The study, led by IBEC in collaboration with IQAC-CSIC, UB, and IRB Barcelona, has shown in cultured neurons and mouse models that P33 partially modulates the enzyme BACE1, responsible for beta-amyloid formation, without causing significant cellular damage. The findings have been published in the journal Bioorganic Chemistry.
Unlike other drugs that aim to completely block BACE1, the team's strategy involved designing chemically modified peptides to act selectively. "P33 stood out because it clearly reduced beta-amyloid without harming cells and, moreover, selectively slowed down BACE1 activity," explains Dayaneth Jácome, the study's first author.
In experiments with genetically modified mice prone to developing amyloid plaques, administration of P33 for eight weeks successfully reduced cerebral A levels by 35.6% and the surface area occupied by these plaques, with no detected side effects in other organs.
The researchers believe these results open a new avenue for chemical research into Alzheimer's disease. "These peptides offer us a versatile chemical platform to continue investigating this pathway," states José A. Del Río, principal investigator at IBEC. The next step will be to expand studies with a larger number of animals and precisely confirm how P33 acts on BACE1.
