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A plaques result from the abnormal cleavage of amyloid precursor protein (APP) by betasecretase (BACE1) and gammasecretase, leading to the production of toxic A peptides, particularly A42, which aggregates and forms insoluble plaques

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In addition, besides it is widely known antioxidant potential, ALA has also many other functions, as it is its involvement in mitochondria producing energy, by acting as cofactor for various enzymes involved in metabolism [5]