerative Diseases”. 10(1-4):34-7. ISSN:1660-2854. IF: 3.454.

 

 

Sebollela A., Freitas-Correa L., Oliveira F.F., Paula-Lima A.C., Cardoso L., Torres C., Leon S., Marcondes J., Carraro, D.M., Brentani H., De Felice, F.G., Ferreira., S.T. 2012 “Amyloid-β oligomers induce differential gene expression in adult human brain slices”.Journal of Biological Chemistry. 287(10):7436-45. ISSN:0021-9258. IF: 4.573.

 

 

Paula-Lima A.C., Adasme T. San Martin C., Sebollela A., Hetz C., Carrasco M.A., Ferreira S.T, Hidalgo C. 2011. “Amyloid-β peptide oligomers stimulate RyR-mediated Ca2+ release inducing mitochondrial fragmentation in hippocampal neurons and prevent RyR-mediated dendritic spine remodeling produced by BDNF prevent ryanodine receptors-mediated spine growth induced by BDNF in hippocampal neurons”. Antioxidants and Redox Signaling. 14(7):1209-23. ISSN 1523-0864. IF: 7.407.