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This rapid increase has been argued to be due either to a release of IGF-1 stores in tissues or due to a proteolytic cleavage of IGFBP-3 either in the plasma or in tissue

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[172] reported that LCMT-1 overexpression protected animals from A-induced impairments, whereas overexpression of phosphatase methylesterase 1 worsened A neurotoxicity [172]