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Approximately 3% of healthy elderly persons living in the community have major depression. Recurrence may be as high as 40%. Suicide rates are nearly twice as high in depressed patients as in the general population. Major depression is more common in medically ill patients who are older than 70 years and hospitalized or institutionalized.
Selegiline acts as a monoamine oxidase inhibitor (MAOI) and thereby increases levels of monoamine neurotransmitters in the brain. [17] [11] [28] [5] At typical clinical doses used for Parkinson's disease, selegiline is a selective and irreversible inhibitor of monoamine oxidase B (MAO-B), increasing brain levels of dopamine.
Serotonin syndrome (SS) is a group of symptoms that may occur with the use of certain serotonergic medications or drugs. [1] The symptoms can range from mild to severe, and are potentially fatal.
Monoamine oxidase inhibitors, or MAOIs, including phenelzine, isocarboxazid, tranylcypromine, selegiline and others. Other antidepressants, including other SSRIs, SNRIs and tricyclic antidepressants
The pharmacology of selegiline pertains to the pharmacodynamic and pharmacokinetic properties of the antiparkinsonian and antidepressant selegiline (L-deprenyl). [2] [7] [14] [19] Selegiline is available in a few different forms, including oral tablets and capsules, orally disintegrating tablets (ODTs), and transdermal patches.
The older MAOIs' heyday was mostly between the years 1957 and 1970. [43] The initial popularity of the 'classic' non-selective irreversible MAO inhibitors began to wane due to their serious interactions with sympathomimetic drugs and tyramine-containing foods that could lead to dangerous hypertensive emergencies. As a result, the use by medical ...
More severe symptoms include fever, seizures, irregular heartbeat, delirium, and coma. [76] [77] [11] If signs or symptoms arise, discontinue treatment with serotonergic agents immediately. [76] It is recommended to washout 4 to 5 half-lives of the serotonergic agent before using an MAO inhibitor. [78]
Brunner syndrome is caused by a monoamine oxidase A (MAOA) deficiency, which leads to an excess of monoamines in the brain, such as serotonin, dopamine, and norepinephrine (noradrenaline). In both mice and humans, a mutation was located on the eighth exon of the MAO-A gene, which created a dysfunctional MAO-A gene.