When is a living organism considered extinct? This is one of the fundamental questions of the artwork presented at Ars Electronica 2022 by Antoni Muntadas, a Catalan artist based in … Read more
The “la Caixa” Foundation will fund a large and innovative research project co-led by IBEC Junior Group Leader Benedetta Bolognesi and by ICREA research professor Ben Lehner at CRG, which aims to gain a better understanding of the genetic causes leading to neurodegenerative diseases. Researchers will combine deep mutagenesis and machine learning techniques to produce a “map of dementia” as a method to predict whether a person is more susceptible to suffer these diseases.
IBEC researchers receive two “Ignite Seed Grants” to combine their skills with other BIST members to seek scientific answers to health challenges. Benedetta Bolognesi will study, with the IRB, Huntington’s disease and other neurodegenerative pathologies without treatment. On the other hand, Juan Manuel Fernández-Costa and researchers at ICFO will develop muscles-on-a-chip and biomagnetism sensors to accelerate the design of new treatments for muscular dystrophy.
Benedetta Bolognesi, junior group leader at IBEC, appears in different media for a recent study published in the eLife magazine. In the study they show the first map with all the possible mutations in the amyloid beta peptide and tested how they influence its aggregation into plaques, a pathological hallmark of Alzheimer’s disease.
The Mayor of Barcelona, Ada Colau, visited IBEC facilities last Friday to learn, by our Director and a group of researchers, how bioengineering can help find solutions to health problems such as COVID19, cancer, or degenerative diseases.
When in early 2020, more than 200 scientists gathered in La Pedrera in Barcelona to discuss the present and future of bioengineering, no one imagined that the world would experience the first pandemic of the 21st century and that science would take on more importance than ever.
Researchers from IBEC and CRG in Barcelona use a technique called high-throughput mutagenesis to study Amyotrophic Lateral Sclerosis (ALS), with unexpected results.
Results showed that aggregation of TDP-43 is not harmful but actually protects cells, changing our understanding of ALS and opening the door to radically new therapeutic approaches.
Amyotrophic lateral sclerosis (ALS) is a devastating and incurable nervous system disease that affects nerve cells in the brain and spinal cord, causing loss of muscle control and normally death within a few years of diagnosis. In ALS, like in other neurodegenerative diseases, specific protein aggregates have long been recognized as the pathological hallmarks, but it is not clear whether they represent the actual cause of the disease. Indeed, alleviating aggregation has repeatedly failed as a therapeutic strategy when trying to treat neurodegenerative diseases such as Alzheimer’s disease.