Albert Quintana Romero

Albert Quintana Romero



Albert Quintana Romero

+34 935 814 967



Department of Cellular Biology, Physiology and Immunology
Institut de Neurociències
Faculty of Medicine (room M1-113)
Universitat Autònoma de Barcelona (UAB)
Bellaterra Campus 08193-Cerdanyola del Vallés

Albert Quintana is an Associate Professor of the Department of Cell Biology, Physiology and Immunology. He earned a Bachelor in Science in Biology (Biomedicine) in 2001 and a PhD in Neuroscience in 2007, both from the Universitat Autònoma de Barcelona. During his PhD focused on the role of cytokines in the development of neuropathology and neuroinflammation in traumatic brain injury. As a postdoc (2008-2013), he joined Dr. Richard Palmiter lab at the University of Washington in Seattle, where he was the lead scientist developing and characterizing a mouse model of mitochondrial disease (Leigh Syndrome). In 2013 he was appointed Assistant Professor in the Department of Pediatrics (University of Washington) and group leader at the Seattle Children’s Research Institute. In 2015 he returned to the Universitat Autònoma de Barcelona as a Ramón y Cajal investigator and ERC grantee (Starting Grant). His research focuses on using a multi-level approach and to develop new tools to identify the molecular determinants of neuronal susceptibility to mitochondrial disease. He has authored over 30 research articles and 2 book chapters.

Dr. Quintana leads the Mitochondrial Neuropathology research group and laboratory (Quintanalab):




Group members:
Irene Bolea
Alex Gella
Pablo Machuca

Fabien Menardy

Kelsey Montgomery
Patricia Prada
Elisenda Sanz

Andrea Urpí


Former members:
Jessica Hui
Benjamin Bauer





Mitochondria are the powerhouses of the cell. Mutations that render mitochondria unable to generate energy cause a group of rare and usually fatal pathologies collectively known as mitochondrial disease. It has been estimated that 1 in 5000 children will develop a mitochondrial disease. Currently, there is no cure for mitochondrial disease and the treatments available are mostly ineffective. Energy-demanding cells such as neurons are especially sensitive to mitochondrial disease, and they account for most of the clinical signs and symptoms observed in humans, such as hypotonia, ataxia, seizures and early death.However, even if every single cell in the body carries the mutation, only specific brain areas seem to be affected by the deficiency.  Our lab investigates the molecular mechanisms defining why some neuronal populations are particularly affected by mitochondrial disease, with the overarching goal of identifying novel targets that lead to improved treatments for mitochondrial disease patients.





The Quintana lab current research focuses on identifying the neuronal populations susceptible to mitochondrial disease and which mechanisms are making these neurons die. This knowledge is essential to understand and fight these incurable diseases. The Quintana lab uses a wide array of approaches, combining molecular biology, stereotaxic surgery, mouse genetics and behavior, biochemistry, histology, optogenetics and in vivo electrophysiology to reveal novel pathways and mechanisms in neuronal function and pathology and open new and unexplored lines of research and therapeutic targets to treat mitochondrial disease encephalopathy.





Mitochondria generate most of the energy that cells require to function properly. Dysfunctions in the mitochondrial energy-producing machinery causes a group of severe and progressive pathologies collectively named mitochondrial disease. 1 in 5000 births will be affected by mitochondrial disease, severely and progressively impairing the normal development of the child. Although the disease is usually fatal, there is no cure, or even effective treatments for mitochondrial disease.

The central nervous system, and neurons in particular, are high energy-requiring tissues and cells. Hence, they are severely affected in mitochondrial disease and alterations in their functioning cause most of the clinical signs and symptoms observed in patients and that ultimately lead to premature death. However, even though usually all neuronal populations present the same mutation only discrete neuronal groups are affected and die. Our research focuses on identifying the cellular mechanisms that underlie this susceptibility to mitochondrial alterations. Our studies combine histological, molecular, electrophysiological, optegenetic and behavioral approaches to identify new neural circuits and mechanisms involved in neuronal function and mitochondrial pathology with the overarching goal to generate new therapeutic targets.





1) Identifying the molecular changes in susceptible neuronal populations.

The cellular mechanisms underlying whether a neuron dies   or survives mitochondrial alterations are not clear. Our results using an animal model of mitochondrial disease have identified the neuronal populations that are affected the most. We hypothesize that transcriptional and translational changes are underlying the neuronal fate of a neuron with mitochondrial alterations. Given the high anatomical and cellular specificity of mitochondrial disease and the heterogeneity of the neural tissue new technologies are required to be able to observe such changes in affected neurons. Our lab is developing new methods to identify these changes with a cell-specific resolution. This will allow the characterization of the mechanisms and cellular pathways involved in the mitochondrial pathologies and identify new potential therapies.


2) Establishing the functional connectome of the vestibular nucleus.

Our studies have identified the vestibular nucleus, in the brainstem, as a key player in the physiological and behavioral changes observed in mice with mitochondrial deficits. The vestibular nucleus is divided in different regions that connect extensively with other brain areas. Even though it is involved in many different functions such as the control of balance, blood pressure or breathing the circuitry underlying all these functions has not been elucidated. Our lab uses stereotaxic surgery and in vivo electrophysiological approaches to identify the vestibular projections involved in these physiological responses and the role they play in mitochondrial disease.


3) Identify new therapeutic targets to mitochondrial encephalopathy.

Our results have identified two signaling cascades that are altered in mice with mitochondrial dysfunction: mTOR and SREBP/JNK. Our lab has characterized that blocking mTOR extends lifespan of affected mice 5-fold and that the administration of antioxidants ameliorates the disease progression and delays the clinical features of the disease. Building upon this, our current studies are focused on characterizing and identifying the downstream factors involved in these positive effects to further our knowledge and to identify new treatments for mitochondrial disease.



  • Dr. Richard Palmiter, Howard Hughes Medical Institute and University of Washington, USA
  • Dr. Nino Ramirez, Seattle Children’s Research Institute, USA
  • Dr. Phil Morgan, Seattle Children’s Research Institute, USA
  • Dr. Margaret Sedensky, Seattle Children’s Research Institute, USA
  • Dr. Hugo Bellen, Howard Hughes Medical Institute and Baylor College of Medicine, USA.
  • Dr. Francois H. van der Westhuizen, North-West University, South Africa
  • Dr. Iain L Campbell, University of Sydney, Australia


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Instituto de Neurociencias


Tel: 93 581 3861
Fax: +34 93 581 3327


Tel: 93 581 33 27

Facultad de Medicina. Edificio M-1
Calle de la Vinya - Campus de la UAB · 08193
Bellaterra (Cerdanyola del Vallès) · Barcelona