Lidiette Angeles Perez
University of Texas Southwestern Medical Center
Investigating the contributions of cerebellar-hippocampal circuitry to social behaviors, cognition, and dementia
About 10% of the United States population will develop age-related dementias, disorders characterized by memory loss, social impairments, and behavioral changes. Despite their high prevalence and increasing cost, there is no effective treatment for dementias. Extensive data supports the hippocampus as one of the first brain regions to be impacted by neurodegeneration; however, the circuit networks working in tandem with the hippocampus in regulation of behaviors impacted in these diseases and whether these networks might offer potential therapeutic targets remain poorly explored. Studies have implicated inputs to hippocampal CA2 from the supramammillary nucleus of the hypothalamus to be necessary for social memory, while we have recently shown important roles for the cerebellum in regulation of these behaviors. We have also evidenced that cerebellar modulation can improve social memory and cognitive flexibility. Furthermore, in this presentation we demonstrate cerebellar modulation can impact both supramamillary nuclear and hippocampal activity. Thus, we hypothesize that the cerebellum impacts hippocampal activity and this modulation will influence hippocampal-dependent social and cognitive behaviors affected in dementia. To test this, I combine in vivo chemogenetic approaches with viral tracing, in vivo eletrophysiology, genetic models, and behavioral evaluation. My results will not only advance the understanding of cerebellar contributions to non-motor functions and delineate novel cerebellar-hippocampal circuit contributions to behavior but could inform new therapeutic avenues for these debilitating illnesses.
SACNAS Virtual National Diversity in STEM Conference, October 25-29, 2021
- Dentel, B, Angeles-Perez, L, Ren, C, Jakkamsetti, V, Holley, AJ, Caballero, D, Oh, E, Gibson, J, Pascual, JM, Huber, KM et al.. Increased glycine contributes to synaptic dysfunction and early mortality in Nprl2 seizure model. iScience 2022; 25 (5): 104334. PubMed PMID:35602938 PubMed Central PMC9118754.