scholarly journals Possible Therapeutic Effect of T-794, a Novel Reversible Inhibitor of Monoamine Oxidase-A, on Post-Stroke Emotional Disturbances, Assessed in Animal Models of Depression.

1997 ◽  
Vol 20 (4) ◽  
pp. 349-353 ◽  
Author(s):  
Masaya KATO ◽  
Hiroshi IWATA ◽  
Taiichi KATAYAMA ◽  
Hidetoshi ASAI ◽  
Hiroshi NARITA ◽  
...  
Keyword(s):  
Animal Models ◽  
Monoamine Oxidase ◽  
Therapeutic Effect ◽  
Emotional Disturbances ◽  
Monoamine Oxidase A ◽  
Reversible Inhibitor ◽  
Post Stroke ◽  
Animal Models Of Depression

Rhamnocitrin isolated from Prunus padus var. seoulensis: A potent and selective reversible inhibitor of human monoamine oxidase A

2019 ◽  
Vol 83 ◽  
pp. 317-325 ◽  
Author(s):  
Seung Cheol Baek ◽  
Mi Hyeon Park ◽  
Hyung Won Ryu ◽  
Jae Pil Lee ◽  
Myung-Gyun Kang ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase A ◽  
Reversible Inhibitor ◽  
Prunus Padus

Post-Stroke Fatigue May Be Associated with the Promoter Region of a Monoamine Oxidase A Gene Polymorphism

2016 ◽  
Vol 43 (1-2) ◽  
pp. 54-58 ◽  
Author(s):  
Smi Choi-Kwon ◽  
Mihye Ko ◽  
Sang-Eun Jun ◽  
Juhan Kim ◽  
Kyung-Hee Cho ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Promoter Region ◽  
Tryptophan Hydroxylase ◽  
Variable Number Tandem Repeat ◽  
Variable Number ◽  
Monoamine Oxidase A ◽  
Potential Contribution ◽  
Female Patients ◽  
Post Stroke ◽  
Mao A

Background: Post-stroke fatigue (PSF) is a common sequela of stroke. Despite reports of serotonergic involvement in the etiology of PSF, the potential contribution of serotonergic genes in the development of PSF needs to be investigated. Methods: A total of 373 patients, who experienced ischemic stroke for PSF, were evaluated 3 months after the stroke. PSF was assessed using the Fatigue Severity Scale. The genomic DNA collected and stored in a -70°C freezer was genotyped for 6 polymorphisms in genes associated with serotonin synthesis (tryptophan hydroxylase 1 (TPH1) A218C, TPH2 rs10879355, and TPH2 rs4641528), transport (the promoter region of the serotonin transporter protein), and catabolism (the 30-bp functional variable number tandem repeat) polymorphism in the promoter region of monoamine oxidase A (MAO-A). Results: Among the 373 patients, 164 (44%) had PSF. All patients were ethnic Koreans. Of the 6 polymorphisms examined, only one marker, that is, low-activity MAO-A was associated with PSF (p < 0.05) in female patients. Multiple logistic regression analyses showed that post-stroke depression (PSD; 95% CI 1.561-14.323, p = 0.006) and low MAO-A activity (95% CI 0.166-0.722, p = 0.005) were factors associated with PSF in female patients, whereas only PSD (95% CI 5.511-65.269, p = 0.000) was associated with PSF in male patients. Conclusions: Our findings suggest that PSF may be associated with a genetic polymorphism involving MAO-A, at least in female stroke patients.

Brofaromine in Panic Disorder: A Pilot Study with a New Reversible Inhibitor of Monoamine Oxidase-A

1992 ◽  
Vol 25 (06) ◽  
pp. 261-264 ◽  
Author(s):  
D. Garcia-Borreguero ◽  
C. Lauer ◽  
A. Özdaglar ◽  
K. Wiedemann ◽  
F. Holsboer ◽  
...  
Keyword(s):  
Pilot Study ◽  
Panic Disorder ◽  
Monoamine Oxidase ◽  
Monoamine Oxidase A ◽  
Reversible Inhibitor

scholarly journals Neurochemical Characterization of T-794, a Novel Reversible Inhibitor of Monoamine Oxidase-A

1997 ◽  
Vol 73 ◽  
pp. 247
Author(s):  
Taiichi Katayama ◽  
Hiroshi Iwata ◽  
Masaya Kato ◽  
Hidetoshi Asai ◽  
Yasuhiro Yamada ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase A ◽  
Reversible Inhibitor

scholarly journals Potentials of Curcumin as an Antidepressant

2009 ◽  
Vol 9 ◽  
pp. 1233-1241 ◽  
Author(s):  
S.K. Kulkarni ◽  
Ashish Dhir ◽  
Kiran Kumar Akula
Keyword(s):  
Major Depression ◽  
Animal Models ◽  
Monoamine Oxidase ◽  
Molecular Mechanisms ◽  
Antidepressant Effect ◽  
Symptoms Of Depression ◽  
Animal Models Of Depression ◽  
Antidepressant Efficacy ◽  
Oxidase Enzyme ◽  
Human Illness

Major depression, a debilitating psychiatric disorder, is predicted to be the second most prevalent human illness by the year 2020. Various antidepressants, ranging from monoamine oxidase inhibitors to recently developed dual reuptake inhibitors, are prescribed for alleviating the symptoms of depression. Despite the availability of these blockbuster molecules, approximately 30% of depressed patients do not respond to the existing drug therapies and the remaining 70% fails to achieve complete remission. Moreover, antidepressants are associated with a plethora of side effects and drug-drug/drug-food interactions. In this context, novel approaches are being tried to find more efficacious and safer drugs for the treatment of major depression. Curcumin is one such molecule that has shown promising efficacy in various animal models of major depression. Although the mechanism of the antidepressant effect of curcumin is not fully understood, it is hypothesized to act through inhibiting the monoamine oxidase enzyme and modulating the release of serotonin and dopamine. Moreover, evidences have shown that curcumin enhances neurogenesis, notably in the frontal cortex and hippocampal regions of the brain. The use of curcumin in clinics for the treatment of major depression is limited due to its poor gastrointestinal absorption. The present review attempts to discuss the pharmacological profile along with molecular mechanisms of the antidepressant effect of curcumin in animal models of depression. A need for clinical trials in order to explore the antidepressant efficacy and safety profile of curcumin is emphasized.

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