ライフサイエンスコーパス: GAD

1 GAD autoantibodies (GADAs) are sensitive markers of isle

2 GAD autoantibodies (GADAs) identify individuals at incre

3 GAD autoantibodies (GADAs), insulinoma-associated antige

4 GAD exists as two isoforms named according to their resp

5 GAD expression was verified with Western blotting.

6 GAD was nearly as prevalent as depression in this cohort

7 GAD(65) mRNA was detected in horizontal cells, and seque

8 GAD, GSP, and GSP/GAD subjects showed no such increases,

9 .65, P<0.001; depression: OR=5.24, P=0.001), GAD-2 items predicted GAD (anxious: OR=4.09, P=0.003; un

10 ith GABA-immunogold staining showed that (1) GAD-positive terminals mainly target dendrites and spine

11 10 received a diagnosis (143 depression, 129 GAD, 30 panic disorder).

12 score (OR, 1.19; 95%CI, 0.95-1.49; P = .14); GAD (OR, 2.46; 95% CI,1.14-5.30;P = .02); elevated anxie

13 ere 90 participants, all medication-free (17 GAD, 12 MDD, 23 GAD/MDD, and 38 control subjects).

14 ee adults with GSP (EER n = 19; TAC n = 18), GAD (EER n = 17; TAC n = 17), GSP/GAD (EER n = 17; TAC n

15 nts (Patient Health Questionnaire-2 [PHQ-2], GAD-2, and an item about panic attacks), and a diagnosti

16 nts, all medication-free (17 GAD, 12 MDD, 23 GAD/MDD, and 38 control subjects).

17 tive behavioral therapy (CBT), 48 adults (25 GAD and 23 PD) reduced (via cognitive reappraisal) or ma

18 .1)], panic disorder [OR = 1.6 (1.01, 2.3)], GAD [OR = 1.8 (1.1, 3.0)], any mood disorder [OR = 1.4 (

19 roinsulin or glutamic acid decarboxylase 65 (GAD)] delayed T1D onset, but published data are conflict

20 ith that for glutamic acid decarboxylase 67 (GAD(67)) mRNA, a synthesizing enzyme for GABA.

21 ls that lack glutamic acid decarboxylase 67 (GAD).

22 2.55;95%confidence interval [CI], 1.38-4.73),GAD(OR, 2.47; 95%CI, 1.23-4.97), elevated BDI-II (OR, 1.

23 ess the effect of bilateral delivery of AAV2-GAD in the subthalamic nucleus compared with sham surger

24 acy and safety of bilateral infusion of AAV2-GAD in the subthalamic nucleus supports its further deve

25 e 6-month endpoint, UPDRS score for the AAV2-GAD group decreased by 8.1 points (SD 1.7, 23.1%; p<0.00

26 The AAV2-GAD group showed a significantly greater improvement fro

27 on were headache (seven patients in the AAV2-GAD group vs two in the sham group) and nausea (six vs t

28 se of bowel obstruction occurred in the AAV2-GAD group, was not attributed to treatment or the surgic

29 omly assigned to sham surgery and 22 to AAV2-GAD infusions; of those, 21 and 16, respectively, were a

30 8); 44% T cell-positive patients) or adults (GAD(311-320); 38%).

31 surface antibodies were not directed against GAD itself.

32 but it is not known if sensory input alters GAD isoforms.

33 tion gradients were abnormally shallow among GAD patients, reflecting less degradation of the conditi

34 ontal cells, and sequencing of the amplified GAD(65) fragment showed approximately 85% identity with

35 yme glutamic acid decarboxylase (GAD(65) and GAD(67) isoforms), the plasma membrane GABA transporters

36 prevalent as depression in this cohort, and GAD-2 was an effective screening tool; however, panic di

37 e use of 2-step screening for depression and GAD beginning with a 4-item scale (GAD-2 plus PHQ-2).

