Tuesday, March 13, 2007

Antidepressants help create new brain cells

Definitely another argument for using antidepressant medications in the treatment of depression.

"The study describes for the first time the molecular mechanisms and the identity of the protein, vascular endothelial growth factor (VEGF), which underlie the actions of antidepressants on new cell growth and behavior."
"Duman said recent studies demonstrated that stress decreases the expression of VEGF in the hippocampus, a region of the brain involved in the control of emotion, mood, learning, and memory, and this could contribute to the atrophy and loss of cells caused by stress and depression.
In prior groundbreaking research Duman found that antidepressants increase the expression of growth factors in the hippocampus and other regions of the brain. Duman also found that antidepressants increase the birth of new neurons in the hippocampus.
According to Duman, future studies could look at VEGF and related pathways for genetic mutations that might contribute to depression, or make a person more susceptible to depression. VEGF signaling also could provide targets for the development of novel, faster acting, and more effective therapeutic agents."

Ideally, this could mean eventually creating drugs that specifically stimulate VEGF to treat depression. But what happens when someone who is not under stress, and not depressed, takes antidepressants?



RichardT said...

I'm particularly interested in how VEGF interoperates with the dictum that "Cognitive-behavior therapy mutes overactivity in the frontal cortex, the seat of reasoning, logic, analysis and higher thought. Antidepressants raise activity there. Cognitive-behavior therapy raises activity in the limbic system, the brain's emotion center. Drug therapy lowers activity there."

Janie said...

That doesn't make much sense to me. I've heard that cognitive behavioral therapies (CBT) do cause brain changes similar to antidepressants over time.
I would think that CBT and antidepressatns (AD) would both be regulating activity in the prefrontal cortex, and that both should be decreasing 'overactivity' in the limbic system.