Results about: Alzheimer

Our research focuses on three angles of peptide and protein chemistry: the design, synthesis and structure of bioactive molecules. From a structural perspective, we apply modern NMR techniques to study complex molecular recognition processes.

Researchers demonstrate the presence of stable beta-amyloid dimers in the brains of patients with Alzheimer’s disease

A study headed by IRB Barcelona provides the first direct evidence of beta-amyloid dimers (two proteins joined together) in patients with Alzheimer’s disease and points to the potential of these molecules as biomarkers.

Beta-amyloid dimers may be the smallest pathological species that trigger Alzheimer’s disease.

Patrick Aloy: “The whole is more than the sum of its parts”

The “Meet Our Scientists” video “Networks of life” explains his work and reveals the personal side of this scientist.

Jens Lüders: “Curiosity should fuel research”

The Meet Our Scientists video series introduces Jens Lüders, who studies microtubules—mini-filaments involved in multiple cell processes. The alteration of these structures is associated with diseases such as cancer and Alzheimer’s and with developmental defects.

In the video “Curiosity as a fuel”, Lüders recalls that transcendental discoveries arise from basic research and that such science is driven exclusively by curiosity, without specifically pursuing its applicability or transfer.

Researchers discover the hidden potential of disordered proteins

The finding paves the way for the identification of new therapeutic targets for many diseases.

Discovery of molecular protection linked to a degenerative neuromuscular disease

Kennedy’s disease leads to progressive muscle wastage. It is a condition that affects only men and it appears between 40 and 50 years of age. There is no specific treatment available.

In individuals with this disease, muscle cells and motor neurons die over the years because they accumulate a protein that is mutated.

Researchers at IRB Barcelona discover that this protein has a self-protective mechanism through which the deleterious effects of the mutation are delayed.