ライフサイエンスコーパス: MAO

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

2 MAO B messenger RNA also correlated with viral loads in

3 MAO B messenger RNA was highest in macaques with the mos

4 MAO subjects also had increased plasma concentrations of

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

6 MAO-A KD decreased basal reactive oxygen species levels

7 MAO-A KD specifically increased the activity of complex

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

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

10 T-cell populations in 9 lean, 12 MNO, and 13 MAO subjects.

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

12 AO-B inhibitor (K(i)(A(2A)) = 260 nM; IC(50)(MAO-B) = 200 nM; IC(50)(MAO-A) = 10 muM) and dose depend

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 thesized compounds were evaluated for MAO-A, MAO-B, and AChE inhibitory activities as potential drug

30 nd by a decrease in the expression of MAO-A, MAO-B, and tryptophan hydroxylase in the dorsal raphe nu

31 targets, the first potent, dual-acting A2AAR/MAO-B inhibitors with a nonxanthine structure were devel

32 may be useful tools for validating the A2AAR/MAO-B dual target approach in PD.

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

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

35 Eight drug molecules, including COX, ACE, MAO, and PDE inhibitors, have been successfully [(18)F]-

36 al stress, which transcriptionally activates MAO A.

37 In contrast, the properties affecting MAO B affinity were the polarity and bulk of the para-su

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

39 derate (~6%) weight gain in MNO (n = 12) and MAO (n = 8) subjects with a mean BMI of 36 +/- 4 kg/m2 w

40 5HTR2A/2B/2C and MAO-A/TPH1 are expressed in cholangiocytes and HSCs from

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

42 ng the monoamine metabolic enzymes MAO A and MAO B (MAO AB-deficient mice) exhibit diminished prolife

43 oamines, because of the absence of MAO A and MAO B, cause functional alterations that are accompanied

44 CSE significantly reduced MAO-A and MAO-B activities in vitro, whereas nicotine did not.

45 ght on how selective inhibition of MAO-A and MAO-B can be achieved by geometric isomers of cis- and t

46 increased research into selective MAO-A and MAO-B inhibitors.

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

48 docking experiments carried out on MAO-A and MAO-B structures proved new information about the enzyme

49 Monoamine oxidases A and B (MAO-A and MAO-B) are enzymes of the outer mitochondrial membrane t

50 xpression of monoamine oxidase-A (MAO-A) and MAO-B in the lateral OFC and by a decrease in the expres

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

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

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

54 With ethylene as the feed and MAO as cocatalyst/activator, SNS-based complexes Ti-C0-C

55 energy of interaction between inhibitor and MAO B residues during inhibitor egress is an effective i

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

57 9 nM; selective versus other AR subtypes and MAO-A), which inhibited A2AAR-induced cAMP accumulation

58 which acts as a dual human A(2a) antagonist/MAO-B inhibitor (K(i)(A(2A)) = 260 nM; IC(50)(MAO-B) = 2

59 mpound is the best balanced A(2A) antagonist/MAO-B inhibitor reported to date, and it could be consid

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

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

62 ns 2-12 showed good inhibitory activities at MAO-B, AChE, and BChE but low selectivity.

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

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

65 l cortex monoamine oxidases A (MAO A) and B (MAO B) determined.

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

67 bitors of monoamine oxidase A (MAO-A) and B (MAO-B) holds a therapeutic relevance in the treatment of

68 monoamine metabolic enzymes MAO A and MAO B (MAO AB-deficient mice) exhibit diminished proliferation

69 otopic membrane protein monoamine oxidase B (MAO B) is an important drug target for Parkinson's disea

70 olinesterase (AChE) and monoamine oxidase B (MAO B), a series of multitarget ligands was properly des

71 was further studied in monoamine oxidase B (MAO-B) and cyclooxygenase-1 (COX-1) enzyme through molec

72 reversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is

73 AARs) and inhibition of monoamine oxidase B (MAO-B) in the brain are considered attractive strategies

74 ne was found to inhibit monoamine oxidase B (MAO-B) with an IC(50) of 18 +/- 7.1 muM in preliminary a

75 eversible inhibitors of monoamine oxidase B (MAO-B).

76 linesterase (AChE), and monoamine oxidase B (MAO-B).

77 mine agonists, and monoamine oxidase type B (MAO-B) inhibitors.

78 r determinants for high affinity toward both MAO isoforms.

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

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

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

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

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

84 nhibitory potency of ciproxifan on rat brain MAO, these findings should be considered, when using hig

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

88 h increased resistance toward degradation by MAO-A.

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

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

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

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

93 in the modulation of aggression mediated by MAO A.

