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By employing a conditional gene expression strategy on an ApoE knockout background to eliminate interference from endogenous central ApoE, the study demonstrated that peripheral expression of ApoE4 alone is sufficient to induce memory impairment, BBB leakage, and perivascular gliosis, with a severity comparable to that observed in systemic ApoE4 expression models [88]

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By the time most people reach their 60s, their natural GHK-Cu is a fraction of what it was in their 20s

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ROS/Ca 2+ signaling mediated by damaged mitochondria through MAMs may further affect chromatin homeostasis and gene transcription [266, 339]