38 Panic disorder and GAD do not contribute to adverse pregnancy complications

39 ChAT, bNOS, glycine, and GAD remain reliable AC markers in the GCL.

40 GSP and GAD both involve reduced capacity for engaging emotion-r

41 nsplastomic plants expressing proinsulin and GAD to protect the autoantigens from degradation in an o

42 ines in SMLC migration and proliferation and GAD development.

43 ties and differences in symptoms in PTSD and GAD.

44 have glutamic acid decarboxylase antibodies (GAD-ab), but these 2 disorders have not been reported to

45 n of glutamic acid decarboxylase antibodies (GAD-abs) in the paraneoplastic context.

46 As GAD-tg mice aged, their T-cell responses to GAD65 remain

47 ulin (insulin autoantibody [IAA]) in 180, as GAD (GAD antibody [GADA]) in 107, and as IA-2 antigen (I

48 s found to associate with select Ags such as GAD in cells and ex vivo.

49 Western blotting were carried out to assess GAD mRNA and protein expression, respectively.

50 e and de novo posttransplant autoantibodies (GAD antibody, insulinoma-associated protein 2 antigen, z

51 efined autoantibodies (insulin autoantibody, GAD antibody, or IA-2 antibody), and 136 subjects presen

52 jection of IgG purified from the 2 available GAD autoantibody-ositive purified IgG preparations did n

53 the early phase of macrophage infection, but GAD contributed to the survival of B. microti in a murin

54 ction of cell bodies of GABAergic neurons by GAD mRNAs.

55 have previously shown that Ig-GAD2, carrying GAD 206-220 peptide, induced in hyperglycemic mice immun

56 ive in situ hybridization, we measured CB1R, GAD(67), and diacylglycerol lipase alpha (the synthesizi

57 ominant and specific to either T1D children (GAD(530-538); 44% T cell-positive patients) or adults (G

58 ), major depressive disorder (MDD), comorbid GAD and MDD (GAD/MDD), or neither GAD nor MDD (control s

59 ow that these regulators usurp the conserved GAD acid stress resistance system to regulate T3S by inc

60 However, these cells did not contain GAD(67), GAT-1, or GAT-3 immunoreactivity.

61 In contrast, GAD(67) mRNA levels were unaltered in CB1R(+/-) andCB1R(

62 er 2 modules are positive for AChE, NADPH-d, GAD, and CO throughout the rostrocaudal LCIC.

63 pression of both glutamic acid decarboxlase (GAD) and synaptic vesicle protein (SV2).

64 ynthetic enzyme glutamic acid decarboxylase (GAD(65) and GAD(67) isoforms), the plasma membrane GABA

65 urons expressed Glutamic Acid Decarboxylase (GAD) 65 and 67, suggesting that they may be GABAergic, s

66 ibodies against glutamic acid decarboxylase (GAD) 65 are commonly observed in patients suffering from

67 he promoter for glutamic acid decarboxylase (GAD) 65 kDa, 67 kDa, or tyrosine hydroxylase (TH).

68 eptor subunits, glutamic acid decarboxylase (GAD) and a GABA transporter in the brains of female rhes

69 hesizing enzyme glutamic acid decarboxylase (GAD) and choline acetyltransferase (ChAT) revealed that

70 ene transfer of glutamic acid decarboxylase (GAD) and other methods that modulate production of GABA

71 fic changes in glutamate acid decarboxylase (GAD) and vesicular GABA transporter expression, these fi

72 toantibodies to glutamic acid decarboxylase (GAD) are well documented in association with stiff perso

73 r either IA2 or glutamic acid decarboxylase (GAD) autoantibodies.

74 erived from two glutamic acid decarboxylase (GAD) genes, GAD1 and GAD2, both of which produce transcr

75 Antibodies to glutamic acid decarboxylase (GAD) have been found in patients with temporal lobe epil

76 nown to express glutamic acid decarboxylase (GAD) in early postnatal development, the functional role

77 r expression of glutamic acid decarboxylase (GAD) in layer V of cortex and in the CA1 of hippocampus,

78 hesizing enzyme glutamic acid decarboxylase (GAD) is decreased in Brodmann area 9 (BA9) of the dorsol

79 gic neurons and glutamic acid decarboxylase (GAD) mRNA expression in the aBST.

