Anti-anxiety drugs include fast-working benzodiazepines and slow-working serotonin and norepinephrin inhibitors. Benzodiazepines, the most well known of which are the muscle relaxant Valium and the neuro-retarding chemical Xanax, quickly reduce anxiety but they have serious detrimental health effects. Because they work by increasing the body's levels of the neurological depressant GABA, they slow down nearly all of the brain's cognitive functions, including working memory and short-term memory, reports a Tel Aviv research team in the August 1, 2010 issue of "Neuron." Benzodiazepines therefore should not be used to reverse memory loss. The slow-working anti-anxiety drugs, on the other hand, show great promise in reversing memory loss and restoring optimal brain function.
Recovery After Stroke
Escitalopram, or Lexapro, is an serotonin reuptake inhibitor approved for the treatment of depression and generalized anxiety disorder. In addition to its anti-anxiety and anti-depressive effects, escitalopram also has regenerative effects on brain tissue, reports a research team in the February 2010 issue of "Archives of General Psychiatry." The team tested the drug in a random trial involving 129 stroke patients and found that the drug can significantly improve learning, thinking and memory.
A stroke is an obstruction of blood flow in the brain that stems from a clot or a hemorrhage. When blood flow is cut off, neurons in the affected area do not get enough oxygen and nutrients and quickly begin to die. Within the first few hours after the occurrence of a stroke, treatment with blood-thinning and anti-swelling medications and surgery may prevent extensive damage. But once damage has occurred, these kinds of treatments are ineffective. Escitalopram, however, can reverse brain damage to some extent because it stimulates the production of molecules required for the brain to grow new neurons.
VEGF Production in the Brain
While escitalopram is the only selective serotonin reuptake inhibitor currently approved for anxiety, many other selective serotonin reuptake inhibitors approved for depression may be effective in the treatment of anxiety as well. As the breakdown of stress hormones requires serotonin, low serotonin levels are predictors of anxiety. Selective serotonin reuptake inhibitors work selective on serotonin transporters in the brain and thereby increase the brain's serotonin levels, leading to a reduction of low-serotonin triggered anxiety.
Besides increasing serotonin levels, serotonin reuptake inhibitors also increase the production of vascular endothelial growth factor, or VEGF, in the hippocampus, the brain's main memory center, reports a Rockefeller research team in the March 2007 issue of "Proceedings of the National Academy of Sciences." Stress and anxiety decrease the expression of VEGF, which can lead to memory loss. Serotonin reuptake inhibitors can reverse this condition by restoring healthy levels of VEGF, which may lead to a regeneration of damaged tissue in the hippocampus.
Tricyclic Antidepressants for Memory Loss
Another group of drugs with anti-anxiety effects are the so-called tricyclic antidepressants. They are prescribed primarily for major depression but also have anti-anxiety and anti-psychotic indications. Most of the drugs in this group are serotonin and norepinephrine reuptake inhibitors. They inhibit serotonin and the norepinephrine transporters and thereby increase the brain's serotonin and norepineprine levels.
Like selective serotonin reuptake inhibitors, tricyclic antidepressants can stimulate the function of brain neurons, reports an Emory University research team in the July 2009 issue of "Chemistry and Biology." The researchers believe that the drug protects memory neurons from glucose and oxygen deprivation. Since degenerative memory diseases such as Alzheimer's and prefrontal-cortical dementia are degenerative diseases that stem from a blockage of nutrients and oxygen to neurons in the hippocampus and the prefrontal cortex, respectively, triclic antidepressant seem promising in slowing down the degenerative effects of these diseases.
References
- "Arch Gen Psychiatry"; Escitalopram and Enhancement of Cognitive Recovery Following Stroke; Ricardo E. Jorge, et al; February 2010
- "PNAS"; VEGF is an Essential Mediator of the Neurogenic and Behavioral Actions of Antidepressants; Jennifer L. Warner-Schmidt and Ronald S. Duman; March 2007
- "Chemistry and Biology"; Amitriptyline is a TrkA and TrkB receptor agonist that promotes TrkA/TrkB heterdodimerization and has potent neurotrophic activity; S-W Jang, et.; July 2009
- "Neuron"; Basal GABA Regulates GABABR Conformation and Release Probability at Single Hippocampal Synapses; Tal Laviv, et al.; August 2010
