“Blessed are the forgetful, for they get the better even of their blunders.” — Friedrich Nietzsche

“Your memory is a monster; you forget—it doesn't. It simply files things away. It keeps things for you, or hides things from you—and summons them to your recall with will of its own. You think you have a memory; but it has you!” — John Irving

“One of the keys to happiness is a bad memory.” — Rita Mae Brown

Memories are not cherished by everyone: Once they start to fade we get scared silly. We fear our brains are failing us. Your mother's voice rings clear and loud in your head: “Once lost brain cells never come back.” That was indeed what we once thought. Luckily, things are not quite that austere. Drugs that can cheer us up are sometimes also good for our brains. Slow-working antidepressants and anti-anxiety drugs show great promise in reversing memory lapses, generating new brain cells and restoring optimal brain function.

According to researchers reporting in the February 2010 issue of Archives of General Psychiatry escitalopram (Lexapro)—a selective serotonin reuptake inhibitor (SSRI) that is regularly prescribed for depression and anxiety disorders—has potential regenerative effects on brain tissue that has undergone damage following a stroke.

A stroke is an obstruction of blood flow in the brain that stems from a clot or a hemorrhage. When a clot or a hemorrhage obstructs blood flow, neurons in the affected area are deprived of oxygen and nutrients and rapidly begin to die. Within the first few hours after a stroke, treatment with blood-thinners and anti-swelling medications and surgery may prevent extensive damage. But once damage is inevitable, these kinds of treatments are ineffective.

According to the research team, however, escitalopram can reverse brain damage to some degree because it enhances the production of molecules required for the growth of new neurons. The team tested the drug in a random trial involving 129 stroke patients and found that it improved thinking, learning and memory in a significant number of the participants.

Serotonin is one of the molecules that may have restorative effects on the brain. High levels of stress are associated with increased processing of negative emotions. As the breakdown of stress hormones requires serotonin, high levels of stress could lead to low serotonin levels. SSRIs work selectively on the brain’s serotonin transporters. These tiny molecules transport serotonin back into the neurons. Once inside the brain cells serotonin cannot facilitate cell communication. By blocking the serotonin transporters, SSRIs increase the brain's serotonin levels, leading to increased levels of serotonin.

Escitalopram is the newest SSRI on the marked. But many other SSRIs approved for depression may have similar, restorative effects on the brain. Besides increasing serotonin levels, SSRIs 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. SSRS can reverse this condition by restoring healthy levels of VEGF. This can lead to a regeneration of damaged tissue in the hippocampus.

Tricyclic antidepressants are another group of drugs with brain-optimizing effects, reports an Emory University research team in the July 2009 issue of Chemistry and Biology. Tricyclic antidepressants are prescribed primarily for major depression but they also have anti-anxiety and anti-psychotic indications. Most chemicals in this group are serotonin and norepinephrine reuptake inhibitors. They inhibit the serotonin and norepinephrine transporters, delaying the absorption of serotonin and norepinephrine into the cells. This increases the extra-cellular levels of the chemical and hence its availability for promoting communication among brain cells.

The Emory researchers believe that tricyclic antidepressants protect memory neurons from glucose and oxygen deprivation. Since degenerative memory diseases, such as prefrontal-cortical dementia and Alzheimer’s disease, stem from a blockage of nutrients and oxygen to neurons in the hippocampus and the prefrontal cortex, tricyclic antidepressants could be promising in slowing down the damaging effects of these diseases.

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