80 d by the enzyme glutamic acid decarboxylase (GAD) of which there are two major isoforms: GAD65 and GA

81 y of the enzyme glutamic acid decarboxylase (GAD) present in neurons.

82 rase (NADPH-d), glutamic acid decarboxylase (GAD), cytochrome oxidase (CO), and calretinin (CR).

83 two isoforms of glutamic acid decarboxylase (GAD), GAD65 (GAD2) and GAD67 (GAD1), the rate-limiting e

84 ity for GABA or glutamic acid decarboxylase (GAD), the enzyme that produces GABA.

85 hesizing enzyme glutamic acid decarboxylase (GAD), with increased GAD-67-immunopositive interneurons

86 calbindin-, or glutamic acid decarboxylase (GAD)-67-positive.

87 tes autoantigen glutamic acid decarboxylase (GAD).

88 es derived from glutamic acid decarboxylase (GAD)65 (sIA(g7)-pGAD65).

89 GABA synthesis, glutamic acid decarboxylase (GAD)65 and GAD67.

90 rter (vGAT) and glutamic acid decarboxylase (GAD)65 in the GABAergic contacts that the overexpressing

91 Additionally, glutamic acid decarboxylase (GAD)65-loaded tolDCs from well-controlled patients decre

92 cent protein or glutamic acid decarboxylase (GAD)65/67 immunoreactivity confirmed these GABAergic pro

93 distribution of glutamic acid decarboxylase (GAD)67 and GLY transporter 2 (T2) in axonal terminals to

94 ntrolled by the glutamic acid decarboxylase (GAD)67 promotor.

95 s of the enzyme glutamic acid decarboxylase (GAD): GAD65 and GAD67.

96 uroendocrine enzyme glutamate decarboxylase (GAD) catalyses the synthesis of the inhibitory neurotran

97 entially functional glutamate decarboxylase (GAD) system involved in extreme acid resistance in sever

98 ts synthetic enzyme glutamate decarboxylase (GAD).

99 [vGluT2-eGFP], glutamic acid decarboxylase [GAD]67-eGFP, and glycine transporter 2 (GlyT2)-eGFP, res

100 GABA signaling (glutamic acid decarboxylase; GAD, and vesicular GABA transporter; VGaT).

101 e by the action of glutamate decarboxylases (GADs).

102 and bipolar disorder (BD) involves decreased GAD(67) expression, although this change involves fundam

103 renia may partially compensate for deficient GAD(67)-mediated GABA synthesis by reducing endogenous c

104 , unlike its name implies, has no detectable GAD activity, but it is able to efficiently catalyze dec

105 We detected GAD autoantibodies at a very high titer (median, 7500 U/

106 o act as a GTPase activated by dimerization (GAD), while recent reports suggest LRRK2 to exist under

107 trongly support the geocentric axial dipole (GAD) hypothesis for the past few million years.

108 Graft arterial disease (GAD) limits long-term solid-organ allograft survival.

109 prominently in generalized anxiety disorder (GAD) and in other anxiety and mood disorders.

110 dividuals with generalized anxiety disorder (GAD) and panic disorder (PD) to generate individual subj

111 pression (MD), generalized anxiety disorder (GAD) and panic disorder (PD), as well as depressed affec

112 care settings, generalized anxiety disorder (GAD) and panic disorder are common but underrecognized i

113 obia (GSP) and generalized anxiety disorder (GAD) are both associated with emotion dysregulation.

114 ic disorder or generalized anxiety disorder (GAD) in pregnancy, or medications used to treat these co

115 Generalized anxiety disorder (GAD) is a chronic disorder in need of reliable data to g

116 Generalized anxiety disorder (GAD) is a common chronic condition that is understudied

117 Generalized anxiety disorder (GAD) is characterized by the core symptom of uncontrolla

118 Generalized anxiety disorder (GAD) is common in older adults; however, access to treat

119 Generalized anxiety disorder (GAD) is one of the most common psychiatric disorders in

120 for late-life generalized anxiety disorder (GAD), but only pilot studies have been conducted in prim

121 der (PTSD) and generalized anxiety disorder (GAD), eg, share elevated anxiety symptoms, but differ wi

122 patients with generalized anxiety disorder (GAD), major depressive disorder (MDD), comorbid GAD and

123 th depression, generalized anxiety disorder (GAD), or panic disorder; understand the predictive value

124 sorder (PTSD), generalized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, soc

125 eralization in generalized anxiety disorder (GAD), results of this meta-analysis do not reveal whethe

126 ies underlying generalized anxiety disorder (GAD).

