Neuroscience & Alzheimer's Research
Neurons are extremely interesting cells because genetic information and most of the synthetic machinery is located in one region of the cell and materials must be transported long distances (sometimes up to 1 meter) to supply the axon terminus. Disruption of this transport and alterations in the structural proteins often lead to protein aggregation and intracellular inclusions associated with neurodegenerative diseases. Neurobiologists within the department are working to decipher why these cellular disruptions occur, and how they lead to disease.
A major focus is on Alzheimer’s disease, with studies aimed at developing an understanding of:
- How microtubule associated proteins abnormally associate to form filamentous inclusions
- How abnormal processing of the beta-amyloid peptide leads to toxic aggregates
- The normal cellular and molecular mechanisms that regulate neurite elongation during development and how toxic cellular aggregate lead to neurite degeneration
- The mechanisms that regulate neural plasticity
Adriana Ferreira Lab
Our work focuses on the mechanisms underlying neurite degeneration and synapse loss in Alzheimer’s disease and related neurodegenerative disorders. We are interested in the relationship between beta-amyloid deposition and the progressive formation of dystrophic neurites and cell death in hippocampal neurons.
Saba Parvez Lab
Our lab is interested in understanding how certain noncoding genomic regions regulate animal development. We employ high-throughput functional genetics in a zebrafish model system to answer these questions. We are specifically interested in poison exons, a class of noncoding alternative exons, whose inclusion results in degradation of the resulting transcript through nonsense mediated decay. Misregulation of poison exons is implicated in several diseases including cardiovascular and neurodevelopmental disorders. We investigate what roles poison exons play in animal development and disease.
