25–30 May 2020, Spetses Island, Greece
Our group is working on neurological diseases with inflammatory etiology. In particular, we are focusing in scaffolding proteins (insulin recpetor substrate, IRS1 and IRS2). mediating trophic factors effect in vivo and in vitro. We also use CRISPR knockout cells generated by collaborators.
In addition, our interest broaden to psichiatric diseases, reward and depression. We are interested in further understanding neuroinflammation and structural proteins in pathological situations. Recently, we have started a study measuring perinuclear nets in our model of neuroinflammation with preliminary, yet interesting results.
Our group uses molecular and cellular biology methods, along with animal models, stereotaxic surgery, behavioral paradigm and postmortem analysis, including ex vivo tests.
We carry out, routinely, protein (western blots) analyiss; quantitaive PCR; and immunohistochemistry immunofluorescence, and confocal microscopy.
We design and clone shRNA; genes and promoters. We can generate AAV derived particules and succesfully inject them by estereotaxia in vivo to study behavioural alterations as a consequence of modulating gene expression.
We are also studing some of the molecular mechanisms regulating neuronal branching.
We are acquantance in behaviour, neuroanatomy, primary cultures, cell lines, and molecular biology.
Primary cultures of neurons and astrocytes and shRNA silencing.
Epigenetic and gene regulation, bioinformatics
Pathophysiology of extracellular matrix regulation.
I am very interested in opening up links between different factors contibuting to degenerative and psiquiatric disease (tipically oxidative stress, inflammation, insulin resistance) to structural damage/alterations. We can design shRNa to knocdown expression or we can overexpress different genes to study their implications in these proceses. Moreover, we have the in vivo models (rodent) to tests different hypothesis that we can propose in the consortium.
1. Central relaxin-3 receptor (RXFP3) activation impairs social recognition and modulates ERK-phosphorylation in specific GABAergic amygdala neurons.
Albert-Gasco H, Sanchez-Sarasua S, Ma S, García-Díaz C, Gundlach AL, Sanchez-Perez AM, Olucha-Bordonau FE.
Brain Struct Funct. 2018 Oct 28. doi: 10.1007/s00429-018-1763-5. [Epub ahead of print]
2. Nucleus incertus ablation disrupted conspecific recognition and modified immediate early gene expression patterns in 'social brain' circuits of rats.
García-Díaz C, Sánchez-Catalán MJ, Castro-Salazar E, García-Avilés A, Albert-Gascó H, Sánchez-Sarasúa de la Bárcena S, Sánchez-Pérez AM, Gundlach AL, Olucha-Bordonau FE.
Behav Brain Res. 2019 Jan 1;356:332-347. doi: 10.1016/j.bbr.2018.08.035. Epub 2018 Sep 5.
3. Abscisic Acid Supplementation Rescues High Fat Diet-Induced Alterations in Hippocampal Inflammation and IRSs Expression.
Ribes-Navarro A, Atef M, Sánchez-Sarasúa S, Beltrán-Bretones MT, Olucha-Bordonau F, Sánchez-Pérez AM.
Mol Neurobiol. 2019 Jan;56(1):454-464. doi: 10.1007/s12035-018-1091-z. Epub 2018 May 2.
4. . The effect of abscisic acid chronic treatment on neuroinflammatory markers and memory in a rat model of high-fat diet induced neuroinflammation.
Sánchez-Sarasúa S, Moustafa S, García-Avilés Á, López-Climent MF, Gómez-Cadenas A, Olucha-Bordonau FE, Sánchez-Pérez AM.
Nutr Metab (Lond). 2016 Oct 26;13:73. doi: 10.1186/s12986-016-0137-3. eCollection 2016.
PMID: 27795733 Free PMC Article
5. Central relaxin-3 receptor (RXFP3) activation increases ERK phosphorylation in septal cholinergic neurons and impairs spatial working memory.
Albert-Gascó H, García-Avilés Á, Moustafa S, Sánchez-Sarasua S, Gundlach AL, Olucha-Bordonau FE, Sánchez-Pérez AM.
Brain Struct Funct. 2017 Jan;222(1):449-463. doi: 10.1007/s00429-016-1227-8. Epub 2016 May 5.
25–30 May 2020, Spetses Island, Greece