127 ministered the Generalized Anxiety Disorder (GAD-7) instrument, whole blood DNA methylation was measu

128 patients with generalized anxiety disorder (GAD; n = 32, female) and healthy controls (n = 25, age-m

129 y the two-item Generalised Anxiety Disorder [GAD]-2 anxiety scale), and post-traumatic stress disorde

130 Panic disorder, GAD, or use of benzodiazepines or serotonin reuptake inh

131 ebrate genes, GAD1 and GAD2, encode distinct GAD proteins: GAD67 and GAD65, respectively.

132 wly developed electrochemiluminescence (ECL)-GAD antibody (GADA) assay and compare its sensitivity an

133 presentation of the exogenous and endogenous GAD Ag.

134 II presentation of exogenous and endogenous GAD, but did not perturb the presentation of several oth

135 prefrontal cortex of genetically engineered GAD(67) heterozygous (GAD(67)(+/-)), CB1R heterozygous (

136 plexing HSP90 with GAD Ag enhanced exogenous GAD Ag presentation.

137 associated with terminal boutons expressing GAD-immunoreactivity in addition.

138 major depressive disorder] and 43 (5.3%) for GAD [generalized anxiety disorder] (11 [1.4%] had comorb

139 Two screening instruments, the GAD-7 for GAD and the Patient Health Questionnaire for panic disor

140 tudies should evaluate patients with CBS for GAD-ab and people with SPS for signs of CBS.

141 ADR variants are susceptibility factors for GAD, further highlighting the critical role of the adren

142 urate and feasible screening instruments for GAD and panic disorder has the potential to improve dete

143 Double-labeling for GAD and synaptophysin confirmed that these were synaptic

144 The genetic association with positivity for GAD autoantibodies (GADAs), IA2 antigen (IA-2A), zinc tr

145 f distinct anatomical modules that stain for GAD-67 as well as other neurochemical markers.

146 Staining for GAD-67 and other markers revealed a single modular netwo

147 The best-performing test for GAD was the Generalized Anxiety Disorder Scale 7 Item (G

148 nctionally identified presynaptic cells from GAD-GFP mice confirmed the pharmacological analyses: Ca(

149 pport the idea that GABA is synthesized from GAD(65), taken up into synaptic vesicles by VGAT, and li

150 se studies demonstrate the presence of GABA, GAD(65), and VGAT in horizontal cells of the guinea pig

151 Specific GABA, GAD(65), and VGAT immunostaining was localized to horizo

152 entate gyrus, interneurons positive for GABA/GAD are sparsely distributed along the edge of the hilus

153 (insulin autoantibody [IAA]) in 180, as GAD (GAD antibody [GADA]) in 107, and as IA-2 antigen (IA-2 a

154 We hypothesized that alum-formulated GAD65 (GAD-alum) can preserve beta-cell function in patients wi

155 sk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-2A), or ZnT8

156 the neural correlates of EER and TAC in GSP, GAD, and GSP/GAD.

157 C n = 18), GAD (EER n = 17; TAC n = 17), GSP/GAD (EER n = 17; TAC n = 15), and no psychopathology (EE

158 GAD, GSP, and GSP/GAD subjects showed no such increases, with all groups d

159 rrelates of EER and TAC in GSP, GAD, and GSP/GAD.

160 ng in cases comorbid for both disorders (GSP/GAD).

161 957 [73.7%]), 98 had panic disorder, 252 had GAD, 67 were treated with a benzodiazepine, and 293 were

162 in only serum samples, five of them also had GAD-65 antibodies.

