Laboratorio de Neurobiología del Centro de Investigación Príncipe Felipe.
Using animal models of chronic hepatic encephalopathy, we are studying the mechanisms responsible for the neurological alterations in patients with hepatic encephalopathy i.e. impairment of cognitive and intellectual function, as well as alterations in motor activity and coordination and in the sleep-waking cycle and in circadian rhythms.
Once we have identified the molecular alteration responsible for the neurological alteration, we try to restore normal cerebral function through pharmacological treatments.
The studies performed have allowed us to:
prevent death induced by acute ammonia intoxication;
prevent or delay death in rats with acute liver failure;
restore learning ability in rats with chronic hepatic encephalopathy and,
reverse hypokinesia in these rats. We have shown that rats with liver failure suffer neuroinflammation which contributes to cognitive and motor impairment. We are studying the mechanisms leading to neuroinflammation and how this leads to cognitive and motor impairment We have shown that acute liver failure leads to activation of NMDA receptors in brain. We have been able to increase the survival time and rate in rats with acute liver failure by blocking NMDA receptors. We are also studying the effects on brain development of neurotoxic compounds present in the environment and in the food chain, such as mercury or PCBs (polychlorinated biphenyls).
We have found, in animal models, that ingestion of food containing these contaminants by female rats leads, when their pups are adult, to impaired cognitive function and altered motor activity and coordination. We are studying the mechanisms responsible for these neurological alterations.
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