Physiopathology of nervous system diseases

Research groups

CELLULAR AND MOLECULAR BASIS OF HUNTIGTON’S DISEASE AND OTHER DISORDERS OF THE BASAL GANGLIA

Alberch Vie, Jordi >

STEM CELLS AND REGENERATION MEDICINE

Canals Coll, Josep Maria >

INTERCELLULAR COMMUNICATION

Aguado, Fernando >

NEURAL DEVELOPMENT

Alcántara Horrillo, Soledad >

NEURODEGENERATION AND NEUROPROTECTION

Auladell, Carme >

GRUP DE RECERCA EN NEUROFARMACOLOGIA: PREVENCIÓ DE L’ENVELLIMENT (GREN)

Camins Espuny, Antoni >

NEUROPHARMACOLOGY AND PAIN

Ciruela, Francisco >

CANCER, NEURAL CELL FATE AND CELL PLURIPOTENCY

Edel, Michael >

FISIOLOGIA I PATOLOGIA DE LA RELACIÓ FUNCIONAL GLIA-NEURONA

Estévez Povedano, Raúl >

NEUROPATHOLOGY

Ferrer, Isidro >

NEURODEGENERATION AND SYNAPTIC DYSFUNCTION IN HUNTINGTON´S DISEASE

Gines Padros, Silvia >

PHYSIOPATHOLOGY AND TOXICOLOGY OF SENSORY AND MOTOR SYSTEMS

Llorens, Jordi >

GRUP DE NEUROQUÍMICA

Mahy Géhenne, Nicole >

MALAGELADA’S LAB

Malagelada Grau, Cristina >

NEUROPHARMACOLOGY IN AGING AND NEURODEGENERATION

Pallas Lliberia, Mercè >

BLOOD-BRAIN BARRIER RESEARCH GROUP

Pelegrí, Carme i Vilaplana, Jordi>

KINASES AND PHOSPHATASES IN NEURONAL FUNCTION AND DYSFUNCTION

Pérez Navarro, Esther >

Representative of the research area

Dr. Silvia Ginés Padrós

Departament de Biomedicina

silviagines (at) ub.edu

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Did you know that neurodegenerative diseases are one of the main causes of disability and loss of quality of life?

The nervous system is one of the most susceptible systems to develop diseases, because it is affected by organic alterations as well as by psychic disorders which may affect patients’ mood and behaviour. These disorders can be caused by neurodegenerative diseases (like Alzheimer, Huntington or Parkinson diseases), cerebrovascular diseases or sensory disturbances (like the retinopathies and the disorders of the vestibular system).

Research groups of this area are interested in defining the physiopathologic mechanisms involved in the loss of functionality, atrophy and neuronal degeneration related to these diseases. A deeper understanding of these mechanisms will allow us to develop new therapeutic strategies to delay or prevent this neurologic diseases.

Some research lines deal with the age-related neurodegenerative processes, especially on the first episodes and symptoms. Particularly, we are interested in understanding the molecular mechanisms involved in Alzheimer’s disease and their possible relation with environmental factors and lifestyles. For instance, we analyse the possible link between Alzheimer’s disease and type II diabetes, or the potential preventive effects of antioxidant substances like resveratrol.

Other research groups study the cellular and molecular mechanisms of Huntington’s disease, a neurodegenerative disease classically characterized by motor deficits, psychiatric alterations and cognition dysfunctions. The main goal of these studies is finding new treatments to stop the progression of the disease and patient’s death. In this sense, researchers studying this disease are working on two different approaches of treatments: pharmacologic therapy and cellular therapy. The research lines focused on pharmacology analyse the role of neurotrophins and several kinases and phosphatases, as well as the potential use of this proteins as therapeutic targets. On the other hand, the research lines focused on cellular therapy explore if neuronal stem cells could replace the populations of damaged neurons.

The study of several molecular aspects of neuronal function is also addressed in this area, to develop new therapeutic tools for pain or skeletal muscle hyperexcitability. We are also interested in the toxic effects caused by some substance on the vestibular system, which provides the sense of balance and spatial orientation. Finally, other research lines study the GPCRs receptor of neurons and its potential use as a pharmacological target, the genetic factors involved in retina pathologies, or diseases affecting myelin (like leucodystrophie).