163 genetically engineered GAD(67) heterozygous (GAD(67)(+/-)), CB1R heterozygous (CB1R(+/-)), CB1R knock

164 seizure-induced hippocampal histopathology, GAD expression loss, upregulated hippocampal GFAP and gr

165 ildren developed at least one persistent IA (GAD antibody, IA-2A, or micro insulin autoantibodies) an

166 Autoantibodies to insulin (IAA), GAD (GADA), islet antigen-2 (IA-2A), and zinc transporte

167 ice and prediction algorithms, we identified GAD and preproinsulin candidate epitopes.

168 In GAD patients, BLA and CMA connectivity patterns were sig

169 In GAD(67)(+/-) mice, GAD(67) and CB1R mRNA levels were sig

170 In GAD, we find evidence of an intra-amygdalar abnormality

171 D65 and other beta-CAAs at different ages in GAD-tg mice and their NOD mouse littermates.

172 ed frontolimbic white matter connectivity in GAD.

173 there was a significantly greater decline in GAD symptoms (difference in improvement, -2.36; 95% CI,

174 ral basis for emotion regulation deficits in GAD.

175 There was no difference in GAD severity in patients receiving CBT vs those receivin

176 toms of worry and autonomic dysregulation in GAD arise from a shared underlying neural mechanism.

177 tic rat models exhibited an ~50% increase in GAD(65) protein as well as a twofold increase in VMH GAB

178 receptors preceded presynaptic increases in GAD-65 puncta size.

179 The thickened intima in GAD contains smooth muscle-like cells (SMLCs), leukocyte

180 red adrenergic function has been reported in GAD, however direct evidence for genetic susceptibility

181 ic circuitry predicts better CBT response in GAD and PD.

182 rs have implicated the amygdala, but work in GAD has yielded conflicting results.

183 tivation of GABAergic neurons, and increased GAD expression in the aBST.

184 and CCR1-deficient recipients, it increased GAD intimal thickening with SMLC proliferation in only t

185 mic acid decarboxylase (GAD), with increased GAD-67-immunopositive interneurons in the stratum oriens

186 DQ and for antibodies (Abs) against insulin, GAD, IA-2 (IA-2A), and zinc transporter-8 (ZnT8A) for pr

187 evel may therefore yield novel insights into GAD.

188 islet antigen-specific approaches involving GAD of 65 kDa (GAD65)-expressing plasmids, as previously

189 e Generalized Anxiety Disorder Scale 7 Item (GAD-7), with a positive likelihood ratio of 5.1 (95% CI,

190 1 complexes were distinct from canonical LAT-GADs-SLP-76 complexes.

191 of LAT-GRB2-SKAP1 complexes relative to LAT-GADs-SLP-76 complexes.

192 with diabetes risk than those to full-length GAD, suggesting that assays using N-terminally truncated

193 roximately 85% identity with other mammalian GAD(65) mRNAs.

194 essive disorder (MDD), comorbid GAD and MDD (GAD/MDD), or neither GAD nor MDD (control subjects).

195 We used immunoblots to measure GAD(65) protein (a rate-limiting enzyme in GABA synthesi

196 In GAD(67)(+/-) mice, GAD(67) and CB1R mRNA levels were significantly reduced

197 f cortex and in the CA1 of hippocampus, more GAD(+) terminals surrounding the pyramidal neurons and l

198 The intimal SMLCs in mouse GAD lesions differ from medial smooth muscle cells in th

199 Neither GAD- nor IA2-specific TCRs mediated T-cell islet infiltr

200 , comorbid GAD and MDD (GAD/MDD), or neither GAD nor MDD (control subjects).

201 ng GIRK2 in gamma-aminobutyric acid neurons (GAD-Cre:Girk2(flox/flox) mice) exhibited a clear deficit

202 Identification of the target of the non-GAD antibodies and peripheral and intrathecal transfer p

203 d be used to demonstrate the role of the non-GAD IgG in SPS.

