ライフサイエンスコーパス: hypofunction

1 otypes in the genetic model of NMDA receptor hypofunction.

2 ction in schizophrenia is secondary to NMDAR hypofunction.

3 rom one side to induce unilateral mandibular hypofunction.

4 al aberrations associated with NMDA receptor hypofunction.

5 eurodevelopmental deficit, and glutamatergic hypofunction.

6 RG1/erbB4 signaling leading to glutamatergic hypofunction.

7 e for disorders characterized by cholinergic hypofunction.

8 ns of residues 316 or 317 would predict MC4R hypofunction.

9 ics to treat disorders associated with NMDAR hypofunction.

10 er in elderly men may be related to HPG axis hypofunction.

11 rmal levels could be used to define salivary hypofunction.

12 ow rates over 6 hours and to define salivary hypofunction.

13 for the treatment of postradiation salivary hypofunction.

14 g or disorders characterized by dopaminergic hypofunction.

15 damage was required for both senescence and hypofunction.

16 growth retardation due to placental vascular hypofunction.

17 schizophrenia genetic risk and NMDA receptor hypofunction.

18 working memory deficits associated with NMDA hypofunction.

19 onstrating inflammation-induced serotonergic hypofunction.

20 ethyl-D-aspartate glutamate receptor (NMDAR) hypofunction.

21 tients with unilateral peripheral vestibular hypofunction.

22 with vagal hyperreactivity rather than vagal hypofunction.

23 order characterized by NMDAR and cholinergic hypofunctions.

24 hic support by NGF to ameliorate cholinergic hypofunctioning.

25 pathway, dopamine hyperfunction and/or NMDA hypofunction abnormalities implicated in schizophrenia m

26 To better understand how NMDAR hypofunction affects the brain, we used magnetic resonan

27 te increase in dopamine release (followed by hypofunction after chronic use) and cue exposure-induced

28 each of humoral self-tolerance, and salivary hypofunction after delivery of a replication-deficient a

29 tural phase signaling, whereas NMDA receptor hypofunction alters interstructural and intrastructural

30 two common vestibular disorders - vestibular hypofunction and benign paroxysmal positional vertigo (B

31 Furthermore, hypofunction and BMP-2 increase the development of trans

32 ongenital sensorineural deafness, vestibular hypofunction and childhood onset retinitis pigmentosa.

33 While this demonstrates causality between MD hypofunction and cognitive inflexibility, questions rema

34 iodine deficiency and mild maternal thyroid hypofunction and decreased child cognition.

35 action similarly reduced the impact of NMDA hypofunction and dopamine hyperfunction on OFC neurons,

36 erferon (IFN) alfa for treatment of salivary hypofunction and dry mouth symptoms in primary Sjogren's

37 Symptoms of both HPG axis hypofunction and dysthymic disorder include dysphoria, f

38 ate network alterations may arise from NMDAR hypofunction and establish a proof of principle whereby

39 Treatments for unilateral vestibular hypofunction and for posterior canal BPPV are effective;

40 Thus, developmental NMDAR hypofunction and glutathione system deficits, separately

41 Prefrontal localized hypofunction and impaired serotonergic responsivity are

42 nt's disease is a direct consequence of CLC5 hypofunction and is not attributable to a gain of functi

43 Vagal hypofunction and prolonged intra-esophageal acidificatio

44 rong positive association between testicular hypofunction and subsequent MS (rate ratio = 4.62, 95% c

45 ted levels of KYNA could contribute to NMDAR hypofunction and the cognitive deficits and negative sym

46 e, decreased susceptibility to tumor-induced hypofunction, and attenuation of IR expression compared

47 nk among chronic stress, prefrontal cortical hypofunction, and behavioral dysfunction.

48 ogy could be linked to NMDA receptor (NMDAR) hypofunction, and thus used the serine racemase-null mut

49 prevalence of xerostomia and salivary gland hypofunction appears to be significantly higher in HIV-p

50 adult mutants, adrenocortical dysplasia and hypofunction are predominant features.

51 te strong evidence for NMDA receptor (NMDAR) hypofunction as an underlying factor for cognitive disor

52 d a potential association between testicular hypofunction, as a proxy for low testosterone levels, an

53 unction precedes the hippocampal cholinergic hypofunction associated with structural cholinergic dege

54 suggest that Shank3 deficiency induces NMDAR hypofunction by interfering with the Rac1/PAK/cofilin/ac

55 uced hippocampal ACh release and cholinergic hypofunction by selective impairment of desensitization

56 ndrome of dRTA and hemolytic anemia in which hypofunction can be discerned by in vitro studies.

