Assumpció Bosch Merino

Assumpció  Bosch Merino

 

 

Assumpció Bosch Merino

Academic Staff

Phone:
+34 935 814 203

Email:
assumpcio.bosch@uab.cat

Adress:

Department of Biochemistry and Molecular Biology
Institut de Neurociències
CBATEG (room H-530)
Universitat Autònoma de Barcelona (UAB)
Bellaterra Campus 08193-Cerdanyola del Vallés

Area

Thesis number in address


Assumpció Bosch obtained a PhD in Biosciences at the Universitat Autònoma of Barcelona (UAB) and did her postdoctoral training on gene therapy strategies using viral vectors at the University of Iowa (IA, USA) and at the Pasteur Institute (Paris, France). Currently, she is Full Professor of Biochemistry and Molecular Biology and group leader at the Neuroscience Institute (UAB), mainly focused on gene therapy strategies for metabolic diseases affecting the nervous system, both central and peripheral. She has published more than 60 peer-reviewed articles, leaded national and European research projects and co-founded two biotech companies on the gene therapy field. Since 2014 she acts as deputy director in the Department of Biochemistry and Molecular Biology at UAB.

She heads the Gene therapy for neurometabolic disorders lab, included in the NeuroGene research group:

 

 

Laboratory members:
Belén García Lareu
Marc Leal Julià
Andrea Onieva

Meritxell Puig Ferrer
Angela Sánchez Osuna
Sergi Verdés

 


STRATEGIC OBJECTIVES

 

The research activity of our group is focused on the development of gene therapy strategies affecting the nervous system, both central (lysosomal storage diseases) and peripheral (pain, genetic and acquired neurophaties) and on the elucidation of the molecular mechanisms implicated in the development of these pathologies combining the use of animal models, tissue cell culture and viral vectors.



MAIN RESEARCH LINES

 

1) Study of the tropism of different gene therapy viral vectors in the peripheral nervous system
Gene transfer to the peripheral nervous system (PNS) is particularly challenging as it involves several cell types, most of them post-mitotic. Efficient gene transfer to certain cell types of the PNS can be of great interest for gene therapy for neurological diseases or for pain treatment. Also important, delivery or inhibition of target molecules with viral vectors can be used as a tool to analyze physiological processes in the PNS, such as interactions between glia and neurons, retrograde or anterograde transport, nerve regeneration, etc. Within the aim to determine the most efficient gene transfer vectors for each cell type in the PNS, we are characterizing the tropism of different pseudotypes of AAV vectors and different human and non-human adenoviral vectors through different routes of administration.

 

2.Gene therapy for diabetic neurological complications
Diabetic complications involve both sensorimotor and autonomic components of the peripheral nervous system (PNS). Sensorimotor neuropathy developed by diabetic patients is the most common peripheral neuropathy affecting in different degrees all types of nerve fibers and causing loss of pain sensation, burst sensation and cutaneous hyperestesia, typically starting at the feet and the lower part of the legs but progressing to hands and arms. In more advanced stages, foot ulcers and neuropathic deformities appear, which could lead to 40% of the non-traumatic limb amputations.

The pathology of diabetic sensorimotor neuropathy is characterized by axonal atrophy and demyelination, leading to nerve fiber loss followed by abnormal regeneration of these fibers. Despite insulin treatment or pancreas transplantation, progression of diabetic neuropathy is not stopped, indicating the need for a specific treatment at early stages of the diabetes.

Our team is studying the molecular mechanisms leading to the development of diabetic neuropathy, using primary cell cultures and mouse models of the disease, with the aim to elucidate new therapeutic targets for this complication of the diabetes. In more detail, we are studying the effect of hyperglicemia in the demyelination of the PNS and the role of trophic factors or other molecules implicated in the cellular signaling between sensory neurons and Schwann cells to stimulate the expression of myelin proteins and the regeneration of the PNS

 

3) Understanding and treating Mucopolysaccharidosis type VII

Gene therapy is one of the most attractive treatments for diseases affecting the central nervous system (CNS) since blood-brain-barrier impairs delivery of systemically administered drugs to the cerebral parenchyma. Currently, some gene therapy clinical trials are ongoing for the treatment of some lysosomal storage diseases (LSD) with neuronal involvement, which are progressive neurological diseases affecting young children. However, the proper development and evaluation of these therapies requires understanding how cell signaling pathways are affected in these diseases and what is the impact on the viability or function of LSD cells and particulary in neurons. Other organs like bone or heart can be difficult to correct, even with high serum enzyme levels. We are paying particular attention to these tissues in a mouse model of Mucopolysaccahridosis type VII.

 

 

FUNDING

 

ISCIII; MINECO; EU; Feder-EU; AGAUR, Marató TV3; Genzyme.

 

  • R. Thwaite, G. Pages, M. Chillon, and A. Bosch. AAVrh.10 immunogenicity in mice and humans. relevance of antibody cross-reactivity in human gene therapy. Gene Therapy: 22: 196-201. 2015.
  • L. Ariza, G. Pagès, B. García-Lareu, X. Navarro, M. Chillon, J. Ruberte, P.Otaegui, and A. Bosch. Experimental diabetes in neonatal mice induces early peripheral sensorimotor neuropathy. Neuroscience: 274:250-9. 2014.
  • L. Ariza, L. Giménez-Llort, A. Cubizolle, G. Pagès, B. García-Lareu, N. Serratrice, D. Cots, M. Chillon, E. Kremer and A. Bosch. CNS delivery of helper-dependent canine adenovirus corrects neuropathology and behavior in Mucopolysaccharidosis type VII mice. Human Gene Therapy: 25(3):199-211. 2014.
  • J. Homs, G. Pages, L. Ariza, C. Casas, M. Chillon, X. Navarro, A. Bosch. Intrathecal Administration of IGF-I by AAVrh10 Improves Sensory and Motor Deficits in a Mouse Model of Diabetic Neuropathy. Molecular Therapy-Methods & Clinical Development: Jan 15;1:7. 2014.
  • M. Chillon and A. Bosch (Editors). Adenovirus: Methods and Protocols. Methods Molecular Biology, Third Edition, New York, USA. Humana Press. Volumen: 1089. ISBN:978-1-62703-678-8.2014.
  • E. Gil, A. Bosch, D. Lampe, J. M. Lizcano, J. C. Perales, O. Danos, M. Chillon. Functional characterization of the human mariner transposase Hsmar2. Plos One: 8(9): e73227:1-12. 2013.
 
See all publications fo A.Bosch at PubMed.

 

Institut de Neurociències
Tel: 93 581 3861 / Fax: +34 93 581 3327

Facultat de Medicina. Edifici M-1
Avinguda de Can Domènech - Campus de la UAB · 08193
Bellaterra (Cerdanyola del Vallès) · Barcelona