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Copper(II) binding to amyloid-beta fibrils of Alzheimers disease reveals a picomolar affinity: stoichiometry and coordination geometry are independent of Abeta oligomeric form

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However, the accumulated data suggest that the overactivation of this signaling system could stem from inactivation or genetic ablation of the tuberous sclerosis complex (TSC) [261, 262], the master negative regulator of mTOR