ライフサイエンスコーパス: MAO-A

1 MAO A is a key enzyme that degrades a number of monoamin

2 MAO A was measured using PET and serial scans with the M

3 MAO-A density (by Western blot) and activity (by [(14)C]

4 MAO-A expression was decreased in 95.4% of human cancer

5 MAO-A inhibition prevents these changes, and also revers

6 MAO-A is the primary enzyme metabolizing catecholamines

7 MAO-A KD decreased basal reactive oxygen species levels

8 MAO-A KD specifically increased the activity of complex

9 MAO-A VT (an index of MAO-A density) was measured using

10 MAO-A VT was significantly greater in the PFC (37%, inde

11 A)) = 260 nM; IC(50)(MAO-B) = 200 nM; IC(50)(MAO-A) = 10 muM) and dose dependently counteracts halope

12 rexpression, R1 small interfering RNA, and a MAO A inhibitor, we found that R1 and MAO A act upstream

13 t study, we compared the protein levels of a MAO A-transcriptional activator, Kruppel-like factor 11

14 nalized on the basis of docking studies to a MAO-A/MAO-B homology model.

15 ized on the basis of docking studies using a MAO-A/MAO-B homology model.

16 Monoamine oxidase A (MAO A) degrades serotonin, norepinephrine, and dopamine

17 otonin-degrading enzyme monoamine oxidase A (MAO A) is an important source of hydrogen peroxide in ra

18 reduced levels of brain monoamine oxidase A (MAO A) leading to speculation that MAO A inhibition by t

19 A spontaneous monoamine oxidase A (MAO A) mutation (A863T) in exon 8 introduced a premature

20 The genetic deletion of monoamine oxidase A (MAO A), an enzyme that breaks down the monoamine neurotr

21 Monoamine oxidase A (MAO A), encoded by the X chromosome, catalyzes the oxida

22 ing evidence shows that monoamine oxidase A (MAO A), the key enzyme catalyzing serotonin (5-hydroxytr

23 has been reported that monoamine oxidase A (MAO A, a major neurotransmitter-degrading enzyme) is sig

24 ucocorticoids and brain monoamine oxidase A (MAO A, which degrades monoamine neurotransmitters).

25 nt rat cerebral cortex monoamine oxidases A (MAO A) and B (MAO B) determined.

26 n mice expressing a dominant-negative MAO-A (MAO-A(neo)), which were more protected against pressure

27 selective inhibitors of monoamine oxidase A (MAO-A) and B (MAO-B) holds a therapeutic relevance in th

28 but suffer from potent monoamine oxidase A (MAO-A) inhibition and low solubility.

29 Monoamine oxidase A (MAO-A) is a key regulator of serotonin metabolism, and p

30 Monoamine oxidase A (MAO-A) is an important brain enzyme that creates oxidati

31 Monoamine oxidase A (MAO-A) is an important enzyme on the outer mitochondrial

32 of the 40% increase in monoamine oxidase A (MAO-A) levels that occurs during PPB, a dietary suppleme

33 abnormality is elevated monoamine oxidase A (MAO-A) levels, which occurs in the prefrontal and anteri

34 f the gene encoding the monoamine oxidase A (MAO-A) to reduce serotonin levels in the brain.

35 We found that monoamine oxidase A (MAO-A) was the most significantly up-regulated gene.

36 vox), are inhibitors of monoamine oxidase A (MAO-A), which presents an undesired side effect.

37 se in the expression of monoamine oxidase-A (MAO-A) and MAO-B in the lateral OFC and by a decrease in

38 Monoamine oxidase-A (MAO-A) is a treatment target in neurodegenerative illnes

39 that high expression of monoamine oxidase-A (MAO-A) is associated with positive ARv7 detection in CRP

40 Monoamine oxidase-A (MAO-A), a key brain enzyme which metabolizes monoamines,

41 thyltransferase (COMT), monoamine oxidase-A (MAO-A), vesicular monoamine transporter (VMAT1,2) and ch

42 he mitochondrial enzyme monoamine oxidase-A (MAO-A), which produces hydrogen peroxide as a catalytic

43 Abnormal MAO A activity has been implicated in several neuropsych

44 on of Sp1 binding with mithramycin abrogated MAO-A mRNA induction.

