A5001710120- Polyomavirus and related diseases
- Tuberous Sclerosis Complex Research
- Chromatin Remodeling and Cancer
- Immune responses and vaccinations
- Epigenetics and DNA Methylation
- Family Support in Illness
University of California, Los Angeles
2021-2024
Postnatal immune activation leads to social deficits in a mouse model of TSC by abnormal interferon production microglia.
There is evidence that viral infections during pre-natal development constitute a risk factor for neuropsychiatric disorders and lead to learning memory deficits. However, little known about why early post-natal have different impact on depending the sex of subject. We previously showed immune activation induces hippocampal-dependent social deficits in male, but not female, mouse model tuberous sclerosis complex (TSC; Tsc2+/− mice). Here, we explored viral-like challenge object memory....
Tuberous sclerosis complex is a genetic disorder associated with high rates of intellectual disability and autism. Mice heterozygous null mutation the Tsc2 gene (Tsc2+/-) show deficits in hippocampal-dependent tasks abnormal long-term potentiation (LTP) hippocampal CA1 region. Although previous studies focused on role neuronal memory phenotypes rodent models tuberous complex, results presented here demonstrate for microglia these deficits.To test possible type I interferon LTP Tsc2+/- mice,...
Abstract Tuberous Sclerosis Complex (TSC) is a genetic disorder associated with high rates of intellectual disability and autism. Although previous studies focused on the role neuronal deficits in memory phenotypes rodent models TSC, results presented here demonstrate for microglia these deficits. Mice heterozygous null mutation Tsc2 gene (Tsc2 +/- ), show hippocampal dependent tasks, as well abnormal long-term potentiation (LTP) CA1 region. Here, we that type I interferon signaling (IFN1)...