Adriana Ferreira
Title: Associate Professor
Research area: Molecular cell biology of synaptogenesis
Degree: M.D., Ph.D., Universidad Nacional de Cordoba (Argentina)
Voice: 312.503.4300
Fax: 312.503.7345
e-mail:  a-ferreira@northwestern.edu

Detailed research description: The research in the Ferreira laboratory is focused on the mechanisms underlying neurite degeneration and synapse loss in Alzheimer’s disease and related neurodegenerative disorders. Specifically, we are interested in the relationship between beta-amyloid deposition and the progressive formation of dystrophic neurites and cell death in hippocampal neurons. Recently, we have determined that the microtubule associated protein tau plays an essential role in beta-amyloid-induced neurite degeneration. These results constitute the first direct evidence of a mechanistic link between beta-amyloid deposition and tau in central neurons. Furthermore, our results indicated that beta-amyloid induces calpain-mediated tau cleavage leading to the generation of a 17 kDa neurotoxic fragment in hippocampal neurons both in culture model systems and in AD human brain samples. Currently, we are analyzing the mechanisms by which this tau fragment mediates beta-amyloid-induced neurite degeneration. These studies are being performed by means of a variety of cell and molecular biology techniques.

 

Representative publications:

Rapoport, M., Dawson, H.N., Binder, L.I., Vitek, M. and Ferreira, A. Tau is essential for beta-amyloid induced neurotoxicity. Proc. Natl. Acad. Sci. USA. 99: 6364-6369, 2002.

 

 Park, S-Y and Ferreira, A. The generation of a 17 kDa neurotoxic fragment: An alternative mechanism by which tau mediates AB-induced neurodegeneration.  J. of Neurosci. 25: 5365-5375, 2005.

 

 Kelly, B., Vassar, R., and Ferreira, A. Beta-amyloid-induced dynamin I depletion in hippocampal neurons: A potential mechanisms for early cognitive decline in Alzheimer’s disease. J. Biol. Chem. 280: 31746-31753, 2005.

 

 Kelly, B., and Ferreira, A. Beta-amyloid-induced dynamin 1 degradation is mediated by NMDA receptors in hippocampal neurons. J. Biol. Chem. 281: 28079-28089, 2006.

 

 Park, S-Y., Tournell, C.E, Sinjoanu, R.C., and Ferreira, A. Caspase 3- and calpain-mediated tau cleavage are differentially prevented by estrogen and testosterone in beta-amyloid-treated hippocampal neurons. Neuroscience 144: 119-127, 2007.

 

 Nicholson, A. and Ferreira, A. Increased membrane cholesterol might render mature hippocampal neurons more susceptible to beta-amyloid-induced calpain activation and tau toxicity. J. Neurosci. 29: 4640-4651, 2009.