ライフサイエンスコーパス: deprenyl

1 he monoamine oxidase inhibitor selegiline (L-deprenyl).

2 larger for 11C-L-deprenyl-D2 than for 11C-L-deprenyl.

3 is a better index of MAO activity than 11C-L-deprenyl.

4 A, was more sensitive to clorgyline than to deprenyl.

5 A low dose of L-deprenyl (0.01 mg/kg, i.p. every other day for 3 weeks b

6 an +/- SD) months of controlled observation, deprenyl 10 mg/day was found to significantly delay the

7 or a placebo and were then placed on active deprenyl (10mg/day).

8 The PET tracer (11)C-deuterium-L-deprenyl ((11)C-DED) has been used to visualize activate

9 and healthy controls using (11)C-deuterium-L-deprenyl ((11)C-DED) to measure monoamine oxidase B loca

10 C-L-deprenyl and deuterium-substituted 11C-L-deprenyl (11C-L-deprenyl-D2).

11 levels could be abrogated by the addition of deprenyl, a specific MAO-B inhibitor.

12 ot confirm previous findings that low dose L-deprenyl administration in vivo after MPTP can rescue SN

13 that obtained with either GM1 or high dose L-deprenyl alone.

14 the monoamine oxidase B (MAO-B) inhibitor L-deprenyl, alone and in combination, on striatal dopamine

15 R-(-)-Deprenyl (deprenyl) ameliorates the progression of disability in e

16 diolabel a novel bis-deuterium substituted l-deprenyl analog (fluorodeprenyl-D2) with (18)F and to ev

17 We show that deprenyl and a related agent, TCH346, in subnanomolar co

18 hibited by stoichiometric amounts of both (-)deprenyl and clorgyline in a mechanism-based reaction, f

19 enylethylamine or dopamine or the IC(50) for deprenyl and clorgyline.

20 udies of the torso area 2 h apart with 11C-L-deprenyl and deuterium-substituted 11C-L-deprenyl (11C-L

21 with the MAO B-specific radiotracers,l-[11C]deprenyl and deuterium-substituted l-[11C]deprenyl (l-[1

22 lations which prevented nigral degeneration (deprenyl and nomifensine pretreatment) also prevented th

23 lso partly by monoamine oxidase B inhibitors deprenyl and pargyline.

24 y Parkinson's disease were randomized in the Deprenyl and Tocopherol Antioxidative Therapy of Parkins

25 Results also suggest the MAOB inhibitor deprenyl as a therapeutic agent to block certain actions

26 s preceded by the injection of clorgyline or deprenyl at a concentration (1 mg/kg) which selectively

27 Co-administration of GM1 and high dose L-deprenyl caused a synergistic increase in striatal DA le

28 ddition of the monoamine (MAO) inhibitors, l-deprenyl, clorgyline, pargyline, or in vivo nialamide pr

29 Short-term incubation of l-deprenyl combined with DAT and NET uptake inhibitors inc

30 caine-withdrawn rats with the MAOB inhibitor deprenyl completely alleviated the behavioral sensitizat

31 A sensitivity analysis showed that 11C-L-deprenyl-D2 is a better index of MAO activity than 11C-L

32 function was significantly larger for 11C-L-deprenyl-D2 than for 11C-L-deprenyl.

33 This study indicates that 11C-L-deprenyl-D2 will be useful for measuring the effects of

34 euterium-substituted l-[11C]deprenyl (l-[11C]deprenyl-D2).

35 deuterium-substituted 11C-L-deprenyl (11C-L-deprenyl-D2).

36 els of MAO B is improved by the use of 11C-L-deprenyl-D2, similar to prior studies on the brain.

37 ttsburgh compound-B (PIB), (11)C-deuterium-L-deprenyl (DED) and (18)F-fluorodeoxyglucose (FDG) respec

38 R-(-)-Deprenyl (deprenyl) ameliorates the progression of disab

39 tantia nigra was similar with clorgyline and deprenyl even if the ratio MAO A/MAO B was approximately

40 e, high glucose, and high glucose plus R-(-)-deprenyl for up to 5 days.

41 s disease patients who had been treated with deprenyl for up to 7 years, compared with patients who w

42 , monoamine oxidase blockers pargyline and l-deprenyl had no effect on DAcyt levels in MPP(+)-treated

43 potent than the prototypical MAO-B inhibitor deprenyl (IC(50) = 334 nM).

44 There were no accompanying benefits of deprenyl in postponing levodopa-related adverse effects

45 A high dose of L-deprenyl, inhibiting MAO-B activity, (10 mg/kg, i.p. eve

46 c activity and had no significant changes on deprenyl inhibition.

47 R-(-)-deprenyl inhibits nuclear accumulation of GAPDH and subs

48 Selegiline (L-deprenyl) is a selective, irreversible inhibitor of mono

49 nti-parkinsonian medications which include L-deprenyl, it will be important to further investigate th

50 1C]deprenyl and deuterium-substituted l-[11C]deprenyl (l-[11C]deprenyl-D2).

51 oxytryptamine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (

52 Therefore, R-(-)-deprenyl offers a strategy to explore the role of GAPDH

53 Combined effects of uptake inhibitors with l-deprenyl on dopamine clearance were additive (up to 99%

54 a second treatment randomization to continue deprenyl or switch to placebo.

55 ,3,6-tetrahydropyridine (MPTP), low doses of deprenyl prevent binding of GAPDH and Siah1 in the dopam

56 R-(-)-deprenyl prevents nuclear translocation of GAPDH and sub

57 monoamine oxidase inhibitors clorgyline and deprenyl resulted in a 42% and 75% reduction in lesion v

58 ial was initiated to examine the benefits of deprenyl (selegiline) and alpha-tocopherol in slowing th

59 Deprenyl (selegiline) delays the need for levodopa thera

60 tivation is much faster with clorgyline than deprenyl, suggesting a closer resemblance to MAO A than

61 etinal Muller cells and the ability of R-(-)-deprenyl to inhibit the translocation of GAPDH and apopt

62 assessing the binding specificity of labeled deprenyl to peripheral MAO B; (b) MAO B can be visualize

63 The addition of R-(-)-deprenyl to these cells incubated in high glucose reduce

64 ive Therapy of Parkinsonism trial to receive deprenyl, tocopherol, combined treatments, or a placebo

65 dopa and who had consented to continuing the deprenyl treatment (D subjects) or changing to a matchin

66 2 years of observation, including open-label deprenyl treatment and a second treatment randomization

67 Co-administration of GM1 and low dose L-deprenyl was not only not synergistic, but caused GM1s e

68 Administration of a 1 mg/kg dose of l-deprenyl yielded 70% inhibition of MAO-B in all regions.