57 These results demonstrate that NMDAR hypofunction can reproduce the numerous hippocampal defi

58 Mediodorsal thalamus hypofunction causes cognitive inflexibility reflected by

59 Cholinergic hypofunction contributes to dementia-related cognitive d

60 stantial evidence that NMDA receptor (NMDAR) hypofunction contributes to the pathophysiology of schiz

61 lation, SAPK/JNK activation, and proteasomal hypofunction cooperate to produce further protein accumu

62 litus (DM2), these findings suggest that IDE hypofunction could mediate human disease.

63 These results indicate that NMDAR hypofunction critically contributes to FTD-associated be

64 To establish whether IDE hypofunction decreases Abeta and insulin degradation in

65 le Pavlovian learning was not affected by MD hypofunction, decreasing MD activity during Pavlovian le

66 a potential target for treatment of salivary hypofunction diseases.

67 strate that a genetic model of NMDA receptor hypofunction displays a reduced ability to extinguish co

68 ns such as why some patients with vestibular hypofunction do not improve with a course of vestibular

69 individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with

70 We show that transient NMDAR hypofunction during early brain development, coinciding

71 Patients with salivary hypofunction exhibit difficulty in chewing and swallowin

72 The modest degree of hypofunction exhibited in vitro by these mutations, howe

73 lular-level abnormalities--eg, NMDA receptor hypofunction, GABA system dysfunction, neural connectivi

74 We tested the hypothesis that hypofunction has a greater influence than ovariectomy on

75 NMDAR hypofunction has been implicated in schizophrenia becaus

76 pact on NMDA receptors (NMDARs), since NMDAR hypofunction has been implicated in schizophrenia.

77 ogical treatment of disorders in which NMDAR hypofunction has been implicated.

78 N-Methyl-D-aspartate (NMDA) receptor (NMDAR) hypofunction has been postulated to contribute to the co

79 chizophrenia, that result from NMDA receptor-hypofunction have been mainly attributed to dysfunction

80 phrenia-1 (DISC1) and D-serine/NMDA receptor hypofunction have both been implicated in the pathophysi

81 ion and experimental models of NMDA receptor hypofunction have proven useful for characterizing neuro

82 The NMDA receptor (NMDAR) hypofunction hypothesis of schizophrenia is supported by

83 have witnessed a rise in the 'NMDA receptor hypofunction' hypothesis for schizophrenia, a devastatin

84 n proposed as a model for the intrinsic NMDA hypofunction hypothesized for schizophrenia.

85 While MD hypofunction impaired reversal learning, it did not affe

86 ary for set-shifting, and that NMDA receptor hypofunction impairs the capacity to modify existing kno

87 ssociated with xerostomia and salivary gland hypofunction in a population of HIV-positive women.

88 T and may act, in part, by normalizing daMCC hypofunction in ADHD.

89 ystemic inflammation and chronic cholinergic hypofunction in delirium and have implications for the r

90 of schizophrenia by promoting NMDA receptor hypofunction in fast-spiking interneurons.

91 The etiology of salivary gland hypofunction in HIV(+) patients is unclear.

92 We have transiently induced NMDAR hypofunction in infant mice during postnatal days 7-11,

93 nd their predictions in the context of NMDAR hypofunction in INs.

94 -DOPS treatment may ameliorate noradrenergic hypofunction in Menkes disease.

95 -DOPS treatment may ameliorate noradrenergic hypofunction in Menkes disease.

96 s, we also discuss the implications of NMDAR hypofunction in other types of INs using computational m

97 N-methyl-D-aspartate receptor (NMDAR) hypofunction in parvalbumin-expressing (PV+) inhibitory

98 rugs for alleviating symptoms of cholinergic hypofunction in patients with advanced Alzheimer's disea

99 However, it remains to be seen if NMDAR hypofunction in PV+ neurons is fundamental to the phenot

100 ta demonstrate for the first time that NMDAR hypofunction in pyramidal cells is sufficient to cause e

101 NMDA receptor hypofunction in schizophrenia has been inferred by a lar

102 hanced NRG1 signaling may contribute to NMDA hypofunction in schizophrenia.