204 adjusted models, neither panic disorder nor GAD was associated with maternal or neonatal complicatio

205 otting showed an increase of GAD-65, but not GAD-67, in the hippocampal homogenate.

206 In the first experiment, we use a novel GAD-Cre rat to show that optogenetic inhibition of LH ga

207 from 10 unique studies for the detection of GAD and panic disorder in primary care patients Across a

208 ctivity and will allow activity detection of GAD positive cells in vitro and in vivo selectively.

209 nts with a DSM-IV-Text Revision diagnosis of GAD and 26 healthy comparison subjects were recruited an

210 years or older with a principal diagnosis of GAD randomized to receive either escitalopram or placebo

211 of 2785 patients assessed had a diagnosis of GAD while 224 of 2637 patients assessed had a diagnosis

212 with a principal or coprincipal diagnosis of GAD who were recruited between January 27, 2011, and Oct

213 Results indicate a sparse distribution of GAD neurons colocalized with D5 receptors in the LAH.

214 tments: four doses of GAD-alum, two doses of GAD-alum followed by two doses of placebo, or four doses

215 one of three study treatments: four doses of GAD-alum, two doses of GAD-alum followed by two doses of

216 ransgenic mice that report the expression of GAD, suggesting that they are predominantly excitatory.

217 essed for double-label immunofluorescence of GAD (a marker for GABA production) and D5 receptors in t

218 Western blotting showed an increase of GAD-65, but not GAD-67, in the hippocampal homogenate.

219 lockade of GABA(A) receptors or knockdown of GAD(65) in the VMH.

220 However, a measure of GAD severity did not indicate greater improvement with C

221 es revealed complex coexpression patterns of GAD with the TRC protein markers gustducin, neural cell

222 The presence of GAD(65) mRNA was also evaluated by using laser capture m

223 iled to perturb MHC class II presentation of GAD.

224 ribute importantly to the psychopathology of GAD by proliferating anxiety cues in the individual's en

225 , accompanied by nonsignificant reduction of GAD-67 synapses in the CA3 region.

226 effect of adverse life events on the risk of GAD.

227 Using two different strains of GAD-GFP mice, as well as immunostaining for GABA, we fou

228 d fluorescence was restricted to a subset of GAD-67-positive cholinergic amacrine cells of both ortho

229 twork, consistent with cognitive theories of GAD.

230 Treatment of GAD with an antidepressant should be continued for at le

231 The use of GAD-alum as compared with placebo did not affect the ins

232 d for dissecting the responses of the AR2 or GAD network of Escherichia coli K-12 to changes in pH, w

233 onses in receptor cells, glial-like cells or GAD-expressing presynaptic cells.

234 dies have examined these processes in GSP or GAD, no work compares findings across the two disorders

235 nsferase), bNOS (brain-type nitric oxidase), GAD (glutamate decarboxylase), and glial markers, and oc

236 on: OR=5.24, P=0.001), GAD-2 items predicted GAD (anxious: OR=4.09, P=0.003; unable to control worryi

237 ptor gamma2 subunit clusters and presynaptic GAD-65 puncta were observed.

238 s significantly higher in pretransplantation GAD autoantibody-positive daclizumab-treated recipients

239 CALM was superior to UC for principal GAD at 6-month (-1.61; 95% confidence interval [CI], -2.

240 planation of increased inflammation in PTSD, GAD, PD, and phobias is via the activation of the stress

241 titer (700 000 U/mL) serum with recombinant GAD indicated that these neuronal surface antibodies wer

242 The findings that reduced GAD(67) mRNA expression can induce lower CB1R mRNA expre

243 ic secondary outcomes included self-reported GAD symptoms (GAD Scale 7 Item) measured at baseline and

244 ssion and GAD beginning with a 4-item scale (GAD-2 plus PHQ-2).

