A study led by the Institute for Bioengineering of Catalonia (IBEC) identifies a molecule, P33, that partially modulates the enzyme that initiates amyloid beta formation. The results, obtained in cell cultures and in mice, open up a new avenue of chemical research into the disease.
IBEC researcher Amayra Hernández-Vega has been awarded a grant from the Pasqual Maragall Researchers Programme to lead a project focused on studying the earliest stages of Alzheimer’s disease. The study will combine in vitro and human models of familial Alzheimer’s disease to identify age-related factors and potential inhibitors that could slow the early progression of the disease. The project was presented at an informative session on sleep and brain health, which was attended by around 500 people.
Amaya Hernández-Vega, a senior researcher at IBEC, will lead one of the two projects selected in the 2024 call for proposals from the Pasqual Maragall Research Programme, which is dedicated to funding research into Alzheimer’s disease and other neurodegenerative conditions. IBEC also celebrates the participation of Jordi Duran, an associate researcher from the Molecular and Cellular Neurobiotechnology group, who will collaborate on the second selected project.
An international team co-led by the Institute for Bioengineering of Catalonia (IBEC) and the West China Hospital Sichuan University (WCHSU) was able to reverse Alzheimer’s in mice after only 3 injections with nanoparticles. The innovative approach to treating the disease focuses on restoring the normal function of the vasculature, rather than acting on neurons or other brain cells, as has usually been done until now. This achievement, published in the Signal Transduction and Targeted Therapy Journal, is a promising step towards an effective treatment for Alzheimer’s disease.
This is an analysis on an unprecedented scale. They studied over 140,000 versions of the Aβ42 peptide, which forms harmful plaques in the brain. It is the first map to reveal how mutations affect a protein in its transition state — a fleeting phase that is difficult to study. This finding opens up new avenues for preventing Alzheimer’s disease and suggests a method that can be applied to studying other proteins involved in different pathologies. The study, published in Science Advances, is a collaboration between the Wellcome Sanger Institute in the United Kingdom, the Institute for Bioengineering of Catalonia, and the Centre for Genomic Regulation in Barcelona.
The new therapy, made of nanofibers and trehalose, a sugar that naturally occurs in plants, traps and neutralizes toxic proteins to stop disease progression. Now trapped, the toxic proteins can no longer enter neurons and instead harmlessly degrade. The study, published in the journal of the American Society, was led by the Institute for Bioengineering of Catalonia and the Northwestern University.
The new AI is able to predict when and why protein aggregation occurs, a mechanism linked to Alzheimer’s and 50 other diseases that affect 500 million people. The results show great potential for research into neurodegenerative diseases and for improving drug production, reducing costs and increasing efficiency. The study, published today in Science Avances, is the result of a collaboration between the Centre for Genomic Regulation (CRG) and the Institute of Bioengineering of Catalonia (IBEC).
This is a molecule that is directly linked to the expression of the cellular prion protein found on the surface of nerve cells. The study, led by the IBEC, opens the door to the early detection of Alzheimer’s disease in asymptomatic stages in blood samples, favouring its diagnosis and treatment.
The researcher at the Institute for Bioengineering of Catalonia has been awarded an ERC Consolidator Grant. This prestigious European funding supports excellent scientists and scholars who are consolidating their independent research teams to pursue their most promising scientific ideas. The €2 million grant over 5 years will allow Bolognesi and her team to develop a new method for identifying mutations that lead to the formation of amyloids—aggregates of proteins that contribute to a variety of diseases, including Alzheimer’s and Parkinson’s.
A study led by the Institute of Bioengineering of Catalonia (IBEC) describes the development of an organ-on-a-chip that mimics the human blood-brain barrier. With this system, researchers can study the barrier permeability to different drugs and screen the most effective ones, avoiding animal tests. The device could also incorporate cells from patients to make a personalized study of the disease.