To discover molecules that make synapses in development and destroy them in Alzheimer's disease is the purpose of our group's research. ADDLs almost instantly block LTP, a classic model for synaptic plasticity and memory. Subsequently, they cause nerve cell death by apoptosis. Gene knockouts show ADDLs act through a signal transduction pathway involving Fyn, a protein tyrosine kinase others have discovered is involved physiologically in LTP and developmental apoptosis and is overexpressed in Alzheimer's disease. Currently part of a novel theory, ADDLs may one day provide a basis for discovery of new drugs to combat Alzheimer's, a devastating disease that afflicts over 4 million people in the United States.
Cholesterol modulates alpha-secretase cleavage of amyloid precursor protein.
Focal adhesion kinase expressed by nerve cell lines shows increased tyrosine phosphorylation in response to Alzheimer's A-beta peptide.