Abstract:Misfolding and accumulation of amyloid-β (Aβ)
to form
senile plaques are the main neuropathological signatures of Alzheimer’s
disease (AD). Decreasing Aβ production, inhibiting Aβ
aggregation, and clearing Aβ plaques are thus considered an
important strategy for AD treatment. However, numerous drugs cannot
enter the AD clinical trials due to unsatisfactory biocompatibility,
poor blood–brain barrier penetration, little biomarker impact,
and/or low therapeutic indicators. Here, a pair of chiral aspartic
acid-mod… Show more
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