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Patients and researchers participate in a scientific workshop on Huntington's disease

The CIMA hosts a meeting where the latest advances in this neurodegenerative pathology will be presented.

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Kashif Mahfooz, Isabel Pérez-Otaño, Rebeca Martínez, John Wesseling, Sonia framework and Joao Covita, Huntington's disease researchers. PHOTO: Manuel Castells
06/10/14 13:47 Mª Pilar Huarte

The research center Applied Medicine (CIMA) of the University of Navarra hosted on Saturday, October 4, a meeting about the Huntington's disease (HD). Patients with this neurodegenerative pathology shared their experience and health professionals and researchers presented the latest scientific advances.

department Drs. Rosario Luquin, Director of the Neurology Program of the University of Navarra, and Sonia Luquin, Director of the Neurosciences Program of the University of Navarra. Clínica Universidad de Navarraand Sonia framework, of the Neurosciences Program of CIMA, addressed general aspects of the disease. For his part, Dr. Saül Martínez Horta, coordinator of the group European HD, spoke about the present and future of the research of this pathology. Nurse Antonia Campolongo focused on aspects related to patient nutrition.

The workshop was attended by Josefina GarreThe Huntington's disease and promoter of the eponymous scholarship to consolidate the research of this disease in the CIMA.

Neurodegenerative disorder

Huntington's disease is the neurodegenerative disease with the highest incidence after Alzheimer's and Parkinson's; it is hereditary and is characterized by the appearance of involuntary and uncontrolled movements. In advanced stages it causes severe motor and cognitive impairment, psychiatric disorders and dementia. Although the mutation Genetics manager of the disease (the abnormal elongation of a protein called huntingtin) was discovered 20 years ago, the mechanisms that cause the loss of connections and neuronal death are unknown and to date there is no cure or effective treatment.

Researchers at CIMA have shown that a molecule, called GluN3A, is abnormally elevated in patients with Huntington's disease, and that suppressing this abnormality prevents the disordered elimination of synapses and corrects the symptoms of this severe neurodegenerative disease in mice.

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