Dicholine salt of succinic acid, a neuronal insulin sensitizer, ameliorates cognitive deficits in rodent models of normal aging, chronic cerebral hypoperfusion, and beta-amyloid peptide-(25–35)-induced amnesia

Table 1 Effect of CS on brain ChAT activity in rats with β-amyloid peptide-(25–35)-induced amnesia.

Treatment Groups	ChAT activity, dpm/mg of tissue
SH	6.15 ± 0.21*
CTR	4.52 ± 0.25^†
CH	4.84 ± 0.68
CS1	5.19 ± 0.35
CS10	5.39 ± 0.41
CS25	5.72 ± 0.38*

ChAT activity in brain cortex homogenates was assayed by radiometry on the day as indicated in the experimental schedule (Figure 11). SH, sham-operated rats (i.p. saline for 7 days); CTR, β-amyloid peptide-(25–35)-induced rats (i.p. saline for 7 days, control); CH, β-amyloid peptide-(25–35)-induced rats treated i.p. for 7 days with choline chloride in dose of 10 mg/kg; CS1, CS10, and CS25, β-amyloid peptide-(25–35)-induced rats treated i.p. for 7 days with CS in doses of 1, 10, or 25 mg/kg respectively. Each group comprised eight rats. Data represent the ChAT activity means ± SEM expressed as dpm/mg of wet tissue. *P < 0.05 vs. CTR. ^†P < 0.05 vs. SH.