ライフサイエンスコーパス: ADHD

1 ADHD and cannabis use are partly determined by genetic f

2 ADHD exhibited poorer accuracy and larger reaction times

3 ADHD is associated with a significantly increased risk f

4 ADHD often co-occurs with intellectual disability, and s

5 ADHD participants made more exploratory decisions (i.e.,

6 ADHD participants reported significantly greater dizzine

7 ADHD PRS explained ~ 1% (p value < 0.0001) of the varian

8 ADHD symptoms reliably cluster into two correlated dimen

9 ADHD was associated with increased procedures (AOR = 1.4

10 ADHD was defined by International Classification of Dise

11 ADHD-specific intracranial volume and hippocampal differ

12 (WGS) data on 875 individuals, including 205 ADHD cases and 670 non-ADHD controls.

13 s, adults with (n = 26) and without (n = 23) ADHD completed the bandit task at baseline, and after me

14 29 patients met study criteria (ASD N = 343; ADHD N = 1175; ASD + ADHD N = 140).

15 icipants were young adult nonsmokers (n = 61 ADHD, n = 75 Control) between the ages of 18-25 years (i

16 ever, given the extensive comorbidity across ADHD and other psychiatric conditions, the extent to whi

17 s the variable clinical course of adolescent ADHD is determined by plasticity of the cerebral cortex.

18 underlying the complex course of adolescent ADHD.

19 -standing selective pressures acting against ADHD-associated alleles until recent times.

20 rior to typical age of experimentation among ADHD patients.

21 ifferences across different age groups among ADHD, ASD, and OCD.

22 medicated at the time of scanning and had an ADHD diagnosis.

23 lation-level and within-individual analyses, ADHD medication was associated with lower odds of suicid

24 after birth in ASD (+ 6.5 h, p < 0.001) and ADHD (+ 3.8 h, p < 0.001), and after non-birth admission

25 mics Consortium for discovery (N=19,210) and ADHD data from the Lundbeck Foundation Initiative for In

26 ion studies on persistent ADHD in adults and ADHD in childhood separately and jointly, and by compari

27 e found that genetic liabilities for ASD and ADHD covary with neuromotor development during infancy.

28 ficant relationships were found with ASD and ADHD diagnoses (p = 0.0006 and p = 0.002, respectively).

29 limitation since ascertaining depression and ADHD from prescriptions omitted affected children receiv

30 oup to differ significantly in education and ADHD PGSs.

31 el the association between PFAS exposure and ADHD in each study, and combined all adjusted study-spec

32 OE) in the forebrain show hyperactivity and ADHD-like pharmacological responses to D-amphetamine.

33 ADHD-inattentive presentation (ADHD-I), and ADHD-combined presentation (ADHD-C).

34 tained ratings of anxiety, irritability, and ADHD, and 10 minutes of resting-state functional magneti

35 antibiotic use in the first year of life and ADHD risk.

36 from records of additional support needs and ADHD and depression through relevant encashed prescripti

37 PFOS) and perfluorooctanoic acid (PFOA), and ADHD in a collaborative study including nine European po

38 3 transcript with risk for schizophrenia and ADHD, and increased expression of an XPNPEP3 transcript

39 h that is sensitive to medication status and ADHD comorbidity.

40 enetically associated with substance use and ADHD, suggesting impulsivity is an endophenotype contrib

41 iation between prenatal Tdap vaccination and ADHD in offspring (hazard ratio = 1.00, 95% confidence i

42 iation between maternal Tdap vaccination and ADHD, with inverse probability of treatment weighting (I

43 ildhood neurodevelopmental disorders such as ADHD, typically onset in early childhood but can persist

44 criteria (ASD N = 343; ADHD N = 1175; ASD + ADHD N = 140).

45 efore age 1 were grouped as ASD, ADHD, ASD + ADHD, or No Diagnosis using retrospective billing codes.

46 ssion in ADHD (+ 1.1 d, p < 0.001) and ASD + ADHD (+ 2.4 d, p = 0.003).

47 lth System before age 1 were grouped as ASD, ADHD, ASD + ADHD, or No Diagnosis using retrospective bi

48 ehavioral measures in 176 children with ASD, ADHD or OCD with complete data that passed quality contr

49 d with intelligence, educational attainment, ADHD, autism, and bipolar disorder and among de novo var

50 with five diagnoses (i.e., anxiety, autism, ADHD, depressive, specific learning) in a large-scale, t

51 udy was to evaluate the associations between ADHD polygenic risk scores (PRS) and a broad range of ch

52 We estimated associations between ADHD PRS, a general psychopathology factor, and several

53 bstantiate the temporal relationship between ADHD and future cannabis use and reinforce the need to c

54 FDR < 0.01), of which 30 were shared between ADHD and educational attainment or general intelligence

55 Both ADHD symptoms and CD symptoms were related to similar an

56 ting and working memory were related to both ADHD and CD traits.