94 de synthase (DHPAAS) is identified to bypass MAO and DDC for direct production of 3,4-dihydroxyphenyl

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

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

97 over, most of the tested compounds displayed MAO inhibitory effect when tested in vivo.

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

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

100 with valuable tools for designing effective MAO B inhibitors as well as outline a method that can be

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

106 These engineered MAO-N biocatalysts have been applied in deracemization r

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

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

109 We re-explored MAO antidepressant agent phenelzine (phenethylhydrazine)

110 % inhibitory concentration of compound 6 for MAO-B was 227 +/- 36.8 nM.

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

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

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

114 line at high doses loses its selectivity for MAO-B, there is no direct evidence that it also inhibits

115 Adipose tissue from MAO individuals contains increased numbers of Th17 and T

116 Adipose tissue from MAO subjects had 3- to 10-fold increases in numbers of C

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 inhibitory activity (IC50 = 30 nM) and good MAO B/A selectivity (selectivity index, SI = 94) along w

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

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

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

123 isplayed good inhibitory activities and high MAO-B selectivity.

124 c substituents producing compounds with high MAO B affinity.

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

126 dole-5-carboxamide (53, PSB-1410, IC50 human MAO-B 0.227 nM, >5700-fold selective versus MAO-A).

127 ole-5-carboxamide (38a, PSB-1491, IC50 human MAO-B 0.386 nM, >25000-fold selective versus MAO-A) and

128 t and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, >16000-fold selective versus MAO-A).

129 zole-5-carboxamide (30, PSB-1434, IC50 human MAO-B 1.59 nM, selectivity versus MAO-A>6000-fold), high

130 amide (17, Ki human A2A, 39.5 nM; IC50 human MAO-B, 34.9 nM; selective versus other AR subtypes and M

131 class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).

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

133 Recombinant human MAO-B and MAO-A enzyme preparations were used to determi

134 dence shows a relationship between the human MAO-B (hMAO-B) enzyme and neuropsychiatric/degenerative

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

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

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

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

139 centrations and secretion rates increased in MAO, but not MNO, subjects.

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

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

142 ge of therapeutic target proteins, including MAO, tyrosine kinases, BACE1, steroid receptors, mGlu5 r

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

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

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

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

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

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

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

150 nalogues of 17f, namely 18b and 19a, inhibit MAO-B with IC(50) of 68 and 48 nM, respectively, being 5

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

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

153 t, and therapeutic use of drugs that inhibit MAO-B are major challenges for future therapy.

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

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

156 unds acting as monoamine oxidase inhibitors (MAO-Is) and bearing a 6'-substituted (E)-2-(benzofuran-3

157 ic antidepressant imipramine, which inhibits MAO activity and reduces oxidative stress.

158 levodopa (IPX066), safinamide which inhibits MAO-B, dopamine uptake and glutamate and pardoprunox whi

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

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

161 show that (1) tranylcypromine (TCP), a known MAO inhibitor, increases sensitivity to the primary rein

162 ats received pre-session injections of known MAO inhibitors.

163 -fluorodeprenyl-D2 was consistent with known MAO-B expression in the human brain.

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

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

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

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

168 using different amounts of methylalumoxane (MAO), giving in each case a very active catalytic mixtur

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

170 Furthermore, it better models MAO inhibition and is more sensitive to stress-induced r

171 ine oxidase variants from Aspergillus niger (MAO-N) which display remarkable substrate scope and tole

172 ated between the affinity for MAO A, but not MAO B, and the levels of 3,4-dihydroxyphenylacetic acid

173 tissue lipogenesis increased in MNO, but not MAO, subjects.

174 o the left, (2) inhibition of MAO-A, but not MAO-B, increases low-dose nicotine self-administration,

175 We also report a novel MAO-N mediated asymmetric oxidative Pictet-Spengler appr

176 These novel MAO-Is may represent promising hits for the development

177 pants were metabolically abnormal and obese (MAO).

178 abolically abnormal insulin-resistant obese (MAO) subjects, metabolically normal insulin-sensitive ob

179 e defined as "metabolically abnormal obese" (MAO), are protected from the adverse metabolic effects o

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

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

182 phorylation is involved in VPA activation of MAO A.

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

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

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

186 Expression of MAO isoforms has been detected in the developing embryo.

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 ts was to further characterize the impact of MAO inhibition on the primary reinforcing and reinforcem

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 dose of l-deprenyl yielded 70% inhibition of MAO-B in all regions.

200 but is unlikely to reflect an involvement of MAO inhibition.

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

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

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

204 olin-2-iminato ligand (L) in the presence of MAO and/or TTPB as cocatalysts have been explored.

