Reversing Cognitive Deficits in the PTEN Knockout Model of ASD
Elste, Noah
Elste, Noah
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Abstract
Despite the prevalence of ASD, the relationship between its underlying genetics and the expression of its varied cognitive deficits remain vexing and complex for clinicians and basic scientists (Srivastava et al., 2014). A candidate gene mutation in some ASD cases is the Phosphatase and Tensin Homolog (PTEN) gene, which codes for the PTEN phosphatase (Busch et al., 2019). When mutated or absent in neurons, cell overgrowth and hyperexcitability occur (Getz et al., 2022). We have found that PTEN loss ultimately leads to a specific cognitive deficit in the association of objects with novel spatial locations during performance of a spatial accuracy task. High density silicon neural probes are also used in a head-fixed apparatus to show functional differences in the local field potentials and action potential properties of hippocampal cells. Further research will help specify how cellular and morphological changes can create a specific behavioral phenotype, and gain insights into the relationship between ASD, epilepsy, and their reciprocal relationship with cognitive function.
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Undergraduate
Date
2024-01-01