We use different methodologies, for instance molecular and electrophysiological techniques, animal models, behaviour studies, pharmacologic methods and clinical trials.

Highlighted publications

· Ansoleaga B, Jové M, Schlüter A, Garcia-Esparcia P, Moreno J, Pujol A, Pamplona R, Portero-Otín M, Ferrer I. (2015) Deregulation of purine metabolism in Alzheimer’s disease. Neurobiology of Aging 36: 68-80.

· Bayod S, Felice P, Andrés P, Rosa P, Camins A, Pallàs M, Canudas AM. (2015) Downregulation of canonical Wnt signaling in hippocampus of SAMP8 mice. Neurobiology of Aging, Feb;36(2):720-9.

· Brito V, Giralt A, Enriquez-Barreto L, Puigdellívol M, Suelves N, Zamora-Moratalla A, Ballesteros JJ, Martín ED, Dominguez-Iturza N, Morales M, Alberch J, Ginés S (2014) Neurotrophin receptor p75(NTR) mediates Huntington’s disease-associated synaptic and memory dysfunction. The Journal of Clinical Investigation, 12(10):4411-28.

· García-Negredo, G., Soto, D., Llorente, J., Morató, X., Galenkamp, K.M.O., Gómez-Soler, M., Fernández-Dueñas, V., Adelman, J.P., Shigemoto, R., Fukozawa, Y., Luján, R. & Ciruela, F. (2014). Co-assembly and coupling of mGlu5 receptors and SK2 channels. Journal of Neuroscience, 34 (44), 14793–14802.

· Hoegg-Beiler MB, Sirisi S, Orozco IJ, Ferrer I, Hohensee S, Auberson M, Gödde K, Vilches C, de Heredia ML, Nunes V, Estévez R, Jentsch TJ. (2014) Disrupting MLC1 and GlialCAM and ClC-2 interactions in leukodystrophy entails glial chloride channel dysfunction. Nature Communications, 19;5:3475.

· Jeworutzki E, López-Hernández T, Capdevila-Nortes X, Sirisi S, Bengtsson L, Montolio M, Zifarelli G, Arnedo T, Müller CS, Schulte U, Nunes V, Martínez A, Jentsch TJ, Gasull X, Pusch M, Estévez R. (2012) GlialCAM, a protein defective in a leukodystrophy, serves as a ClC-2 Cl(-) channel auxiliary subunit. Neuron, 8;73(5):951-61.

· Malagelada C, López-Toledano MA, Willett RT, Jin ZH, Shelanski ML, Greene LA. (2011) RTP801/REDD1 regulates the timing of cortical neurogenesis and neuron migration. The Journal of Neuroscience, 31(9):3186-96.

· Saavedra A, Giralt A, Rué L, Xifró X, Xu J, Ortega Z, Lucas JJ, Lombroso PJ, Alberch J, Pérez-Navarro E (2011) Striatal-enriched protein tyrosine phosphatase expression and activity in Huntington’s disease: a STEP in the resistance to excitotoxicity. The Journal of Neuroscience, 31:8150-62.

· Ciruela, F., Vilardaga, J.P. & Fernández-Dueñas. V. (2010). Lighting up multiprotein complexes: lessons from GPCR oligomerization. Trends in Biotechnology, 28 (8), 407-415.

· Aasen T, Raya A, Barrero MJ, Garreta E, Consiglio A, Gonzalez F, Vassena R, Bilic J, Pekarik V, Tiscornia G, Edel MJ, Boué S, Izpisúa Belmonte JC. (2008) Efficient and rapid generation of induced pluripotent stem cells from human keratinocytes. Nature Biotechnology, Nov;26(11):1276-84.

· Epping MT, Wang L, Edel MJ, Carlée L, Hernandez M, Bernards R. (2005) The human tumor antigen PRAME is a dominant repressor of retinoic acid receptor signaling. Cell, Sep 23;122(6)835-47.

· Estévez R, Schroeder BC, Accardi A, Jentsch TJ, Pusch M. (2003) Conservation of chloride channel structure revealed by an inhibitor binding site in ClC-1. Neuron, 10;38(1):47-59.

Highlighted projects