Carlos A. Saura Antolín

Carlos A. Saura Antolín

     

 

Carlos A. Saura Antolín

Academic Staff

Phone:
+34 935 868 398

Email:
carlos.saura@uab.cat

Adress:

Department of Biochemistry and Molecular Biology
Institut de Neurociències
Faculty  of Medicine (room M2-113)
Universitat Autònoma de Barcelona (UAB)
Bellaterra Campus 08193-Cerdanyola del Vallés

Area

Thesis number in address


Carlos A. Saura obtained his Ph.D. in Chemistry from the University of Barcelona (Spain) in 1998. Following postdoctoral training at Johns Hopkins University and University of Chicago under the mentoring of Dr. G. Thinakaran, he was appointed Instructor at the Department of Neurology at Harvard Medical School (Boston, USA) in 2000. Under the supervision of Dr. J. Shen, he investigated the role of presenilins in memory and neurodegeneration in novel transgenic and knockout disease mouse models. In 2004, he was appointed Ramón y Cajal Research Professor at the Universitat Autònoma de Barcelona (Spain). Dr. C. Saura is currently an Associate Professor in the Department of Biochemistry and Molecular Biology at the Institut de Neurociències of the Universitat Autònoma de Barcelona. Dr. Saura has published more than 30 peer-reviewed articles in molecular aspects of brain function and neurodegeneration, has directed several European research projects and is an active collaborator of several national and international founding agencies and scientific journals.

Dr. Carlos Saura is a Principal Investigator at the Biomedical research group in Neurodegeneration and leads his own laboratory:
 
 
 
Laboratory members:
Paula Conde Rubio
Anna del Ser
Miriam Javier Torrent
Laura Rubió Ferrarons
Carlos Soto Faguás
Ohiane Ussia
 
Past members:
Dr. Sergi Marco Martín
Dr. Judit España
Dr. Vidalba Rocher Ros
Dr. Jorge Valero
Dr. Meng Chen
Dr. Arnaldo Parra Damas
Dr. Muriel Arimón Bedós
Dr. Lilian Enríquez
 
 
 
RESEARCH INTERESTS
 
Dr. Carlos Saura´s research interest focuses in understanding the molecular mechanisms that regulate neuronal function in the brain during normal and pathological aging. He is passionate in understanding how brain functions during memory processing and the mechanisms involved in synapse and memory dysfunction in age-related cognitive disorders. Particularly, Dr. Saura investigates the role of specific genes and the mechanisms that regulate gene expression programs implicated in Alzheimer´s disease and other dementias. Dr. Saura has used pioneering approaches to generate novel transgenic and knockout mouse models of neurodegeneration that are used for assessing new pharmacological, cognitive stimulation and gene therapy strategies  as alternative therapies in dementia. His projects provide knowledge of novel molecular targets and new therapeutic strategies for early treatment of Alzheimer´s and related neurological disorders.
 
 
MAIN RESEARCH LINES

1. Mechanisms of synaptic dysfunction in Alzheimer´s disease
The molecular mechanisms underlying gene expression changes and synapse and cognitive dysfunction in cognitive disorders are largely unknown. Recent studies from our lab indicate that specific gene expression programs induced by synaptic activity are essential for memory processing, whereas deregulation of these programs causes memory impairment in mouse models of AD. We investigate the role of the transcription factor cAMP-response element binding protein (CREB) and its transcripcional coactivators CREB binding protein (CBP) and CREB-regulated transcription coactivator-1 (CRTC1) on regulation of specific gene expression programs in cells and transgenic mice that overexpress mutant APP and presenilin genes. Our results indicate that deregulation of specific CREB-dependent gene expression programs plays a role in synaptic and cognitive dysfunction, and regulation of specific gene networks is relevant to develop therapeutic interventions for age-related cognitive disorders. These signaling pathways are being tested as potential drug targets in AD experimental models.

2. Novel therapeutic strategies in Alzheimer´s disease
The discovery of novel molecular mechanisms underlying synaptic dysfunction and memory loss in transgenic and knockout mouse models of AD allow us to design new therapeutic strategies to prevent and/or reverse cognitive dysfunction in this disease. We have described that inactivation of presenilin-1/γ-secretase reduces age-dependent amyloid pathology and memory deficits in APP transgenic mice, whereas inactivation of both presenilins results in memory deficits and neurodegeneration through deregulation of synaptic proteins and the CREB signaling pathway. Similarly, accumulation of Aβ alters expression of CREB target genes required for memory by deregulating the coactivator CRTC1. We are currently employing novel gene therapy and pharmacological approaches to activate  CRTC1 signaling and reverse memory deficits in transgenic mouse models of AD. Finally, we study the cellular mechanisms by which cognitive stimulation has beneficial effects on adult neurogenesis and memory in AD.
  • Saura C.A.*, Yu H.*, Choi S-Y., Sun L.D., Yang X., Handler M., Kawarabayashi T., Younkin L., Fedeles B., Wilson M.A., Younkin S., Kandel E.R., Kirkwood A. and Shen J. APP processing and synaptic plasticity in presenilin-1 conditional (2001). Neuron, 31 (5): 713-726
  • Saura C. A., Choi S.-Y., Beglopoulos V., Malkani S., Zhang D., Shankaranarayana Rao B. S., Chattarji S., Kelleher III R. J., Kandel E. R., Duff K., Kirkwood A. and Shen J. Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration (2004). Neuron, 42: 23-36.
  • Saura C.A., Chen G., Malkani S., Choi S.-Y., Zhang D., Takahashi R.H., Gouras G.K., Kirkwood A., Morris R.G.M. and Shen J. Conditional inactivation of presenilin-1 prevents amyloid accumulation and temporarily rescues associative and working memory impairments in APP transgenic mice (2005). J. Neurosci. 25(29):6755-64
  • España J., Giménez-Llort L., Valero Gómez-Lobo J., Miñano A., Rábano A., Rodríguez-Alvarez J., LaFerla F.M. and Saura C.A.Intraneuronal Aβaccumulation in the amygdala enhances fear and anxiety in Alzheimer’s disease transgenic mice (2010). Biol. Psychiatry 67(6): 513-521.
  • Parra-Damas A., Valero J., Chen M., España J., Martin E., Ferrer I., Rodríguez-Alvarez J. and Saura C.A.  Crtc1 activates a transcriptional program deregulated at early Alzheimer´s disease-related stages  (2014). J. Neurosci. 34(17): 5776-87.
  • Saura C.A., Parra-Damas A.J. and Enríquez-Barreto L. Gene expression parallels synaptic excitability and plasticity changes in Alzheimer´s disease (2015). Front. Cell. Neurosci, 9:318
See all Carlos A. Saura publications 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