LAUSR

HighlightsBetulinic acid could prevent neurobehavioral deficits in AD‐induced rats.Betulinic acid could prevent LTP deficits in AD‐induced rats.There is the best effect of 1:4 molar ratio toward A&bgr; to BA interaction.Congo‐red staining showed reduced A&bgr; fibril plaque number in BA pretreated rats. Abstract Alzheimer's disease (AD) is a common disorder characterized by aggregation and conversion of amyloid beta (A&bgr;) monomers to fibrils. Betulinic acid (BA) strongly accelerated this pathway through circumventing the oligomeric intermediate state. BA at doses of 0.2 and 0.4 &mgr;M/10 &mgr;l/rat (intra‐hippocampal or i.h injection, vehicle: DMSO) was bilaterally administrated 180 and 10 min before co‐administration of A&bgr; (0.1 &mgr;M/5 &mgr;l/rat, i.h injection, vehicle: PBS) and Streptozotocin (STZ, 1.5 mg/kg/10 &mgr;l/rat, intracerebroventricular or i.c.v. injection, vehicle: aCSF). The behavioral assessments (spatial and passive avoidance memory, anxiety, locomotion, depression, and motor coordination), electrophysiological evaluations (hippocampal long‐ term potentiation (LTP)) as well as histological changes were evaluated 30 days after injections. The indices of spatial and passive avoidance memory, anxiety/depression and LTP records were significantly impaired in AD rats in comparison with the sham. Pretreatment of BA (0.4 &mgr;M) showed a more significant effect on memory, anxiety, all LTP parameters, and histological damage compared to a low dose in contrast to the AD group. Overall, BA pretreatment was able to prevent AD‐induced neurobehavioral and LTP deficits in rats and the best effect was observed in molar ratio of 1:4 (A&bgr; to BA).