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 Aß 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.
A major factor contributing to Alzheimer’s disease is the formation of pathogenic Aß plaques in the brain when the molecule APP is abnormally cut by the enzyme BACE1, producing Aß. Because of this, developing drugs that prevent BACE1 from cleaving APP is a central focus of Alzheimer’s research. A major stumbling block in these efforts however, is finding a way to do this without disturbing vital processes in the brain and body that are regulated by normal BACE1 activity.
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