57 A network of 66 genes was supported by ADHD-relevant phenotypes in the cross-species database.

58 r predicting treatment outcomes in childhood ADHD.

59 dies report that adolescents whose childhood ADHD symptoms have remitted are indistinguishable from n

60 We classified ADHD using recommended cutoff points for each instrument

61 rongest driver of absenteeism and coexisting ADHD the strongest driver of exclusion.

62 ed consecutively (29 inattentive or combined ADHD subtype and 27 controls) between 7 and 16 years old

63 independent cohort of patients with combined ADHD and insomnia that 8 of 62 patients and 0 of 369 con

64 ted multigenerational families with combined ADHD and insomnia.

65 of ADHD status and methylphenidate, a common ADHD medication, on explore/exploit decisions using a 6-

66 WM encoding, binding and retrieval comparing ADHD and non-ADHD matched adolescents.

67 The objective of this study was to define ADHD-associated candidate genes and their associated mol

68 ge 9.4 (SD 1.9) years; 45 with DSM 5-defined ADHD) as they completed the continuous performance task

69 We derived ADHD PRS for 13,457 children aged 9 or 12 from the Child

70 etween PS and reading and math disabilities, ADHD-inattentive presentation (ADHD-I), and ADHD-combine

71 These include Parkinson's disease, ADHD, schizophrenia, and mood disorders, which show star

72 of attention deficit hyperactivity disorder (ADHD) and associated cognitive anomalies, particularly i

73 ), attention-deficit hyperactivity disorder (ADHD) and autism (AUT).

74 th attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD).

75 of attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD).

76 Attention-Deficit/Hyperactivity Disorder (ADHD) and conduct disorder (CD) exemplify top-down dysre

77 or attention deficit hyperactivity disorder (ADHD) and depression have more school absences and exclu

78 th attention deficit hyperactivity disorder (ADHD) are at increased risk for adverse cigarette smokin

79 nd attention-deficit/hyperactivity disorder (ADHD) are clinically and biologically heterogeneous neur

80 nd attention-deficit/hyperactivity disorder (ADHD) as common, impactful, co-occurring problems.

81 al attention-deficit/hyperactivity disorder (ADHD) diagnoses and symptoms in the general population.

82 of attention-deficit/hyperactivity disorder (ADHD) has been stable over the past 3 decades, prescript

83 or attention deficit hyperactivity disorder (ADHD) have 2-3 times increased healthcare utilization an

84 of attention-deficit hyperactivity disorder (ADHD) have suggested that structural variants (SVs) play

85 of attention-deficit/hyperactivity disorder (ADHD) in offspring.

86 Attention deficit/hyperactivity disorder (ADHD) is a common and heritable phenotype frequently acc

87 Attention deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder characteri

88 Attention deficit hyperactivity disorder (ADHD) is a common neuropsychiatric condition that has be

89 Attention deficit hyperactivity disorder (ADHD) is a common, highly heritable neuropsychiatric dis

90 Attention deficit hyperactivity disorder (ADHD) is a highly heritable psychiatric disorder.

91 Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder that is consisten

92 Attention-deficit/hyperactivity disorder (ADHD) is a risk factor for suicidal behavior, but the ef

93 Attention-deficit/hyperactivity disorder (ADHD) is a severely impairing neurodevelopmental disorde

94 Attention-deficit/hyperactivity disorder (ADHD) is an impairing neurodevelopmental condition highl

95 Attention-deficit hyperactivity disorder (ADHD) is associated with pervasive impairments in attent

96 Attention-deficit/hyperactivity disorder (ADHD) is emblematic of the problems in the existing psyc

97 of attention-deficit/hyperactivity disorder (ADHD) is heritable.

98 ttention deficit and hyperactivity disorder (ADHD) is inconclusive.

99 of attention-deficit/hyperactivity disorder (ADHD) run a variable course through adolescence.

100 od attention deficit hyperactivity disorder (ADHD) shows a highly variable course with age: some indi

101 nd attention-deficit/hyperactivity disorder (ADHD) using genome-wide association study summary statis

102 ng attention-deficit hyperactivity disorder (ADHD), a highly heritable disorder with an array of cand

103 Attention deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and obsessive-com

104 of attention deficit hyperactivity disorder (ADHD), autism spectrum disorder, bipolar disorder, major

105 de attention-deficit/hyperactivity disorder (ADHD), autism, mild facial dysmorphism, craniosynostosis

106 Attention-deficit hyperactivity disorder (ADHD), like other psychiatric disorders, represents an e

107 th attention-deficit/hyperactivity disorder (ADHD), potentially due to deficient catecholamine transm

108 nd attention-deficit hyperactivity disorder (ADHD), the entire range of neurodevelopmental disorders

109 th Attention-Deficit/Hyperactivity Disorder (ADHD).