45 BPD was associated with greater PFC and ACC MAO-A VT compared with moderate BPD, MDE, and healthy co

46 In BPD, PFC and ACC MAO-A VT were positively correlated with mood symptoms (

47 ptional complex and synergistically activate MAO A transcription.

48 al stress, which transcriptionally activates MAO A.

49 in the detection limit of the assay, against MAO-A.

50 reveals for the first time that KLF11 is an MAO A regulator and is produced in response to neuronal

51 MAO B and MAO A are more selective for the R-enantiomer (rasagilin

52 nhibitor isatin binds to all known MAO B and MAO A with similar affinities.

53 ly 16-fold and 2.4-fold higher for MAO B and MAO A, respectively.

54 p38 kinase inhibitor, R1 overexpression, and MAO A inhibitor, we have shown that MAO A and R1 are dow

55 and a MAO A inhibitor, we found that R1 and MAO A act upstream of cyclin D1 and E2F1.

56 eir affinity for dopamine D(2) receptors and MAO A.

57 5HTR2A/2B/2C and MAO-A/TPH1 are expressed in cholangiocytes and HSCs from

58 ytes and human HSCs express 5HTR2A/2B/2C and MAO-A/TPH1; treatment of these cell lines with 5HTR2A/2B

59 al function, notably complex I activity, and MAO-A may be a target for protection against neurodegene

60 Recombinant human MAO-B and MAO-A enzyme preparations were used to determine inhibit

61 Expression of 5-HT(B) and MAO-A was suppressed in the AMY of female pigs; 5-HT(B)

62 orter stress or glucocorticoid exposures and MAO-A levels/activity is not well established.

63 T(B), 5-HT(A), 5-HT(B), and D receptors, and MAO-A was determined by Q-RT-PCR and data subjected to m

64 9 nM; selective versus other AR subtypes and MAO-A), which inhibited A2AAR-induced cAMP accumulation

65 our results show that targeting the Enz/ARv7/MAO-A signaling with the antidepressants phenelzine or c

66 As MAO-A creates oxidative stress, facilitates apoptosis, a

67 On average, MAO-A VT in perimenopausal age was elevated by 34% compa

68 creased levels of monoamine oxidase A and B (MAO A and B) leading to increased dopamine turnover in t

69 including human monoamine oxidases A and B (MAO A and MAO B) show aromatic amino acid residues orien

70 the membrane-bound forms of MAO A and MAO B (MAO A Y444 mutant enzymes are found to be unstable on me

71 The monoamine oxidases A and B (MAO-A and -B) genes, which are involved in serotonin and

72 Monoamine oxidases A and B (MAO-A and MAO-B) are enzymes of the outer mitochondrial

73 toward SSAO over monoamine oxidases A and B (MAO-A and MAO-B).

74 Because MAO A breaks down serotonin, norepinephrine, dopamine, a

75 ure studies should investigate links between MAO-A suppression and the development of cancer to deter

76 We demonstrated that SRY activates both MAO A-promoter and catalytic activities in a human male

77 Brain MAO A activity was measured in vivo in healthy nonsmokin

78 ctivity of a MAO inhibitor against rat brain MAO A and B in vivo.

79 Here we report for the first time that brain MAO A correlates inversely with the MPQ trait measure of

80 sma levels of selegiline are elevated, brain MAO-A might also be inhibited.

81 direct evidence that it also inhibits brain MAO-A in humans.

82 ositron emission tomography to measure brain MAO-A V(T) on two different days: One under acute psycho

83 We measured brain MAO-A in 18 healthy men after a 28-day treatment with Zy

84 s provide the first direct evidence of brain MAO-A inhibition in humans by formulations of selegiline

85 postulated but not verified to target brain MAO-A in addition to MAO-B.

