A science dissemination contest was organized at our research institute for Sant Jordi. Laura Sánchez won the first prize with this amazing masterpiece, which shows our lab and the things you can find in it! She rocks!

We have received a Proof of Concept UAB grant to transfer our mito-based technology to develop a diagnostic kit for bacteria resistance. The project, which is a collaboration with Hospital Parc Taulí, will consist of creating a fast and highly sensitive approach to detect antimicrobial resistance (AMR), based on checking the expression of different resistance genes. The development of this disruptive methodology could represent a significant step forward in the fight against AMR, allowing clinicians to find a precise antibiotic for each case 👩‍🔬🦠💪👏

These grants are supported by the Secretaria d’Universitats i Recerca of the Departament d’Empresa i Coneixement de la Generalitat de Catalunya and are funded by the Fons Europeu de Desenvolupament Regional (FEDER).

More info about the project

As the new year begins, we would like to look back to 2020 for a last minute. It was a tough year, but the scientific community got two amazing new doctors!

Pati defended her PhD, ESTUDIO DEL PERFIL TRADUCCIONAL CITOSÓLICO Y MITOCONDRIAL DE POBLACIONES NEURONALES SUSCEPTIBLES A LA DEFICIENCIA DEL COMPLEJO I MITOCONDRIAL, in December, giving an excellent presentation that led to a very interesting discussion.

And Pablo defended his thesis, GLUTAMATERGIC VESTIBULAR NEURONS SUSTAIN MOTION-INDUCED AUTONOMIC AND AVERSIVE RESPONSES, online in July. He did a super-great job as well, it was a great presentation with a very nice discussion. Look at him holding his little baby:

We are veeeery proud of them, and wish all the best for their scientific careers! We already have their pictures on our hall of fame:

We have big good news at Quintanalab.

1. Pati already deposited her PhD
2. Eli was selected to be a Ramon y Cajal researcher
3. Albert is now a tenured associate professor

Everything was adequately celebrated with pizza last Friday:

We are very happy!

Cheeeers!

Albert and Eli participated in an international study published in Nature, which describes the processes occurring in the hippocampal neurons to create long-lasting memories.

Long-term memory is a brain mechanism that allows us to encode and retain an almost unlimited amount of information throughout our lifetime. Key proteins that activate protein synthesis, such as the eIF2 initiation factor, are involved in the process.

In this study, coordinated by McGill University (Montreal, Canada), they observed that eIF2 is involved in the formation of new long duration memories through its activity in two types of neurons in the hippocampus: excitatory neurons and neurons expressing somatostatin, a group of inhibitory neurons.

In parallel and autonomously, the reduction of eIF2 bound to a phosphorus molecule (phosphorylated) in these two subpopulations is enough to increase protein synthesis, strengthen connections between neurons, and improve long-term memory.

“To study these effects, we used a technique we had developed, that showed that the changes in the excitatory neurons during learning are similar to those observed by genetically preventing eIF2a phosphorylation in these neurons”, explains Eli. This is important because it validated the genetic model and allowed identifying the changes that learning produces at a transcriptional level.

“The existence of two autonomous processes for memory consolidation mediated by the non-phosphorylated form of eIF2a may respond to an evolutionary advantage in ensuring and regulating the duration of a given memory”, says Albert.

The study is the first to analyze separately the role of excitatory and inhibitory neurons in the hippocampus in the consolidation of these types of memories, and helps to understand the creation and maintenance of memories phenomenon, which continues to belargely unknown.

Read the article

We are very happy to announce we have been selected to receive a grant from La Caixa Foundation to investigate new therapies for mitochondrial disease! It has been a very competitive process, in which only 8 projects were selected out over 150 proposals, so we have some cava in the fridge!

Our project will focus on studying the alterations that occur in a specific area of ​​the brain, the basal ganglia, in mitochondrial pathologies. We suspect that these alterations are caused by signals initiated in the mitochondria that drive cells to their death. Thanks to the funding from La Caixa Foundation (500,000 euros in 3 years), we will investigate how to reverse these signals and look for new therapies.

