Monoamine Oxidase (MAO)
The relay of information between neurons underlies both unconscious and conscious human behaviour.Neurons communicate with one another using neurotransmitters -an endogenous chemical- as the medium of information. Regulating the synaptic cleft level of neurotransmitter is a key component to regulating the communication between neurons. One way of maintaining neurotransmitter level is through degrading enzymes. Monoamine oxidase (MAO) is a mitochondrial enzyme, which degrades neurotransmitters such as Dopaine, epinephrine, norepinephrine and tryptamines via oxidative deamination.[1]Oxidative deamination is the process in which enzymes use oxygen to switch an amine group into analdehyde group.There exist two subtypes of monoamine oxidase: MAO-A and MAO-B. Although MAO-A and B have approximately 70% DNA sequence similarity and exist adjacent to one another on the X chromosome, each subtype has their own substrate specificity and unique pharmacological inhibitors.[2] MAOs are thought to contribute to many psychiatric and neurological diseases because of their role in regulating neurotransmitter in the synapse. Dysregulation of MAO activity has been associated with pathologies such as mood disorder, changes in behaviour and neurological disorders.

Activity of Monoamine Oxidase
Activity of Monoamine Oxidase
Cartoon diagram of human MAO-B
Cartoon diagram of human MAO-B




1. MAO in depression (Mohamed M.)


1. Amine Hypothesis
2. Neurotransmitters involved
3. Affected brain region
4. Monoamine Oxidase A
4.1 Mechanisms
5. Association to Major Depression Disorder
6. Specific treatments.
6.1 MAO-A Inhibitors
7. Future Insight


2. MAO and Schizophrenia (Hyun Kyung L)


2.1 MAO on brain
2.1.1 Effect of MAO on abnormal behaviour
2.2 Correlation between MAO and Schizophrenia
2.2.1 Platelet MAO level.
2.2.2 Methylation on MAO promoter
2.3 Clinical Approach
2.3.1 MAO B inhibitors
2.3.2 Gene Therapy

3. MAO and Parkinson’s disease (Mohamed R.)


3.1 Overview
3.2 Apoptosis ER stress induced
3.2.1 Overview
3.2.2 UPR
3.2.3 ER stress pathway
3.2.4 ER stress & ER permeability
3.3 Treatment for Parkinson’s disease
3.3.1 Current MAO-B Inhibitors Overview
3.3.2 PF9601N
3.3.2.1 Overview
3.3.2.2 Inhibition of ER stress & Anti-apoptotic
3.4 Clinical Potential
3.4.1 PF9601N

4. MAO and Behavior (Teba I)


4.1 Genes to Behavior
4.1.1 Norepinephrine Effects on Behavior
4.1.2 Serotonin Effects on Behavior
4.2 Monoamine Oxidase and Criminal Behavior
4.2.1 Case Studies and Experiments
4.2.2 Environmental Factors
4.2.3 Criticisms
4.3 Applications and Treatments
4.3.1 MAO-Inhibitors and Medication
4.3.2 Therapy and Preventative Measures


5. MAO and Bipolar Disorder (Cathy D)


5.2 MAO Deficiency
5.2.1 Genetics
5.2.2 Preclinical and Clinical Findings
5.3 Endophenotypes
5.4 Treatments and Future Perspectives




References
[1] Kalgutkar, A and et al. Interaction of nitrogen-containing xenobiotics with monoamine oxidase (MAO) isozymes Aand B: SAR studies on MAO substrates and inhibitors. Chemical Research in Toxicology. (2001) 14: 1139-162.
[2] SHIH J. Molecular basis of human MAO A and B. Neuropsychopharmachology. (1991) 4(1): 1-7