New Research
A potential protein therapy for autism
Archived article from Sep 26, 2005
By Joseph Blumberg
Bonnie Firestein likens nerve cells to trees. Some are short and bushy with many branches while others are tall with a few branches coming out of one or two main trunks. Different branching patterns correlate with specific disorders and Firestein’s quest is to discover how these dissimilar patterns come about and why.
Firestein, an assistant professor of cell biology and neuroscience in Piscataway, is examining the role of the protein snapin in nerve branch, or dendrite, patterning and its potential as a drug target in therapies aimed at learning and memory disorders. While disorders like autism may arise from a multiplicity of causes, research at the cellular level, such as that by Firestein and her Rutgers team, is creating an important point of entry for early intervention with therapeutic drugs.
Dendrites are the input centers of neurons, where nerve cells receive information that they pass on to another nerve cell or to the brain. Abnormal decreases in dendrite branches mean fewer sites to receive information, which may impede communication.
Individuals with disorders such as autism and Rett syndrome display not only fewer branches, but also show two quite different dendrite patterns. Firestein’s most recent work explores the how and why of dendrite branching and patterning.
Patterning affects the way a cell signals, and understanding the patterning could be just as important as understanding how many branches are there, Firestein said. “Ultimately, this could lead to new drugs designed to modulate the patterning activity.”
Firestein has worked extensively with cypin, a protein that regulates dendrite numbers. Cypin works on the protein tubulin, a structural building block of the dendrite skeleton. Now Firestein’s research group has turned its attention to the protein snapin. When snapin binds to cypin, tubulin is crowded out, so fewer dendrites assemble and more branching occurs. When researchers over-expressed snapin in hippocampal neurons in the lab, the number of primary dendrites growing out of the cell body decreased, but many more secondary dendrites branched off them.
This is significant not just in identifying snapin as a protein that shapes the dendrites, but also in pinpointing a drug target to regulate the interaction of snapin with cypin, Firestein said.
Return to the Sep 26, 2005 issue
|
