Intracerebroventricular administration of adiponectin attenuates streptozotocin-induced memory impairment in rats.

Alzheimer's disease (AD) has been reported to be linked with diabetes mellitus and insulin resistance. Adiponectin (ADN), an adipocytokine secreted from adipose tissue, is involved in the regulation of insulin sensitivity, energy homeostasis, and mitochondrial dysfunction. In this study, we examined the effect of ADN on passive avoidance memory in animal model of sporadic AD (sAD). On days 1 and 3 after cannulation, rats received intracerebroventricular (icv) injection of streptozotocin (STZ) (3 mg/kg). Thirty minutes before the learning process, animals received saline or ADN in different doses (6, 60, and 600 µg). The step-through latency (STL) and total time spent in the dark compartment (TDC) were recorded and analyzed. In STZ-treated rats, STL was significantly decreased, whereas TDC showed a dramatic increase. In ADN-treated rats, STL was significantly increased (P < 0.01) in all treatment doses. The number of entries was decreased in all applied doses; however, TDC was reduced only by the application of 6 ng of ADN (P < 0.05). It can be concluded that ADN is useful to improve the STZ-induced memory impairment. This study showed, for the first time, that icv administration of ADN could improve the memory acquisition in animal model of sAD.