Lab-designed molecule reduces amyloid beta, the protein linked to Alzheimer's disease, in mice

Researchers at the Institute for Bioengineering of Catalonia and several other institutions have identified a synthetic peptide called P33 that may help reduce the production of amyloid beta (Aβ) in the brain. Aβ is a protein linked to Alzheimer's disease. The study, published in Bioorganic Chemistry, involved both lab tests on cultured neurons and a mouse model of the disease.

Enzyme BACE1 is responsible for producing Aβ, which then aggregates into plaques in the brain. Previous drug attempts to block BACE1 entirely have failed due to side effects. The team took a different approach by designing peptides that can enter cells and selectively block BACE1 activity. Of 50 tested molecules, P33 showed the most promise.

In lab tests, P33 reduced Aβ release by over 50% and decreased BACE1 activity without harming the cells. In the mouse model, eight weeks of P33 treatment decreased brain Aβ levels by 35.6% and plaque-affected areas in the cortex and hippocampus. Importantly, the treatment did not damage other organs or affect inflammation markers.

Researchers note that this peptide provides a versatile tool to continue investigating BACE1's role in amyloid beta production. They plan to expand the studies with more animals, measure P33's penetration into the brain, and further understand how it impacts BACE1. The team is also interested in confirming any improvements in memory observed in the treated mice through larger trials.