Topic: engram reactivation

The dentate gyrus (DG) plays a key role in memory encoding and retrieval, facilitating discrimination of the environmental inputs by separating them into non-overlapping patterns and reducing interference of stored representations. It is highly susceptible to aging-related structural and physiological changes and thought to contribute to age-related cognitive dysfunctions. In this study we examined possible age-related changes in pattern separation function and associated changes in DG cellular engrams using a contextual fear conditioning task. Young adult (3-month-old) and healthy aged (24-mo

Neuronal network imbalance and synaptic dysfunction both critically contribute to cognitive decline in AD. Network imbalance is increasingly recognized as an early characteristic of AD, which might precede and drive clinical symptoms. Early alterations in parvalbumin (PV+) interneurons contribute to this network dysfunction in AD mouse models. However, to what extent this shapes how memories are stored within the brain and drives cognitive decline remains to be determined. Our objective is to investigate synaptic, local, and network imbalances in AD, as well as their mutual dependence.We used

A de novo mutation in the DNA methyltransferase 3A gene (Dnmt3a) causes Tatton-Brown-Rahman syndrome (TBRS), a recently described genetic neurodevelopmental disorder that currently has no treatment. Patients display tall stature and intellectual disability. Dnmt3a encodes for the enzymes Dnmt3a1 and Dnmt3a2. These enzymes, according to literature as well as published and unpublished work from our lab, play a crucial role in memory formation in the adult hippocampus. However, how brain and neuronal function is affected in TBRS remains poorly understood. This project aims to bridge this gap of k