86 erved a significant reduction in whole-brain MAO-A binding as reflected by reductions in 10 of 11 bra

87 The characteristics exhibited by MAO A/B KO mice highlight the potential of these animals

88 ntial role of hydrogen peroxide generated by MAO A in cardiomyocyte hypertrophy by serotonin.

89 in the modulation of aggression mediated by MAO A.

90 nin requires hydrogen peroxide production by MAO A and ERK1/2 activation.

91 ssure overload, norepinephrine catabolism by MAO-A is increased accompanied by exacerbated oxidative

92 The presence and degradability by MAO-A of serotonin in plasma extracts were confirmed by

93 h increased resistance toward degradation by MAO-A.

94 sible metabolism of certain hallucinogens by MAO-A, which would cause a bias in the detectability of

95 dative/pro-apoptotic processes implicated by MAO-A overexpression.

96 lying defective brain development induced by MAO-A knockdown during in vitro embryogenesis.

97 glucocorticoid administration and decreased MAO-A binding, activity and protein levels.

98 onal and glial cells significantly decreased MAO-A activity and protein levels.

99 croRNA (miRNA) was used to stably knock down MAO-A mRNA, protein, and catalytic activity by 60-70% in

100 Moreover, dysfunctional MAO-A expression led to elevated levels of embryonic ser

101 nt designed to counter functions of elevated MAO-A activity eliminates vulnerability to depressed moo

102 These results suggest that elevated MAO-A VT is associated with multiple indicators of BPD s

103 nistration typically associate with elevated MAO-A levels/activity.

104 ative symptoms were associated with elevated MAO-A VT in the PFC and ACC (MANOVA, severity: F(2,38)=5

105 sis that a polymorphism in the gene encoding MAO-A contributes to the genetic risk for conduct disord

106 In summary, endogenous MAO-A levels influence mitochondrial function, notably c

107 Rv7 expression can transcriptionally enhance MAO-A expression resulting in Enz resistance via alterin

108 rgic receptor-dependent mechanisms, enhanced MAO-A activity coupled with increased intramyocardial no

109 mice lacking the monoamine metabolic enzymes MAO A and MAO B (MAO AB-deficient mice) exhibit diminish

110 on was demonstrated between the affinity for MAO A, but not MAO B, and the levels of 3,4-dihydroxyphe

111 esults suggest that FoxO1 is a repressor for MAO A transcription, and its phosphorylation is involved

112 tomography using a radioligand specific for MAO A (clorgyline labeled with carbon 11).

113 The synthesized compounds were evaluated for MAO-A, MAO-B, and AChE inhibitory activities as potentia

114 osis is reduced in cortical brain cells from MAO A-deficient mice compared with WT.

115 avior in the MAO A/B KO mice, different from MAO A or B single KO mice, suggest that varying monoamin

116 ic MAO A transgenic mice were generated from MAO A knock-out (KO) mice by using the promoter of calci

117 Furthermore, MAO-A KD protected against inhibitors of complex I, III,

118 n KLF11 levels and those of its target gene, MAO A, both in association with MDD.

119 Hence, greater MAO-A VT during perimenopause may represent a new target

120 D and a microarray analysis reported greater MAO-A messenger RNA in the PFC of rodents exposed to alc

121 drinking correlated positively with greater MAO-A VT in the PFC (r = .67, p = .005) and all brain re

122 ; ACC: r = .38, p = .046), while hippocampus MAO-A VT was negatively correlated with verbal memory (r

123 The presence of human MAO A transgene and its expression were verified by PCR

124 ect on either bovine or sheep MAO B or human MAO A.

125 While the cis isomers are potent human MAO-A inhibitors, the trans analogues selectively target

126 ctively countered the enhanced aggression in MAO A KO mice, at doses that did not inherently affect m

127 nd glia cells indicate that these changes in MAO A and B are a direct consequence of loss of insulin

128 he is conserved in the analogous position in MAO A sequences.

129 esence of a functional FoxO1-binding site in MAO A core promoter.