110 th attention deficit hyperactivity disorder (ADHD).

111 or attention deficit hyperactivity disorder (ADHD).

112 th attention-deficit/hyperactivity disorder (ADHD).

113 nd attention deficit hyperactivity disorder (ADHD).

114 th attention-deficit/hyperactivity disorder (ADHD).

115 r, attention deficit hyperactivity disorder (ADHD)] in children of preeclamptic pregnancies, as well

116 nd Attention-Deficit-Hyperactivity-Disorder (ADHD), but their impact on functional connectivity (FC)

117 ], attention deficit/hyperactivity disorder [ADHD], bipolar disorder, schizophrenia, alcohol dependen

118 odes (Ninth or Tenth Revision) and dispensed ADHD medication after age 3 years.

119 ren were followed to the date of their first ADHD diagnosis, the end of Kaiser Permanente membership,

120 a, 5 of 40 for major depression, 3 of 11 for ADHD and 1 of 2 for autism.

121 given the lack of genomic data available for ADHD, these theories have not been empirically tested.

122 sociated to CD symptoms when controlling for ADHD symptoms.

123 FDR < 0.01) and 46 were novel risk loci for ADHD.

124 on may be a potential therapeutic option for ADHD-associated impairments in sustained attention, inhi

125 Higher PRSs for ADHD were associated with less optimal senses.

126 n of common genetic variants to the risk for ADHD across the lifespan by conducting meta-analyses of

127 between common variant (polygenic) risk for ADHD and its core symptoms.

128 delineate a pathway from polygenic risk for ADHD to hyperactive-impulsive symptoms through white mat

129 We found that polygenic risk for ADHD was associated with symptoms of hyperactivity-impul

130 t of 362 youth, we ask if polygenic risk for ADHD, combined with baseline neural and cognitive featur

131 ptoms carried the highest polygenic risk for ADHD, followed by those with stable symptoms, then those

132 d others spared by the etiological risks for ADHD.

133 matic review of PubMed articles screened for ADHD medications and potential cardiovascular toxicity a

134 yzed independent GWAS summary statistics for ADHD (19,099 cases and 34,194 controls) and BD (20,352 c

135 ide association study summary statistics for ADHD (19,099 cases and 34,194 controls), educational att

136 the latest genome-wide association study for ADHD showed that among those 26 genes, POLR3C and RBFOX1

137 are compatible with the mismatch theory for ADHD but suggest a much older time frame for the evoluti

138 PRSs for ASD and those for ADHD both were associated with autistic traits.

139 ssociations between medication treatment for ADHD and risk of suicide attempts.

140 richment of common genetic risk variants for ADHD within implicated gene sets suggests an environment

141 al of 399 children were classified as having ADHD, with a prevalence ranging from 2.3% to 7.3% in the

142 The relatively small number of heritable, ADHD-associated developmental neural phenotypes can serv

143 Higher ADHD PRS were statistically significantly associated wit

144 rd value may be a key feature of hyperactive ADHD symptoms.

145 were positively associated with hyperactive ADHD symptoms across all participants.

146 m (ASD) and attention deficit hyperactivity (ADHD) disorders.

147 table bioinformatics approaches can identify ADHD candidate genes at increased levels of credibility.

148 acids, which could be helpful for improving ADHD symptoms.

149 p < 0.001), and after non-birth admission in ADHD (+ 1.1 d, p < 0.001) and ASD + ADHD (+ 2.4 d, p = 0

150 rther determined associations with change in ADHD symptoms.

151 l models of increased exploratory choices in ADHD and suggest the unexplained variance in ADHD decisi

152 Comorbid conditions in ADHD play a key role in symptom progression, disorder co

153 ience model of cognitive control deficits in ADHD, and suggests specific circuit biomarkers for predi

154 izes findings from subphenotyping efforts in ADHD that use cognitive, emotion-related, and other feat

155 ogressed Neanderthal alleles are enriched in ADHD risk variants.

156 associated genes have not been identified in ADHD and ASD GWASs before.

