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This model posits that during the early stages of AD, particularly in the preclinical phase, cerebral iron overload—triggered by genetic factors (e.g., APOE ϵ4) or aging—along with the resultant oxidative stress, constitutes a key upstream event that initiates the pathological cascade

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Linear regression was examined between AUC values obtained after BPC157 IM administration and BPC157 doses and between C max values and BPC157 doses