103 No conventional therapy exists for salivary hypofunction in surviving head and neck cancer patients

104 The findings suggest hypofunction in the anterior cingulate cortex in schizop

105 The neonatal sensitivity to NMDA receptor hypofunction in the BSTC, and in its main thalamic targe

106 ics and brain imaging implicate dopaminergic hypofunction in the frontal lobes and basal ganglia in A

107 of type III Nrg1 heterozygous mice revealed hypofunction in the medial prefrontal cortex and the hip

108 The results suggest that the NMDA receptor hypofunction in the NR1 -/- mice is not global but regio

109 ical and clinical studies implicate dopamine hypofunction in the pathophysiology of depression.

110 ansmission and N-methyl-D-aspartate receptor hypofunction in the pathophysiology of psychotic disorde

111 ated with cognitive dysfunction and dopamine hypofunction in the prefrontal cortex, particularly schi

112 macological demonstration that glutamatergic hypofunction in the ventral hippocampus lies at the core

113 ch is associated with adult serotonin system hypofunction in the ventral hippocampus.

114 ur findings provide evidence for overlapping hypofunction in ventral striatal and orbitofrontal regio

115 bute to core symptoms arising from glutamate hypofunction, including cognitive impairments.

116 results suggest that 8-OH-DPAT-induced 5-HT hypofunction increases thirst without substantially affe

117 nditions and during a state of relative NMDA hypofunction induced by ketamine administration, at a do

118 Salivary hypofunction is associated with oral and pharyngeal diso

119 showed that in female rats with DM, salivary hypofunction is correlated with decreased submandibular

120 GABAergic interneuron hypofunction is hypothesized to underlie hippocampal dys

121 NMDA-receptor (NMDAR) hypofunction is strongly implicated in the pathophysiolo

122 One strategy to correct NMDAR hypofunction is to stimulate alpha-amino-3-hydroxy-5-met

123 efrontal cortex (PFC), but the origin of the hypofunction is unclear.

124 Hypofunction led to alveolar bone becoming more highly m

125 t the disruption of circuit function by Pten hypofunction may be ongoing well beyond early developmen

126 dingly, experimental models of NMDA receptor hypofunction may be useful for testing potential new ant

127 NMDA receptor hypofunction may contribute to the comorbidity of substa

128 h the hypothesis that thalamic glutamatergic hypofunction may contribute to the pathophysiology of th

129 dence, our in vivo findings suggest that IDE hypofunction may underlie or contribute to some forms of

130 ment of new antipsychotics based on the NMDA hypofunction model for schizophrenia.

131 The N-methyl-d-aspartic acid receptor hypofunction model of schizophrenia predicts a paradoxic

132 The N-methyl-D-aspartate receptor hypofunction model of schizophrenia predicts dysfunction

133 lices using the N-methyl-D-asparate receptor hypofunction model show that delta frequency bursting is

134 ted by the N-methyl-d-aspartic acid receptor hypofunction model.

135 Notably, gene expression induced during TIL hypofunction more closely resembled self-tolerance than

136 utyric acid-ergic interneuron-specific NMDAR hypofunction mouse model (Ppp1r2-Cre/fGluN1 knockout [KO

137 imer's disease (AD) is marked by cholinergic hypofunction, neuronal marker loss, and decreased nicoti

138 mice with genetically induced NMDA receptor hypofunction [NMDA receptor subunit-1 knockdown (NR1-KD)

139 l object recognition memory in NMDA receptor hypofunctioning NR1-knockdown mice, and were essentially

140 In addition, an NMDA receptor hypofunction (NRHypo) state may play a role in neurodege

141 Consistent with NMDA-mediated hypofunction observed in schizophrenic subjects, adminis

142 ging theory of schizophrenia postulates that hypofunction of adenosine signaling may contribute to it

143 Upregulation of NMDARs might contribute to hypofunction of AMPARs via subcellular redistribution.

144 gnized dependence of hypermutated tumours on hypofunction of genes that are involved in chromatin rem

145 ing coagonist D-serine was able to attenuate hypofunction of GluN2B(p.P553T)-containing NMDARs.

146 ic patients, exhibit behavioral deficits and hypofunction of glutamatergic and GABAergic pathways.

147 est that decreased outward K(+) current from hypofunction of Kir2.6 predisposes the sarcolemma to hyp

148 As hypofunction of N-methyl-d-aspartate (NMDA) receptor-dri

149 Hypofunction of N-methyl-d-aspartate (NMDA) receptors ha

150 the early 1990s it has been postulated that hypofunction of N-methyl-d-aspartate (NMDA) receptors in

151 bit behavioral abnormalities consistent with hypofunction of NMDA neurotransmission.

