Researchers at the RIKEN-Max Planck Joint Research Center in Japan have demonstrated that hallmark symptoms of Alzheimer’s disease can be reduced when sugars are prevented from binding to one of the key enzymes implicated in the disease. The new findings, reported in EMBO Molecular Medicine, show that abnormal attachment of a particular sugar to the enzyme BACE1 is a critical factor leading to the formation of A? plaques in the brain, and that plaques were reduced and cognitive performance improved when this action was prevented in mice through loss of the enzyme GnT-III. In doing so, this work has revealed a novel mechanism for Alzheimer’s disease development, potentially opening the way to a new approach for treatment.
Immunostaining of A? plaques showed that while the normal mouse model for Alzheimer’s disease displayed numerous A? plaques (left, black arrows), the number of plaques was significantly reduced when these mice lacked the GnT-III enzyme (right). Scale bar, 300 ?m.