AsianScientist (Oct. 6, 2016) – Scientists have found that mutations in a gene called BIN1 disrupt the intracellular transport of enzymes responsible for the production of amyloid-β (Aβ) plaques, a hallmark of Alzheimer’s disease. The study was published in Human Molecular Genetics.
While over 20 genes have been identified in recent years as genetic risk factors for Alzheimer’s, little is known about the mechanisms that bring on the disease.
In earlier studies, the research group led by Professor Taisuke Tomita at the Graduate School of Pharmaceutical Sciences at the University of Tokyo found that a protein called CALM regulates the production of toxic variants of Aβ. CALM, which is involved in vesicular transport, is known to be a risk factor for Alzheimer’s.
In the current study, the group analyzed the role of BIN1, considered the most dangerous among the vesicular trafficking-related risk factors for Alzheimer’s. They found that it regulates intracellular transport of β-secretase, and is a molecule that affects Aβ production. These results imply that disruption in the intracellular trafficking of Aβ-producing enzymes is related to the onset of Alzheimer’s disease, and mechanisms targeting BIN1 and CALM could be developed to combat the disease.
“These results indicate that intracellular transport is a key mechanism involved in the onset of Alzheimer’s disease. We will apply these results to the development of prevention, diagnosis and therapeutic drugs for Alzheimer’s disease, and we will also continue our research on other risk factors,” said Tomita.
The current result is expected to lead to the development of preventive and therapeutic strategies to combat Alzheimer’s drugs for intracellular transport that suppress the production of Aβ.
The article can be found at: Miyagawa et al. (2016) BIN1 Regulates BACE1 Intracellular Trafficking and Amyloid-β Production.
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Source: University of Tokyo.
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