THE JOINT UNIT ON NEUROLOGICAL IMPAIRMENT CIPF-INCLIVA PERFORMS BASIC AND TRANSLATIONAL RESEARCH ON COGNITIVE, MOTOR, SLEEP AND CIRCADIAN RHYTHMS ALTERATIONS IN DIFFERENT PATHOLOGICAL SITUATIONS, INCLUDING: MINIMAL AND CLINICAL HEPATIC ENCEPHALOPATHY (HE), HYPERAMMONEMIA AND DEVELOPMENTAL EXPOSURE TO FOOD AND ENVIRONMENTAL CONTAMINANTS.
We also apply our wide range of methodologies to other pathological situations. The aims are:
In animal models:
- Unveil the molecular mechanisms leading to neurological impairment.
- Identify new therapeutic targets for its treatment.
- Design and assess new therapeutic procedures to reverse neurological impairment.
In patients:
- Study the mechanisms, diagnosis and treatment of neurological impairment.
- Identify early diagnostic procedures for neurological impairment.
- Bring to the clinic the diagnostic procedures identified.
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Sustained hyperammonemia induces TNF-a IN Purkinje neurons by activating the TNFR1-NF-kappa B pathway
Journal of Neuroinflammation 2020 Feb,  DOI:  10.1186/s12974-020-01746-z,  Vol. 17,  pag. 70-70
Motor and Cognitive Performance in Patients with Liver Cirrhosis with Minimal Hepatic Encephalopathy
Journal of Clinical Medicine 2020 Jul,  DOI:  10.3390/jcm9072154,  Vol. 9,  pag. 
Hyperammonemia alters the mismatch negativity in the auditory evoked potential by altering functional connectivity and neurotransmission
JOURNAL OF NEUROCHEMISTRY 2020 Jul,  DOI:  10.1111/jnc.14941,  Vol. 154,  pag. 56-70