According to the conclusions of a new study by investigators at the Mayo Clinic, it would appear that the enzyme BACE2 is very efficient at destroying beta-amyloid, the protein that builds up to form plaques in the brains of patients suffering from Alzheimer's disease.
These plaques emerge between neurons, and can eventually lead to their destruction. Therefore, the beta-amyloid protein is one of the primary molecular actors involved in the development of this neurodegenerative form of dementia.
Though closely related to BACE1, an enzyme known to promote the development of beta-amyloid plaques, BACE2 has the exact opposite effects, investigators at the Clinic uncovered, according to PsychCentral
“The fact that BACE2 can lower beta-amyloid by two distinct mechanisms makes this enzyme an especially attractive candidate for gene therapy to treat Alzheimer’s disease,” Mayo neuroscientist at first study author, Samer Abdul-Hay, PhD, says.