130 our findings suggest that excessive 5-HT in MAO-A-deficient mouse embryos triggers cellular signalin

131 III and IV resulted in a similar increase in MAO-A expression, while up-regulation of MAO-A was lower

132 eover, we found that elevated 5-HT levels in MAO-A knockdown embryos coincided with an enhanced activ

133 dexamethasone) and androgen (R1881) increase MAO A promoter and catalytic activities in human neurobl

134 in the rat brain, which results in increased MAO A mRNA and enzymatic activity.

135 y regulatory mechanisms leading to increased MAO A catalytic activity and mRNA levels because of dire

136 Increased MAO-A level, when greater severity and reversed neuroveg

137 Increased MAO-A levels in prefrontal cortex (PFC) and anterior cin

138 F11 knockdown reduces glucocorticoid-induced MAO A expression in cultured neurons; 3) induction of KL

139 ates the relationship between stress-induced MAO A and the transcription factor Kruppel-like factor 1

140 lly repressed both the basal and VPA-induced MAO A catalytic and promoter activities to 30 to 60%.

141 ctor were required for dexamethasone-induced MAO-A mRNA expression, as blockade of the GR with RU 486

142 oamine oxidase B (MAO B) that do not inhibit MAO A have been described in the literature.

143 hen variability in constituents that inhibit MAO-A could impact smoking.

144 st cigarette smoke constituents that inhibit MAO-A, in the range seen in chronic smokers, are likely

145 but not DAT; and while Emsam also inhibited MAO-A (33.2+/-28.9 (range 9-68%) the difference did not

146 ydis selegiline dose significantly inhibited MAO-A (36.9+/-19.7%, range 11-70%, p<0.007)) but not DAT

147 The monoamine oxidase isoenzymes (MAOs) A and B play important roles in the homeostasis of

148 um starvation-induced apoptosis, p38 kinase, MAO A, and caspase-3 were increased, whereas Bcl-2 and R

149 The novel glucocorticoid-KLF11-MAO A pathway may play a crucial role in modulating dist

150 After declines in estrogen level, MAO-A density may be elevated for a month or longer, and

151 m, and polymorphic variation in the X-linked MAO-A gene influences its expression.

152 comparison with male wild-type littermates, MAO A/B KO mice exhibited abnormally high and overgenera

153 sorder severity in patients carrying the low MAO-A activity allele.

154 ading some of these substances, reduced lung MAO A may contribute to some of the physiologic effects

155 Accordingly, male MAO A-deficient humans and mice exhibit an extreme predi

156 We measured MAO A in peripheral organs in a group of 9 smokers and c

157 armine positron emission tomography measured MAO-A total distribution volume (MAO-A VT), an index of

158 In comparison with WT male mice, MAO A KO counterparts exhibited increases in 5-HT and NE

159 ested in mice expressing a dominant-negative MAO-A (MAO-A(neo)), which were more protected against pr

160 ons of monoamines, because of the absence of MAO A and MAO B, cause functional alterations that are a

161 ed mRNA decay and resulted in the absence of MAO A transcript, protein, and catalytic activity and ab

162 ve form of FoxO1 abolished the activation of MAO A by VPA and Akt.

163 phorylation is involved in VPA activation of MAO A.

164 ase inhibitor) reduced the VPA activation of MAO A.

165 The combined deficiency of MAO A and B results in significantly elevated levels of

166 Thus, the lack of MAO A in the forebrain of MAO A KO mice may underlie their phenotypes.

167 ce at 94 GHz (W-band) on the radical form of MAO A.