Cheeeeers!

What was last Saturday’s day number? Yes, it was the 4th of July. What happens on every 4th of July? Yes, we celebrate a BBQ to commemorate the United States’ Independence Declaration. O say, can you see by the dawn’s early light…  You can tell we miss Seattle 😀

We went to El Bosc Tancat, in Cerdanyola, with our cars full of hot dogs, burgers (+ veggie burgers), chorizo, chicken, omelettes, beers, and a bit of sadness, as it was Fab’s farewell as well.

Marco and Adan were the BBQ chefs, and Fab was in charge of them having enough drinks. They did an excellent job, as the food was de-li-ci-ous. Isabella brought this almost-non-alcoholic potion they drink in Serbia, rakija, to help the food disintegrate in the guts.

After the lunch, we gave Fab some presents, such as a magnific apron he is committed to wear every time he cooks Spanish food:

Then, some dared into the swimmingpool to have an afternoon bath and show how tanned they got during lock-down:

What a pleasure to be part of this group of amazing people! <3

We are very glad to announce that our MitoCBD project has been selected for a CaixaImpulse grant.

MitoCBD consists in investigating the use of Cannabidiol (CBD), a substance obtained from the cannabis plant, for the treatment of mitochondrial disease.

It has been proved that CBD has anti-inflammatory and neuroprotective properties, and it was also found to restore deficits and prolong life expectancy in a mitochondrial disease model.

The aim of this project is to test the effectiveness of the CBD in other preclinical models of mitochondrial disease, with the final objective of finding a treatment for these devastating rare diseases.

There has only been 21 projects selected from all around the UE, so we are veeeery happy that MitoCBD is one of them!

We published our first preprint last week. For those who aren’t familiarized, a preprint is a study to be published in a Journal, that has not been reviewed yet. The aim is to make the results available as soon as possible so Science can advance faster. We are very excited about it, and very happy because it has been featured by the preprint platform Biorxiv for reaching the top 5% altmetric score within their first days after releasing it; and it has also been selected as one of the ERC Research results of the week! So cool!

But what is it about?

As you may know, dysfunctions of the mitochondrial energy-generating machinery cause a series of usually fatal diseases collectively known as mitochondrial disease. In this disease, high energy-requiring organs, like the brain, are especially affected, showing many severe symptoms such as motor alterations, respiratory deficits or epilepsy that, in many cases, can be fatal. Hence, our group is driven to better understand these pathologies, with the overarching goal of finding effective therapies to treat them.

This time, we focused on Leigh Syndrome, the most common presentation of mitochondrial disease with a predominant affectation of the central nervous system, particularly in two brain areas, the brainstem (that controls all basic functions that keep us alive) and the basal ganglia, involved in refining motor coordination. We knew that one protein in the mitochondria is critical in this disease: the Complex I subunit NDUFS4, because animal models lacking this subunit in all their cells reproduce the classical signs of Leigh Syndrome described before. However, there were some pressing questions remaining: do symptoms appear due to all cells in the body not working properly, or some specific cells are responsible for them?

To study this, we selectively inactivate NDUFS4 in three neuronal populations we suspected could be key, and keep NDUFS4 working in all other cells in the body. Observing what symptoms remained we could know the role of these neurons in the brain alterations these patients suffer.

What we found was that the inactivation of this subunit in a certain kind of excitatory neurons (the fancy-scientist name is vlgut2-expression glutamatergic neurons) caused brainstem inflammation, motor and respiratory deficits, and early death; and that its inactivation in inhibitory (GABAergic neurons) led to basal ganglia inflammation, severe refractory epileptic seizures and premature death.

Bottom line, these results are very important to contribute understand the underlying cellular mechanisms of mitochondrial disease in general, and Leigh Syndrome in particular, as we have identified which specific neurons are behind the brain lesions observed in this pathology and their specific contribution to the symptoms. Therefore, now we have new knowledge to try to identify which cellular aspects are failing in those cells so we can start to envisage different methods to correct them.

Happy #MitoAwarenessWeek!