152 Schizophrenia may involve hypofunction of NMDA receptor (NMDAR)-mediated signaling

153 in schizophrenia, which is characterized by hypofunction of NMDA receptor (NMDAR)-mediated transmiss

154 This experimental design models the proposed hypofunction of NMDA receptor and gamma-aminobutyric aci

155 cal theories of schizophrenia emphasize that hypofunction of NMDA receptors at critical sites in loca

156 c agents directed toward diseases related to hypofunction of NMDAR.

157 ow dopaminergic activation induces long-term hypofunction of NMDARs, which can contribute to disorder

158 rtical synaptic transmission at two sites: a hypofunction of postsynaptic NMDA receptors, and by redu

159 These results provide direct evidence that hypofunction of striatal FSIs can produce movement abnor

160 ominant-negative SNARE expression leads to a hypofunction of synaptic NMDARs, we conclude that astroc

161 he prevailing models of schizophrenia invoke hypofunction of the glutamatergic synapse and defects in

162 and PET/SPECT studies support the theory of hypofunction of the N-methyl-D-aspartate receptor (NMDAR

163 that this behavior involves cocaine-induced hypofunction of the prefrontal cortex (PFC) or "hypofron

164 n schizophrenia are thought to derive from a hypofunction of the prefrontal cortex (PFC), but the ori

165 Hypofunction of the serotonergic system is often associa

166 ce that traumatic brain injury (TBI) induces hypofunction of the striatal dopaminergic system, the me

167 Hypofunctioning of a specific orbitofrontal cortical net

168 d that N-methyl-d-aspartate receptor (NMDAR) hypofunction on gamma-aminobutyric acid (GABA) interneur

169 chotic efficacy, reversed the impact of NMDA hypofunction on OFC cells and on behavior.

170 on the treatment of patients with vestibular hypofunction or with benign paroxysmal positional vertig

171 tivity contributes to organ failure, whereas hypofunction permits sepsis.

172 N-methyl-D-aspartate receptor (NMDA-R) hypofunction plays an important role in cognitive impair

173 Because this nonstructural cholinergic hypofunction precedes the hippocampal cholinergic hypofu

174 tal disorders characterized by NMDA receptor-hypofunction.Proper brain function depends on the correc

175 induced in the N-methyl-D-asparate receptor hypofunction rat model.

176 l alterations that results from serotonergic hypofunction remain poorly understood.

177 istent with the theory that individuals with hypofunctioning reward circuitry overeat to compensate f

178 Significant associations between a hypofunctioning reward response and obesity suggest the

179 in osteocyte density in alveolar bone, while hypofunction showed an increase compared with controls.

180 -dependent NMDA antagonist to model the NMDA hypofunction state that may occur in schizophrenia.

181 Conclusions: Results suggest hypofunction stimulates early bone formation.

182 Previous studies have reported hypofunction, structural abnormalities, and biochemical

183 rebrain and to model diseases of cholinergic hypofunction such as Alzheimer's disease.

184 n NR1 phosphorylation leads to glutamatergic hypofunction that can contribute to behavioral deficits

185 is not necessarily accompanied by the DLPFC hypofunction that was seen in schizophrenia.

186 Consistent with the NMDAR hypofunction theory of schizophrenia, distinct schizophr

187 s about the mechanisms that might link NMDAR hypofunction to alterations of FS neurons in schizophren

188 a mouse model of radiation-induced salivary hypofunction to investigate the outcomes of DNA damage i

189 hat is overtly symptomatic, and link torsinA hypofunction to neurodegeneration and abnormal twisting

190 ent with the theorized contribution of NMDAR hypofunction to predictive coding deficits in schizophre

191 a dystonic motor phenotype and link torsinA hypofunction to the development of early neuropathologic

192 t link N-methyl-D-aspartate receptor (NMDAR) hypofunction to the etiology of schizophrenia.

193 test the hypothesized contribution of NMDAR hypofunction to this disruption, we examined the effects

194 prevented both senescence and salivary gland hypofunction via a mechanism involving enhanced DNA dama

195 Recently, NMDA receptor hypofunction was described in patients with psychotic ma

196 This platelet hypofunction was reversible and associated with purinerg

197 Using a pharmacogenetic approach to model MD hypofunction, we recently showed that decreasing MD acti

198 gs support the hypothesis that NMDA receptor hypofunction, which has been implicated in the pathophys

199 association of xerostomia and salivary gland hypofunction with HIV infection has been established for

200 autism, our data raise the possibility that hypofunction within this meta-circuit is a shared featur