168 so observed with the membrane-bound forms of MAO A and MAO B (MAO A Y444 mutant enzymes are found to

169 ry, this study demonstrates the functions of MAO A and its repressor R1 in apoptotic signaling pathwa

170 labeling of 5-HT, and immunocytochemistry of MAO A were found in the frontal cortex, striatum, and hi

171 Inhibition of MAO A prevents cell apoptosis.

172 Thus, the lack of MAO A in the forebrain of MAO A KO mice may underlie the

173 norepinephrine, and DA and higher levels of MAO A metabolite 5-hydroxyindoleacetic acid were found i

174 2) overexpressing KLF11 increases levels of MAO A mRNA and enzymatic activity, which is further enha

175 nowledge of the structures and mechanisms of MAO A and MAO B, which are pharmacological targets for s

176 Notably, the prefrontal cortex (PFC) of MAO A KO mice exhibited higher expression of NR2A and NR

177 t in healthy adult males the gene product of MAO A in the brain, rather than the gene per se, would b

178 w insights on the differential regulation of MAO A by glucocorticoid and androgen.

179 r, these results underscore the relevance of MAO A as a neurochemical substrate of aberrant aggressio

180 Our findings suggest that the role of MAO A in pathological aggression may be mediated by chan

181 This study reports the roles of MAO A and R1 in apoptosis and proliferation.

182 n the present study, the cognitive status of MAO A/B knockout (KO) mice was examined with a wide arra

183 level was much lower, whereas the amount of MAO-A protein was not determined due to the lack of a su

184 sis found that significant downregulation of MAO-A, the enzyme that metabolizes serotonin, occurred i

185 ability demonstrated a significant effect of MAO-A genotype in the raphe nuclei, medial and inferior

186 The effects of MAO-A knockdown (KD) on ATP, oxidative stress, electron

187 l OFC and by a decrease in the expression of MAO-A, MAO-B, and tryptophan hydroxylase in the dorsal r

188 The functions of MAO-A influence oxidative stress and apoptosis, 2 proces

189 nduced dose- and time-dependent increases of MAO-A gene and protein expression, while its effects on

190 MAO-A VT (an index of MAO-A density) was measured using [(11)C]harmine positro

191 of acute stress upon MAO-A V(T,) an index of MAO-A density, in human brain and acute glucocorticoid e

192 distribution volume (MAO-A VT), an index of MAO-A density, in severe BPD subjects (n = 14), moderate

193 We hypothesized that MAO-A VT, an index of MAO-A level, is elevated in the prefrontal cortex (PFC)

194 D1 demonstrated moderate inhibition of MAO-A (IC50 = 48.848 +/- 1.935 muM), potency (pEC50 = 6.

195 Although CSE inhibition of MAO-A activity in vitro was found to be partially irreve

196 we shed light on how selective inhibition of MAO-A and MAO-B can be achieved by geometric isomers of

197 for nicotine to the left, (2) inhibition of MAO-A, but not MAO-B, increases low-dose nicotine self-a

198 ty can be strongly enhanced by inhibition of MAO-A.

199 ntrast, targeted inhibition and knockdown of MAO-A expression (E7.5-E10.5) caused structural abnormal

200 nd reduced ATP, followed by up-regulation of MAO-A mRNA, protein, and enzyme activity levels.

201 in MAO-A expression, while up-regulation of MAO-A was lower following complex II inhibition.

202 To determine the role of MAO-A and -B in the development of PD, we screened a sam

203 Here, we investigated the role of MAO-A in maladaptive hypertrophy and heart failure.

204 The specific role of MAO-A was further tested in mice expressing a dominant-n

205 Previous association studies of MAO-A and -B in PD have been inconclusive.

206 Values of MAO-A VT in the prefrontal cortex, anterior cingulate co

207 ta and gamma) increased the transcription of MAOs A and B; the effects were abolished by parkin, but

208 attenuated the stimulating effect of VPA on MAO A.

209 anism apparently unrelated to its actions on MAO(A).

210 The docking experiments carried out on MAO-A and MAO-B structures proved new information about

211 ity and reversed neurovegetative symptoms on MAO-A VT in the PFC and ACC was analyzed using a multiva

212 t and selective MAO-B (high selectivity over MAO-A) and AChE inhibitor in the series with IC(50) valu

213 the functionally related monoamine oxidase (MAO) -A and MAO-B is >10 microM.

214 , and evaluated for their monoamine oxidase (MAO) A and B inhibiting effect.

215 ed the activities of both monoamine oxidase (MAO) A and B.

