What are we working on?

The Neurobiotechnology group at the University of Jaume I, Castellon, was established in 2013 to decipher the nervous system’s pathophysiology using biotechnological tools. We focus on studying how neuroinflammation and insulin resistance are associated and how they affect neuronal signaling and survival, and how these processes prompt the transition health-disease at the onset of neurological and psychiatric disorders. Furthermore, we aim to develop and test new formulations with improved therapeutic potential for treating these diseases.

Targeting neuroinflammation to treat Attention-Deficit/hyperactivity disorder. Elucidating sex-difference in disease and treatments.

Using a mice model of ADHD we have shown the sex differences in ADHD symptoms and response to treatment. In addition, we intend to dissect anterior cingulate circuits underlying ADHD subtypes using interference ARN (shRNA and AAV vectors).

Role of Insulin signaling (IRS1) in the brain, synaptic plasticity, and memory. Sex-dependent effects.

We have designed interfering RNA and cloned it into a micron environment site (using RNA polymerase II promoters). We studied the loss of function of IRS1 in specific hippocampus-septum circuits.

AAV-CMV-shIRS1-EGFP in GABAergic cells in the hippocampus.

We demonstrated that IRS1 in GABAergic neurons of the hippocampal-septum connection regulates memory in female and male rats. In addition, we have shown that IRS1 is required for mature synaptic spines (in vivo studies) and the neuritic tree (in vitro studies).

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Downregulation of IRS1 reduces spines density
IRS1 declines with age and is required to maintain mature spines and neurites.

Development of new formulations

In addition to biotechnological tools, our group has developed an in vitro and in vivo platform to evaluate the neuroprotective effects of natural and synthetic molecules. Thus, we have shown that treatment with phytohormone ABA (Abscisic Acid) significantly reduces neuroinflammation, regulates altered gene expression, and prevents cognitive impairment in two animal models of neuroinflammation and memory loss; the metabolic syndrome and transgenic mice model for Alzheimer’s disease.

Expression and purification of PETase to improve PET degradation.

We are generating various enzymatic tools to improve plastic and mixed textile biodegradation and generate products of added value.