The ventral hippocampus (vHPC) is particularly sensitive to the pathology of Alzheimer’s disease (AD). Proper activity of the vHPC is mediated by parvalbumin (PV) interneurons, which constitute 25% of all inhibitory GABAergic cells. They play a crucial role in processing prepulse inhibition of the acoustic startle reflex (PPI) and social memory, which are managed by the vHPC. In this study, we first investigated the vHPC-related deficits in PPI and social novelty preference in 10-month-old APP/PS1 mice, a transgenic model of AD. We found a significant impairment in startle reduction in APP/PS1 mice when compared to wild types. While sociability was not affected in these mice, results from the three-chamber task indicate a reduced preference for social novelty. Subsequently, we tested whether these deficits could be alleviated by chemogenetic activation of PV interneurons in the vHPC. We observed no effect of PV interneuron activation on sociability; the analysis of social novelty preference and PPI is currently ongoing. Preliminary results suggest that this activation alone may not be sufficient to mitigate AD-related behavioral deficits. However, further data analysis is necessary to draw more conclusions. This research was supported by project No. LX22NPO5107 (MŠMT) funded by the European Union – Next Generation EU.