216 t time that VPA activates monoamine oxidase (MAO) A catalytic activity, mRNA level, and promoter acti

217 ed that partially reduced monoamine oxidase (MAO) A contains an equilibrium mixture of an anionic fla

218 lished that abrogation of monoamine oxidase (MAO) A expression leads to a neurochemical, morphologica

219 Monoamine oxidase (MAO) A is a key enzyme for the degradation of neurotrans

220 nd selective inhibitor of monoamine oxidase (MAO) A.

221 d dopamine receptors, and monoamine oxidase (MAO)-A in brains of sub-adult pigs were evaluated.

222 an hydroxylase (TPH1) and monoamine oxidase (MAO-A) are the key enzymes for the synthesis and catabol

223 gous to the mitochondrial monoamine oxidases MAO-A/B and produces hydrogen peroxide in the nucleus as

224 Monoamine oxidases (MAO) A and B catalyze the oxidative deamination of many

225 se nicotine self-administration, (3) partial MAO-A inhibition, to the degree observed in chronic ciga

226 duced a premature stop codon, which produced MAO A/B double knock-out (KO) mice in a MAO B KO mouse c

227 ch higher than moclobemide) and a pronounced MAO-A/B selectivity.

228 Genotypes with greater putative MAO-A activity were associated with greater 5-HT(1A) rec

229 state (M2)-specific genes (Mannose receptor, MAO-A, and CD36) and therefore conclude that Hck acts as

230 ined whether smokers would also have reduced MAO A in peripheral organs.

231 g sites; 4) KLF11 knockout mice show reduced MAO A mRNA and catalytic activity in the brain cortex co

232 CSE significantly reduced MAO-A and MAO-B activities in vitro, whereas nicotine di

233 y substituents yielded significantly reduced MAO-A inhibition relative to the unsubstituted compound

234 Androgen also up-regulates MAO A gene expression by direct interaction of androgen

235 teracts with Sp1-binding sites and represses MAO A gene expression.

236 requirements for highly specific reversible MAO A inhibitors.

237 s promoted increased research into selective MAO-A and MAO-B inhibitors.

238 Significant MAO A catalytic activity, autoradiographic labeling of 5

239 Since MAO-A metabolizes monoamines, this phenomenon may explai

240 Forebrain-specific MAO A transgenic mice were generated from MAO A knock-ou

241 signaling and are inhibited by the specific MAO-A inhibitor clorgyline.

242 Targeting MAO-A with phenelzine or clorgyline, the FDA-approved dr

243 ken together, these results demonstrate that MAO A is a novel target for VPA via Akt/FoxO1 signaling

244 In addition, we found that MAO A and R1 are involved in the c-Myc-induced prolifera

245 Recently, we found that MAO A was a putative target gene directly regulated by a

246 ion, and MAO A inhibitor, we have shown that MAO A and R1 are downstream of p38 kinase and Bcl-2, but

247 xidase A (MAO A) leading to speculation that MAO A inhibition by tobacco smoke may underlie some of t

248 These results suggest that MAO A is specifically expressed in the forebrain regions

249 pment of cancer to determine the extent that MAO-A suppression contributes to increased cancer risk.

250 We hypothesized that MAO-A levels in PFC and ACC would be highest in severe B

251 We hypothesized that MAO-A levels in the PFC and ACC are most elevated in MDE

252 We hypothesized that MAO-A VT, an index of MAO-A level, is elevated in the pr

253 METHODS AND We report that MAO-A activity is triggered in isolated neonatal and adu

254 We suggest that MAO-A-mediated oxidative stress can lead to cell damage,

255 The MAO A/B KO mice showed reduced body weight compared with

256 A functional SRY-binding site in the MAO A core promoter was identified and validated by elec

257 Therefore, a common polymorphism in the MAO A gene (MAOA, Mendelian Inheritance in Men database

258 hase/escape and anxiety-like behavior in the MAO A/B KO mice, different from MAO A or B single KO mic

259 on factor R1 (RAM2/CDCA7L/JPO2) inhibits the MAO A promoter and enzymatic activities.

