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Cyclic AMP response element binding protein and brain-derived neurotrophic factor: molecules that modulate our mood?
1Department of Biological Sciences, Tata Institute of Fundamental Research, Homi Bhabha Road, Colaba, Mumbai 400 005, India.
Journal of Biosciences
|September 29, 2006
Summary
Depression pathophysiology involves neuro-circuitry damage. Cyclic AMP response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) are key molecules in depression and antidepressant action.
Area of Science:
- Neuroscience
- Psychiatry
- Molecular Biology
Background:
- Depression affects 20% of the population, with poorly understood pathophysiology.
- Mechanisms of antidepressant action remain elusive despite decades of use.
- Neuro-circuitry plasticity is increasingly implicated in depression's etiology and treatment.
Purpose of the Study:
- To review the role of CREB and BDNF in depression.
- To discuss CREB and BDNF as targets and mediators of antidepressant action.
Main Methods:
- Literature review focusing on molecular pathways.
- Analysis of studies on CREB and BDNF regulation in depression models and patients.
- Examination of antidepressant effects on CREB and BDNF.
Main Results:
- Evidence suggests damage to limbic regions contributes to depression.
- Antidepressants may reverse damage and promote adaptive plasticity.
- CREB and BDNF are regulated in depression and targeted by antidepressants.
Conclusions:
- CREB and BDNF are crucial molecules in neuronal plasticity.
- These molecules play a significant role in mood modulation.
- Targeting CREB and BDNF pathways offers potential for novel depression therapies.
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