Activity-dependent genetic labeling during behavioral learning shows Fragile-X syndrome model mice exhibit impaired hippocampal engram reactivation, and that enriched environment experience improves fear memory retrieval by enhancing engram reactivation efficacy.

The capacity for new cerebellum-dependent learning is influenced by the recent history of neural activity in a mouse model of Fragile X syndrome, suggesting a role for metaplasticity.

Behavioral and pharmaceutical interventions reverse defects associated with increased cerebellar long-term depression in a mouse model of Fragile X syndrome.

Computational modeling and analysis of mouse neural population data finds that the excitation/inhibition imbalance theory of brain disorders is too limited to account for key changes in neural activity statistics.

Targeting Abelson kinase can be beneficial for treating disorders characterized by dysregulated Down Syndrome Cell Adhesion Molecule signaling.

An automatic computer vision analysis approach can assist in the diagnosis of rare genetic disorders by using ordinary photographs of patients.

Circuit-based intervention corrects irreconcilable excitability defects between dentate granule cells and mossy cells in Fmr1 knockout mice, representing a promising strategy to restore the dentate excitation/inhibition balance and circuit computations.

The molecular determinants for neuronal subcellular RNA transport by FMRP are defined, with interactions between RNA G-quadruplexes and the RGG domain of FMRP being of critical importance.

A novel neurodevelopmental role for FMRP in collaboration with MAP1B, jointly orchestrating neuronal migration by influencing the microtubular cytoskeleton.

Postnatal, postsynaptic loss of FMRP specifically weakens callosal synaptic inputs onto L2/3 pyramidal neurons, in requirement ofnormal sensory experience, through downregulating AMPA receptor transmission and without affecting local synaptic inputs during cortical circuit development.