260 personality traits) such that the lower the MAO A activity in cortical and subcortical brain regions

261 as unaffected following the same dose of the MAO A inhibitor clorgyline.

262 A levels because of direct activation of the MAO A promoter via Sp/KLF-binding sites; 4) KLF11 knocko

263 scription factor on Sp1-binding sites of the MAO A promoter.

264 measured using PET and serial scans with the MAO A-specific radiotracers (11)C-clorgyline and deuteri

265 (3) dopamine agonist, can be modified by the MAO(A) inhibitor clorgyline, by a mechanism apparently u

266 The MAO-A SAR can be rationalized on the basis of docking st

267 The MAO-A SAR can be rationalized on the basis of docking st

268 ) using positron emission tomography and the MAO-A radiotracer [(11)C]clorgyline.

269 We hypothesized that polymorphism in the MAO-A gene would be associated with sex-specific variati

270 onferred by a functional polymorphism in the MAO-A gene.

271 The selective inhibition of the MAO-A and MAO-B isoforms was confirmed ex vivo in mouse

272 m repeat polymorphism in the promoter of the MAO-A gene.

273 lysine 49 to increase its activation of the MAO-A promoter.

274 ic inhibition of 5-Htr6 activity rescued the MAO-A knockdown phenotype and restored apoptotic activit

275 low dipole moment increased the affinity to MAO A, whereas groups with high dipole moment yielded co

276 es peripheral organs as well as the brain to MAO A-inhibitory compounds, we determined whether smoker

277 rreversible binding of labeled clorgyline to MAO A.

278 ivatives exhibited outstanding affinities to MAO-A (7.0 nM < IC50 < 49 nM, much higher than moclobemi

279 n vitro high affinity and selectivity toward MAO-A isoenzyme, compared to clorgyline and moclobemide,

280 Modulation of the TPH1/MAO-A/5HT/5HTR2A/2B/2C axis may represent a therapeutic

281 brain and acute glucocorticoid exposure upon MAO-A levels in human neuronal and glial cell lines.

282 s are to assess effects of acute stress upon MAO-A V(T,) an index of MAO-A density, in human brain an

283 n an important role of KLF11 in upregulating MAO A in MDD and chronic social stress, suggesting that

284 4d, 14e, and 14g) showing selectivity versus MAO A and remarkably inhibiting colony formation in THP-

285 MAO-B 0.386 nM, >25000-fold selective versus MAO-A) and N-(3,4-dichlorophenyl)-1H-indole-5-carboxamid

286 MAO-B 0.612 nM, >16000-fold selective versus MAO-A).

287 MAO-B 0.227 nM, >5700-fold selective versus MAO-A).

288 IC50 human MAO-B 1.59 nM, selectivity versus MAO-A>6000-fold), high potency and selectivity are optim

289 hy measured MAO-A total distribution volume (MAO-A VT), an index of MAO-A density, in severe BPD subj

290 ontains a noncovalently bound flavin whereas MAO A contains a flavin covalently bound to a cysteinyl

291 It is unknown whether MAO-A levels are abnormal in AD.

292 gression of neural disorders associated with MAO A dysfunction.

293 ortex barrel field structure associated with MAO A KO mice was restored and became morphologically si

294 Also, compared with MAO A KO mice, lower levels of 5-HT, norepinephrine, and

295 ersible inhibitors without interference with MAO A function in neurotransmitter metabolism.

296 Indeed, treating animals with MAO-A inhibitors or selective serotonin reuptake inhibit

297 Depression diagnosis was not associated with MAO-A genotype or 5-HT(1A) receptor availability in thes

298 strual cycle length, was not associated with MAO-A VT (F8,18 = 0.548; P = .81) but tendency to cry wa

299 ndency to cry was positively correlated with MAO-A VT in the prefrontal cortex (r = 0.54; P = .008).

300 5-HT2AR antagonist or after incubation with MAO-A (monoamine oxidase-A).