Monoamine Oxidases (MAOs) as Privileged Molecular Targets in Neuroscience: Research Literature Analysis

Abstract

Background : Monoamine oxidases (MAOs) were discovered nearly a century ago. This article aims to analyze the research literature landscape associated with MAOs as privileged class of neuronal enzymes (neuroenzymes) with key functions in the processes of neurodegeneration, serving as important biological targets in neuroscience. With the accumulating publications on this topic, we aimed to evaluate the publication and citation performance of the contributors, reveal the popular research themes, and identify its historical roots. Methods : The electronic database of Web of Science (WoS) Core Collection was searched to identify publications related to MAOs, which were analyzed according to their publication year, authorship, institutions, countries/regions, journal title, WoS category, total citation count, and publication type. VOSviewer was utilized to visualize the citation patterns of the words appearing in the titles and abstracts, and author keywords. CRExplorer was utilized to identify seminal references cited by the MAO publications. Results : The literature analysis was based on 19,854 publications. Most of them were original articles ( n = 15,148, 76.3%) and reviews ( n = 2,039, 10.3%). The top five WoS categories of the analyzed MAO publications were Pharmacology/Pharmacy ( n = 4,664, 23.5%), Neurosciences ( n = 4,416, 22.2%), Psychiatry ( n = 2,906, 14.6%), Biochemistry/Molecular Biology ( n = 2,691, 13.6%), and Clinical Neurology ( n = 1,754, 8.8%). The top 10 institutions are scattered in the United States, UK, France, Sweden, Canada, Israel, and Russia, while the top 10 countries/regions with the most intensive research on the field of MAOs are the United States, followed by European and Asian countries. More highly cited publications generally involved neurotransmitters, such as dopamine (DA), serotonin, and norepinephrine (NE), as well as the MAO-A inhibitors moclobemide and clorgyline, and the irreversible MAO-B inhibitors selegiline and rasagiline. Conclusion : Through decades of research, the literature has accumulated many publications investigating the therapeutic effects of MAO inhibitors (MAOIs) on various neurological conditions, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and depression. We envision that MAO literature will continue to grow steadily, with more new therapeutic candidates being tested for better management of neurological conditions, in particular, with the development of multi-target acting drugs against neurodegenerative diseases.

Pharmacological Mechanisms Underlying the Neuroprotective Effects of Alpinia oxyphylla Miq. on Alzheimer’s Disease

“…Based on the manual annotation map, terpenes demonstrated a function on regulating the synthesis and release of neurotransmitters, as well as signal transmission, dendritic growth, and spine formation, including synaptic plasticity in the nervous system ( Figure 6). The left panel of Figure 6 shows that SLC18A1, 2, and 3 may have a role in synaptic vesicle cycling, acetylcholinesterase (ACHE) [43], and amine oxidase [flavin-containing] A (MAOA) [44,45] signaling, which have been shown to be involved in tryptophan metabolism, clycerophospholipid metabolism, and also related to cocaine and amphetamine addiction, as well as alcoholism, and Parkinson's disease in the presynaptic nerve terminal. Neurotransmitters, such as dopamine (DA, hsa04728), serotonin (5-HT, hsa04726), and acetylcholine (ACh, has04725) work on muscarinic acetylcholine receptor M2 (CHRM2) [46] and MAOA for DA metabolism in glial cells, as well as on CHRNA7 [47] and CHRM1 [48] for calcium (Ca 2+ ) storage by Ca 2+ -induced Ca 2+ release (CICR) [49], and on HTR2A-SLC6A4-IP3-TRPC1 [50,51] pathway for Ca 2+ transport, respectively.…”

“…On the postsynaptic cell membrane, DA, is the prototypical slow neurotransmitter of the mammalian brain, which interacts with D1-like receptors DRD1 and DRD5 [52,53], both positively coupled to adenylyl cyclase (AC) and cAMP production, which are activated and regulated downstream of PTGS1 and NOS1 expression. While the activation of D2-like receptors DRD2, DRD3, and DRD4 have exactly the reverse effect on regulating the production of AC and cAMP in dopaminergic synapse pathway The left panel of Figure 6 shows that SLC18A1, 2, and 3 may have a role in synaptic vesicle cycling, acetylcholinesterase (ACHE) [42], and amine oxidase [flavin-containing] A (MAOA) [43,44] signaling, which have been shown to be involved in tryptophan metabolism, clycerophospholipid metabolism, and also related to cocaine and amphetamine addiction, as well as alcoholism, and Parkinson's disease in the presynaptic nerve terminal. Neurotransmitters, such as dopamine (DA, hsa04728), serotonin (5-HT, hsa04726), and acetylcholine (ACh, has04725) work on muscarinic acetylcholine receptor M2 (CHRM2) [45] and MAOA for DA metabolism in glial cells, as well as on CHRNA7 [46] and CHRM1 [47] for calcium (Ca 2+ ) storage by Ca 2+ -induced Ca 2+ release (CICR) [48], and on HTR2A-SLC6A4-IP3-TRPC1 [49,50] pathway for Ca 2+ transport, respectively.…”

Neuroprotective Mechanisms of Three Natural Antioxidants on a Rat Model of Parkinson’s Disease: A Comparative Study

“…Current therapy for the disease is symptomatic and fails to influence the course of the disease and its progression [10,11].…”

Hyperlipidemia Downregulate Brain Antioxidant Defense Enzymes and Neurotrophins in Rats: Assessment of the Modulatory Potential of EPA+DHA and Zerumbone

“…The monoamine oxidase catalyzes the oxidation of neurotransmitters and influence brain function. [ 27 ] Surprisingly, hyperlipidemia increased the monoamine oxidase activity in the brain, indicating a larger effect of elevated lipids (as observed in hyperlipidemia) on neurotransmitters level that may have a bearing on the neurodegenerative diseases. Also, the potential link between the diminished brain antioxidant defense enzymes and regulation of monoamine oxidase activity needs to be further elucidated.…”