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Despite a variety of therapies currently under investigation against Alzheimer's disease the discovery of a cure does not seem to be within reach at this point. A more holistic approach of the disease and its treatment that takes into account its multifactorial etiology, should help us to establish new and more efficient conceptual and therapeutic paradigms. This requires finding new targets beyond those that have been classically investigated over the last decades, in particular proteins known as secretases, and whose biological/protease activity contributes to the toxic accumulation of beta-amyloid molecules. We have found that another protease (MT1-MMP), which is different from the aforementioned secretases, also contributes to the accumulation of beta-amyloid and may therefore constitute a new molecular therapeutic target. In the process of validating this potential new target it is necessary to better understand how MT1-MMP interacts with other proteins and what are the cellular mechanisms at stake. Our work sheds light on some of these original mechanisms and provides ground to take a step forward towards the validation of MT1-MMP as a new potential target in Alzheimer's disease.

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This page is a summary of: Proamyloidogenic effects of membrane type 1 matrix metalloproteinase involve MMP-2 and BACE-1 activities, and the modulation of APP trafficking, The FASEB Journal, February 2019, Federation of American Societies For Experimental Biology (FASEB),
DOI: 10.1096/fj.201801076r.
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