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 was nearly as prevalent as depression in this cohort

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

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

8 .65, P<0.001; depression: OR=5.24, P=0.001), GAD-2 items predicted GAD (anxious: OR=4.09, P=0.003; un

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

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

11 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

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

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

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

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

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

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

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

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

20 (PHQ-9), the Generalised Anxiety Disorder-7 (GAD-7) questionnaire, and 12-Item Short Form Health Surv

21 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.

22 ng hormone levels were not associated with a GAD diagnosis overall (p = 0.19, g = 0.25), PACAP may be

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 bed in 1988, but several controversies about GAD autoimmunity still remain.

31 8); 44% T cell-positive patients) or adults (GAD(311-320); 38%).

32 surface antibodies were not directed against GAD itself.

33 -wide signals preceding the first IA against GAD (GADA-first) or against insulin (IAA-first).

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

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

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

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

38 ned reduction in headache days and PHQ-9 and GAD-7 scores in the analysis population (n=715) over 108

39 PHQ-9 and GAD-7 scores were significantly reduced at all time poin

40 >=1 severity category reduction in PHQ-9 and GAD-7.

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

42 after Chrimson expression in VGLUT2-cre and GAD-cre mice, respectively.

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

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

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

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

47 mechanisms and treatment targets in MDD and GAD.

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

49 ties and differences in symptoms in PTSD and GAD.

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

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

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

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

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

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

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

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

58 ed by specific disruption of GAD function by GAD antibodies.

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

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

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

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

63 We detect circulating GAD-reactive B cells in peripheral blood that readily di

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

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

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

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

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

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

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

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

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

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

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

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

76 ibodies against glutamic acid decarboxylase (GAD) are observed in patients with different neurologica

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

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

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

80 Antibodies to glutamic acid decarboxylase (GAD) have been associated with several neurological synd

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

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

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

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

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

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

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

88 measurements of glutamic acid decarboxylase (GAD), a PLP-dependent enzyme synthesizing the neurotrans

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

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

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

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

93 synthesized by glutamic acid decarboxylase (GAD).

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

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

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

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

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

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

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

101 ls that contain glutamic acid decarboxylase (GAD; GAD2-cre).

102 n and activation of glutamate decarboxylase (GAD) 65.

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

104 es predominant when glutamate decarboxylase (GAD) function is compromised.

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

106 hydroxylase (TH) or glutamate decarboxylase (GAD) to systematically compare the proportion of dopamin

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

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

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

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

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

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

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

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

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

116 y diagnosis of generalized anxiety disorder (GAD) and nonpsychiatric controls.

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

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

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

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

121 rder (MDD) and generalized anxiety disorder (GAD) are highly prevalent and debilitating disorders.

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

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

124 Generalized anxiety disorder (GAD) is a common and disabling illness that is often und

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

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

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

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

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

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

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

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

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

134 re (PHQ-9) and Generalised Anxiety Disorder (GAD-7) scales were used to assess the effects of onabotu

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

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

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

138 nxiety (7-item Generalized Anxiety Disorder; GAD-7), level of depression (9-item Patient Health Quest

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

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

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

142 = 38 unmedicated patients with first-episode GAD, MDD, respectively, and n = 35 healthy controls).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 957 [73.7%]), 98 had panic disorder, 252 had GAD, 67 were treated with a benzodiazepine, and 293 were

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

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

169 confidence interval (CI) 1.04-4.66), higher GAD-7 (anxiety) (OR = 1.05, 95% CI 1.0-1.10) and SHI (po

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

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

172 ped persistent insulin autoantibodies (IAA), GAD autoantibodies (GADA), insulinoma-associated antigen

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

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

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

176 ed frontolimbic white matter connectivity in GAD.

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

178 ral basis for emotion regulation deficits in GAD.

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

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

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

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

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

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

185 p complaints were associated with increasing GAD-7 scores, as well as higher SHI scores (p<0.001).

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

187 munity requires demonstration of intrathecal GAD antibody synthesis.

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

189 which may be relevant to disorders involving GAD dysfunction such as schizophrenia or vitamin B6 defi

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

191 1 complexes were distinct from canonical LAT-GADs-SLP-76 complexes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 re directly caused by specific disruption of GAD function by GAD antibodies.

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

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

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

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

216 The identification of GAD-antibody-producing cells has implications for the se

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

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

219 review the evidence on the pathogenicity of GAD antibodies.

220 drome is usually autoimmune, the presence of GAD antibodies in the cerebrospinal fluid is sufficient

221 a neurological syndrome and the presence of GAD antibodies, and we critically review the evidence on

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

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

224 rrow cells represent an additional source of GAD antibodies.

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

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

227 n Americans and one for African Americans on GAD-2 score.

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

229 antibody only against insulin (IAA-first) or GAD (GADA-first) by unsupervised clustering of temporal

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

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

232 We used six clinical parameters (GAD autoantibodies, age at diabetes onset, HbA(1c), BMI,

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

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

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

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

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

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

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

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

241 d and emotional learning processes represent GAD-specific markers.

242 ), the Generalized Anxiety Disorder-7 Scale (GAD-7), and the Sleep Hygiene Index (SHI).

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

244 e Generalized Anxiety Disorder 2-item scale [GAD-2], N=199,611) as the primary analysis and self-repo

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

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

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

248 Nevertheless, the evidence that GAD antibodies are directly pathogenic is not yet convin

249 The GAD autoantibodies were high affinity (antibody dissocia

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

251 The GAD-7 questionnaire showed no difference between the gro

252 significant genetic correlation between the GAD-2 score results and previous GWASs for anxiety (r(g)

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 logical syndrome is pathogenically linked to GAD antibodies, often leading to the assumption that any

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

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

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

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

268 r relatives retested positive with truncated GAD.

269 ly, YhaJ was found to override the universal GAD acid tolerance system but exclusively in EHEC, there

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 tal and dorsolateral prefrontal cortex while GAD was specifically characterized by decreased whole-br

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

274 and depressive symptoms in older adults with GAD.

275 .19, g = 0.25), PACAP may be associated with GAD in females (p = 0.04, g = 0.33).

276 aintaining anxiety and worry associated with GAD.

277 four SNPs were significantly associated with GAD.

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

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

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

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

282 that confirmation of a pathogenic link with GAD autoimmunity requires demonstration of intrathecal G

283 sufficient to confirm a pathogenic link with GAD autoimmunity.

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

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

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

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

288 Patients with GAD are at increased risk for suicide as well as cardiov

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

290 Additionally, among patients with GAD, the risk genotype identified in the PTSD literature

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 ls are highly elevated in most patients with GAD-antibody-associated disorders (n = 15) compared to c

294 tion of conditioned fear among patients with GAD.

295 bic structural connectivity in patients with GAD.

296 of perseverative cognitions in patients with GAD.

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

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

299 eneralization across adults with and without GAD.

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