Neurosciences

We have establish that the synaptic modulator reelin is a critical mediator of psychiatric vulnerability because (1) periadolescent High Fat Diet (pHFD) selectively downregulates prefrontal RELN+ cells and (2) augmenting mPFC RELN levels prevents the pHFD-induced prefrontal cognitive deficits. Our findings have primary relevance to obese individuals who are at an increased risk of developing neurological cognitive comorbidities.

We have shown that pyramidal neurons, mossy cells, and some parvalbumin (PARV)-positive hippocampal interneurons in 2- and 8-month-old (mo) VLW mice accumulate phosphorylated forms of Tau (P-Tau). We propose that alterations in the GABAergic SHP, together with a dysfunction of P-Tau–accumulating PARV-positive neurons, contribute to the cognitive deficits and altered patterns of hippocampal activity present in tauopathies.

We have shown that loss?of?function of SNARE complex members results in motor axon guidance defects in fly and chick embryos. Our data point to an evolutionarily conserved role of the SNARE complex proteins in motor axon guidance, thereby pinpointing an important function of SNARE proteins in axonal navigation in vivo.

We have developed a new method to validate somatic DNA mutations. We combine a recently developed software with a method that cuts DNA by using restriction enzymes at the sites of the variation.

Ack1 (activated Cdc42-associated tyrosine kinase) is a non-receptor tyrosine kinase that is highly expressed in brain. Here we screened mouse brain samples to identify proteins that interact with this kinase. Using mass spectrometry analysis, we identified new putative partners for Ack1 including cytoskeletal proteins and synapse mediators.