Excessive amyloid‑β (Aβ) production, driven by β‑site APP cleaving enzyme‑1 (BACE1), is central to the pathogenesis of Alzheimer’s disease (AD), yet active‑site BACE1 inhibitors have failed in trials because of efficacy and safety limitations. Targeting BACE1 transcription offers an orthogonal strategy that may enable partial, context‑dependent suppression compatible with neuronal function. 1
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Park et al. (2026) studied this question.
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