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Pharmacology and receptor saturation suggest diminishing returns above the studied range, which is part of why the trials stopped at 12 mg

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However, this review also critically evaluates alternative explanations for the translational gap, including limited central nervous system penetration, insufficient pharmacodynamic target engagement, a mismatch between the drugs metabolic mechanisms and the amyloid-driven pathology of established AD, and the inherent limitations of preclinical models

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