245 Characterization of serum GAD antibodies from patients with SPS and evidence for p

246 ounts and acutely dissociated retinas showed GAD(65) and VGAT immunoreactivity in both A-type and B-t

247 Across the subregions, GAD patients had increased connectivity with a previousl

248 utcomes included self-reported GAD symptoms (GAD Scale 7 Item) measured at baseline and 4 months' fol

249 geted by all of these antibodies (other than GAD) and the often dramatic clinical and serological res

250 The GAD autoantibodies were high affinity (antibody dissocia

251 The GAD(+) interneurons showed relatively low expression of

252 in the target tissue, which may explain the GAD-tg mouse's usual disease incidence.

253 Mutants affected in the GAD system lost this resistance, demonstrating its direc

254 Two screening instruments, the GAD-7 for GAD and the Patient Health Questionnaire for p

255 This work provides first evidence that the GAD system might play an essential role in the resistanc

256 General anxiety was assessed using the GAD-7 scale.

257 rologous complementation of mutants with the GAD systems of Escherichia coli or B. microti confirmed

258 s formed patches that interdigitate with the GAD-67-positive modules.

259 h generalization abnormalities also apply to GAD.

260 Autoantibodies to GAD are associated with antibodies that bind to the surf

261 Autoantibodies to GAD might be the causative agent or a disease marker.

262 3.4 +/- 13.9 microT) that also correspond to GAD directions suggests that the overall average paleoma

263 er, these neural features are also linked to GAD, most likely via an vmPFC fear generalization.

264 r was observed in a subset TRCs paracrine to GAD-expressing TRCs.

265 We used transgenic GAD-GFP mice to show that cAMP-triggered Ca(2+) response

266 RBAs and suggest that N-terminally truncated GAD labels will enable more specific measurement of GADA

267 ing that assays using N-terminally truncated GAD should be used to select participants for interventi

268 d with full-length or N-terminally truncated GAD using the National Institute of Diabetes and Digesti

269 r relatives retested positive with truncated GAD.

270 We have identified a third vertebrate GAD gene, GAD3.

271 B. microti was GAD positive and able to export its product, gamma-amino

272 terized the superior olivary nuclei, whereas GAD immunoreactivity characterized many neurons in the n

273 variants in adrenergic receptors (ADRs) with GAD, with the involvement of stressful events.

274 Older adults with GAD randomized to escitalopram had a higher cumulative r

275 RIs) are efficacious for younger adults with GAD, but benefits and risks may be different in older ad

276 and depressive symptoms in older adults with GAD.

277 , a marker for cholinergic neurons, and with GAD C38, a marker for GABAergic neurons, in the caudate

278 aintaining anxiety and worry associated with GAD.

279 four SNPs were significantly associated with GAD.

280 amma2 subunit clusters that colocalized with GAD-65 were larger at 12 h, coinciding in time with the

281 Anterograde tracer also colocalized with GAD-67-positive puncta in labeled fibers, which in some

282 daclizumab-treated recipients compared with GAD autoantibody-negative or ATG-treated recipients.

283 some cases made close synaptic contact with GAD-67-labeled NI neurons.

284 Precomplexing HSP90 with GAD Ag enhanced exogenous GAD Ag presentation.

285 e patients' autoantibodies co-localized with GAD on immunohistochemistry and in permeabilized culture

286 Patients with GAD also display a characteristic pattern of autonomic d

287 (heart rate variability) in 19 patients with GAD and 21 control subjects to define neural correlates

288 ectivity patterns increased in patients with GAD and decreased in control subjects, and these changes

289 eneral mental health for older patients with GAD in primary care.

290 fety (GS least similar to CS); patients with GAD showed less discrimination between threat and safety

291 We report 2 patients with GAD-ab-positive SPS who also had signs suggestive of CBS

292 Patients with GAD-abs must be screened for an underlying cancer if the

293 tion of conditioned fear among patients with GAD.

294 bic structural connectivity in patients with GAD.

295 of perseverative cognitions in patients with GAD.

296 Among women, those with GAD or PD had shorter telomeres than those with no anxio

297 Treatment with GAD-alum did not significantly reduce the loss of stimul

298 eneralization across adults with and without GAD.

299 o telephone-delivered NST in reducing worry, GAD symptoms, and depressive symptoms in older adults wi

300 In young GAD-tg mice, Th1 responses to GAD65's dominant determina