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How can nerve cell communication in the brain be repaired in Alzheimer’s disease?
Farr Niere, Ph.D.
Wake Forest University Health Sciences
Winston-Salem, NC - United States
Background
Learning and memory rely on communication between nerve cells in the brain. Nerve cells communicate with each other through specialized cell structures called synapses. The synapse must contain a specific amount of molecules for these messages to move between nerve cells. One of these molecules is Calcium; calcium plays a key role in communication between nerve cells and the level of calcium in the synapse is controlled by proteins on the surface of the nerve cells that allow calcium to enter or exit the cell. Past studies have found altered levels of calcium molecules and the proteins that transport calcium in the brains of people with Alzheimer’s disease.
In preliminary studies, Dr. Farr Niere discovered that a protein called alpha2delta2 is lower in the brains of people with Alzheimer's disease. Alpha2delta2 is known to be important for calcium transport. Dr. Fierre also found that another protein, DJ-1, blocks the formation of alpha2delta2, and is higher in the brains of people with Alzheimer’s disease. Based on these findings, Dr. Niere believes that low levels of alpha2delta2 could impact calcium molecule levels in synapses leading to a disruption in nerve cell communication.
Research Plan
For their study, Dr. Niere and colleagues will use genetically engineered Alzheimer’s-like mice. The researchers will delete the gene that provides instructions to make DJ-1. Dr. Niere will then determine whether mice that lack DJ-1 have restored levels of calcium and transport in the synapses. Furthermore, the researchers will also determine if lacking the DJ-1 improves learning and memory in these Alzheimer’s-like mice at 6 and 13 months of age.
Impact
The study results may provide further understanding of how the loss of calcium in the brain contributes to impaired nerve cell communication and impact progression of Alzheimer's disease.
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