Professor Shelanski's laboratory is investigating the mechanism of memory disruption and synaptic dysfunction in Alzheimer's Disease. The lab uses a combination of cell culture and transgenic animal approaches in an attempt to understand why the over-expression of the amyloid precursor protein (APP) or direct application of its active peptide, A-beta, inhibits intracellular signaling in neuronal cells and leads to alterations of electrical activity, dendritic spine morphology and behavior. In the past two years, Shelanski's attention has been on the PKA-CREB signaling pathway and on the role of ubiquitin c-terminal hydrolase-L1 (Uch-L1) in regulating these events.
Lopez-Toledano MA, Shelanski ML. Increased neurogenesis in young transgenic mice overexpressing human APP(Sw, Ind). J Alzheimers Dis. 2007 Nov;12(3):229-40.
Vitolo O, Gong B, Cao Z, Ishii H, Jaracz S, Nakanishi K, Arancio O, Dzyuba SV, Lefort R, Shelanski M. Protection against beta-amyloid induced abnormal synaptic function and cell death by Ginkgolide J. Neurobiol Aging. 2007 Jul 17. [Epub ahead of print]
Padmanabhan J, Brown K, Shelanski ML. Cell cycle inhibition and retinoblastoma protein overexpression prevent Purkinje cell death in organotypic slice cultures. Dev Neurobiol. 2007 May;67(6):818-26.