Search results
Results from the WOW.Com Content Network
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.
Monoamine oxidase A, also known as MAO-A, is an enzyme (E.C. 1.4.3.4) that in humans is encoded by the MAOA gene. [ 5 ] [ 6 ] This gene is one of two neighboring gene family members that encode mitochondrial enzymes which catalyze the oxidative deamination of amines , such as dopamine , norepinephrine , and serotonin .
Monoamine oxidases (MAO) (EC 1.4.3.4) are a family of enzymes that catalyze the oxidation of monoamines, employing oxygen to clip off their amine group. [ 1 ] [ 2 ] They are found bound to the outer membrane of mitochondria in most cell types of the body.
2-NAP is a potent monoamine oxidase inhibitor (MAOI), specifically of monoamine oxidase A (MAO-A) (IC 50 Tooltip half-maximal effective concentration = 420 nM). [8] [3] 1-NAP is an MAOI as well, also of MAO-A (IC 50 = 5,630 nM), but was about 13-fold less potent than 2-NAP. [3] Neither 2-NAP or 1-NAP inhibited monoamine oxidase B (MAO-B) (IC 50 ...
In addition to its MRA activity, 4-MTDMA is a fairly potent monoamine oxidase A (MAO-A) inhibitor, with an IC 50 Tooltip half-maximal inhibitory concentration of 2,100 nM. [4] [5] Potent monoamine oxidase inhibition by amphetamines has been associated with dangerous and sometimes fatal toxicity in humans. [4] [5]
Monoamine oxidase inhibitors (MAOIs) are a class of drugs that inhibit the activity of one or both monoamine oxidase enzymes: monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B). They are best known as effective antidepressants , especially for treatment-resistant depression and atypical depression . [ 1 ]
An offshoot of the monoamine hypothesis suggests that monoamine oxidase A (MAO-A), an enzyme which metabolizes monoamines, may be overly active in depressed people. This would, in turn, cause the lowered levels of monoamines.
After release into the synaptic cleft, monoamine neurotransmitter action is ended by reuptake into the presynaptic terminal. There, they can be repackaged into synaptic vesicles or degraded by the enzyme monoamine oxidase (MAO), which is a target of monoamine oxidase inhibitors, a class of antidepressants. [citation needed]