Tampa, FL (Sept. 15, 2011) -- Decreasing expression of a protein associated with susceptibility to depression made old mice resistant to depressive-like behavior while improving their hormonal response to stress, a study led by researchers at the University of South Florida found. The lack of this protein, FKBP51, did not adversely affect their memory, learning, or basic motor functions.
The study suggests that drug discovery efforts aimed at reducing levels of the protein FKBP51 may yield new antidepressant therapies. The findings appear online today (Sept. 15, 2011) in the journal PLoS ONE.
The multidisciplinary research team included scientists from Vanderbilt University Medical Center and the University of Texas at El Paso as well as the USF Health Byrd Alzheimer's Institute.
"About a third of patients are resistant to treatment with standard antidepressant medications, so we need to look for other potential therapeutic targets," said principal investigator Chad Dickey, PhD, assistant professor of molecular medicine at the USF Health Byrd Alzheimer's Institute.
"We've shown that, because FKBP51 appears to act on the genetic liability to abnormal mood and anxiety states, it may offer a much needed treatment tool for secondary prevention of depression recurrence and relapse."
Dickey and his colleagues were using a mouse model with the FKBP5 gene deleted to help study the potential role of the protein it produces, FKBP51, in the progression of Alzheimer's disease. The protein increases with old age, and a reduction of FKBP51 levels has been shown to decrease the burden of tau, a hallmark protein associated with Alzheimer's disease.
FKBP51, a protein encoded by the FKBP5 gene, is highly expressed in the hypothalamus-pituitary-adrenal (HPA) axis, a major part of the brain's circuitry that controls neuroendocrine system responses to stress. Human genetic studies over the last decade have indicate
|Contact: Anne DeLotto Baier|
University of South Florida (USF Health)