PHOENIX, Ariz. Jan. 15, 2009 A scientific group led by the Translational Genomics Research Institute (TGen) have identified three kinases, or proteins, that dismantle connections within brain cells, which may lead to memory loss associated with Alzheimer's disease.
These findings, the results of a multi-year TGen study, are published in this month's edition of BMC Genomics in a paper titled: High-content siRNA screening of the kinome identifies kinases involved in Alzheimer's disease-related tau hyperphosphorylation.
The three kinases were found to cause a malfunction in tau, a protein critical to the formation of the microtubule bridges within brain cells, or neurons. These bridges support the synaptic connections that, like computer circuits, allow neurons to communicate with each other.
"The ultimate result of tau dysfunction is that neurons lose their connections to other neurons, and when neurons are no longer communicating, that has profound effects on cognition the ability to think and reason,'' said Dr. Travis Dunckley, an Associate Investigator in TGen's Neurodegenerative Research Unit and the scientific paper's senior author.
Tau performs a critical role in the brain by helping bind together microtubules, which are sub-cellular structures that create scaffolding in the neurons, allowing them to stretch out along bridges called axons. The axons support the synaptic, or chemical, connections with other neurons.
Under normal circumstances, kinases regulate tau by adding phosphates. This process, called tau phosphorylation, enables the microtubules to unbind and then bind again, allowing brain cells to connect and reconnect with other brain cells.
"That facilitates synaptic plasticity. It facilitates the ability of people to form new memories to form new connections between different neurons and maintain those memories. So, it's an essential function,'' Dr. Dunckley said.
|Contact: Steve Yozwiak|
The Translational Genomics Research Institute