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While the scopolamine model is often used to assess the cognitive enhancing capacity of experimental molecules it clearly initiates learning deficits in a non-physiological manner that only results in acute deficits

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alkylation of a C3-amino-quinoline derived precursor, such as compound 8 may be achieved via reductive amination with, for example, triethyl orthoformate in TFA followed by treatment with NaBH 4 to give the corresponding secondary C3-amine derivative (such as N-methyl-C3-amino-quinoline 9)