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

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

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

208 en possible to expand the substrate scope of MAO-N to accommodate amine substrates containing bulky a

209 Atomistic molecular dynamics simulations of MAO B either embedded in a lipid bilayer or free in solu

210 Additional MD simulations of MAO B in complex with seven different reversible inhibit

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

212 However, suppression of MAO-B does not induce developmental alterations.

213 e the impetus for increased transcription of MAO B and that MAO, and more broadly, oxidative stress,

214 Use of MAO-SLC7A1 knockdown in conceptuses decreased arginine t

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

216 uitable PET radioligand for visualization of MAO-B activity in the human brain.

217 n vivo morpholino antisense oligonucleotide (MAO)-mediated knockdown of SLC7A1 mRNA, the arginine tra

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

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

220 attenuated the stimulating effect of VPA on MAO A.

221 arkers of DA and 5-HT function in the DMS or MAO expression in the ventral tegmental area of low- vs

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

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

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

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

226 ect evidence of increased monoamine oxidase (MAO) activity in the brain of a simian immunodeficiency

227 or antagonist) as well as monoamine oxidase (MAO) and functional binding assays were conducted to inv

228 ous studies have utilized monoamine oxidase (MAO) and L-3,4-dihydroxyphenylalanine decarboxylase (DDC

229 to visualize and quantify monoamine oxidase (MAO) B activity in vivo.

230 ine levels partly through monoamine oxidase (MAO) inhibition.

231 rats pretreated with the monoamine oxidase (MAO) inhibitor clorgyline.

232 line ligand agmatine, the monoamine oxidase (MAO) inhibitor harmane, the alpha(2)-adrenoceptor agonis

233 constituents that inhibit monoamine oxidase (MAO) may increase the reinforcing value of low doses of

234 Monoamine oxidase (MAO) metabolizes cytosolic dopamine (DA), thereby limiti

235 The flavoenzyme monoamine oxidase (MAO) regulates mammalian behavioral patterns by modulati

236 monoamine metabolized by monoamine oxidase (MAO), exists widely in plants, animals, fermented foods,

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

238 t omega-transaminase (TA)/monoamine oxidase (MAO-N) cascade process for the synthesis of chiral 2,5-d

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

240 prepared, and tested as monoamine oxidases (MAOs) and acetyl- and butyryl-cholinesterase (AChE and B

241 esurgence of interest in monoamine oxidases (MAOs) has been fueled by recent correlations of this enz

242 (CREDs), hydrolases and monoamine oxidases (MAOs), providing a comprehensive overview of their uses,

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

244 The most potent MAO-B inhibitors were N-(3'-chlorophenyl)-4-oxo-4H-chrom

245 , were identified as a novel class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).

246 nding 6'-benzyloxy derivatives showed potent MAO-B inhibition and inverted selectivity profile.

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

248 g 5-7-fold more potent than the prototypical MAO-B inhibitor deprenyl (IC(50) = 334 nM).

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

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

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

252 irreversibility than did previously reported MAO-B radioligands.

253 umulation and showed competitive, reversible MAO-B inhibition.

254 as found to be the most potent and selective MAO-B (high selectivity over MAO-A) and AChE inhibitor i

255 r novel class of highly potent and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, >16000-fold

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

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

258 Furthermore, in humans, striatal MAO activity was elevated in individuals with HIV enceph

259 In the adult central nervous system, MAOs have important functions for neurotransmitter homeo

260 arge dietary intake of tyramine while taking MAO inhibitors has been reported; therefore, the measure

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

262 or increased transcription of MAO B and that MAO, and more broadly, oxidative stress, have significan

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

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

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

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

267 We show that MAO metabolism of DA does not increase cytosolic H(2)O(2

268 The MAO and MANO phenotypes had more gallstones than the MHO

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

270 also had a higher risk of gallstones in the MAO (OR = 5.41, 95% CI = 2.31-12.66), MANO (OR = 3.18, 9

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

272 brain cortex in vitro in the presence of the MAO inhibitor pargyline.

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

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

275 trans analogues selectively target only the MAO-B isoform.

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

277 Thus, MAO-B represents an attractive target for the treatment

278 erified to target brain MAO-A in addition to MAO-B.

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

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

281 evelopment and abnormal function compared to MAO control.

282 cal features with a preferential response to MAO inhibitors, which is especially well-evidenced for r

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

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

285 This is dependent upon MAO anchoring to the outer mitochondrial membrane and sh

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

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

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

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

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

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

292 4d, 14e, and 14g) showing selectivity versus MAO A and remarkably inhibiting colony formation in THP-

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

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

295 trate that MNO people are resistant, whereas MAO people are predisposed, to the adverse metabolic eff

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

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

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).

301 viors that can be reversed by treatment with MAO inhibitors, as well as the tricyclic antidepressant