157 Working memory (WM) impairments in ADHD have been consistently reported along with deficits

158 while binding processes seem to be intact in ADHD, attention-related encoding and retrieval processes

159 functional connectivity at rest is lower in ADHD patients when compared with healthy controls, howev

160 coding regions may play an important role in ADHD development and that WGS could be a powerful discov

161 ovides novel mechanistic clues about SBRV in ADHD.

162 lective brain region vulnerability (SBRV) in ADHD.

163 evelopment genes with smaller brain sizes in ADHD, along with associations to regional abundances of

164 ADHD and suggest the unexplained variance in ADHD decisions may be due to less value tracking.

165 odevelopmental SOXopathy that often includes ADHD and abnormal skeletal and other features.

166 tified 58 linkage disequilibrium-independent ADHD-associated loci (conditional FDR < 0.01), of which

167 a-based Mendelian randomization to integrate ADHD and ASD GWAS data with fetal brain expression and m

168 tly captured shared aspects of irritability, ADHD, and anxiety, while the third was specific to anxie

169 y as well as nondrug strategies for managing ADHD.

170 tion (MR) analyses were conducted, with MDD, ADHD, and schizophrenia emerging as the most plausible c

171 iduals, including 205 ADHD cases and 670 non-ADHD controls.

172 binding and retrieval comparing ADHD and non-ADHD matched adolescents.

173 P3 were significantly correlated only in non-ADHD.

174 accuracy and larger reaction times than non-ADHD on all conditions but especially when a change acro

175 Encoding P3 was larger in the non-ADHD group.

176 eval P3 discriminated change only in the non-ADHD group.

177 fects across all conditions, compared to non-ADHD non-smokers.

178 ns, duplications, idiopathic ASD, SZ but not ADHD.

179 ging this enrichment, we identified 19 novel ADHD risk loci and 40 novel BD risk loci at condFDR <0.0

180 ntified TRAPPC9, MEF2C, and ST3GAL3 as novel ADHD candidate genes.

181 The aim of this study was to identify novel ADHD genes by investigating whether genes carrying rare

182 sential to clarify the risks and benefits of ADHD stimulant medications and to explore nonpharmacolog

183 regional changes in brain sizes in cases of ADHD.

184 allenge current conceptions of the causes of ADHD in ways that might have the potential to alter clin

185 consider substance misuse in the context of ADHD in clinical interventions.

186 t similar patterns of genetic correlation of ADHD with other ADHD-related datasets and different trai

187 icant associations with the future course of ADHD symptoms and may have modest predictive power.

188 original studies did not report diagnoses of ADHD or ASD.

189 142 singletons; 150 (52%) had a diagnosis of ADHD (determined by clinician interview with parent); 18

190 tor for suicidal behavior, but the effect of ADHD medication on suicidal behavior remains unclear.

191 of studies that investigated the effects of ADHD medication on behavioral and neuropsychiatric outco

192 Here, we examined the effects of ADHD status and methylphenidate, a common ADHD medicatio

193 ing to disentangle the complex etiologies of ADHD, educational attainment, and general intelligence.

194 a much older time frame for the evolution of ADHD-associated alleles compared to previous hypotheses.

195 35,000 controls, to assess the evolution of ADHD-associated alleles in European populations using ar

196 of genome-wide association studies (GWAS) of ADHD (n = 53,293) and lifetime cannabis use (n = 32,330)

197 ined by genetic factors; the heritability of ADHD is estimated at 70-80% and of cannabis use initiati

198 t informative about children's likelihood of ADHD and ASD diagnoses.

199 ool for studying the molecular mechanisms of ADHD.

200 t subcortical anomalies reflect the onset of ADHD and remain throughout life regardless of symptom ch

201 tanding of the causes and pathophysiology of ADHD on the basis of science over the past decade or so.

202 ring childhood predicting the persistence of ADHD symptoms into adulthood, the genetic architecture u

203 did not identify an increased prevalence of ADHD in association with early life exposure to PFOS and

204 that there may be an increased prevalence of ADHD in association with PFAS exposure in girls, in chil

205 rwa et al. reported a 20%-30% higher risk of ADHD and ASD following prenatal acetaminophen exposure.

206 ependently associated with a reduced risk of ADHD.

207 rial evidence addressing long-term safety of ADHD medications, particularly among adults.

208 alysis of genome-wide association studies of ADHD diagnosis and symptoms.

209 ts in FOV as a mechanism linking symptoms of ADHD and deficits in focused attention and in the gather

210 ic architecture underlying the trajectory of ADHD over time is still unclear.

211 he diagnosis, epidemiology, and treatment of ADHD from the perspective of both the fifth edition of t

212 both the current models and the treatment of ADHD, and the ways in which these findings can promote n

213 755 individuals with idiopathic ASD, SZ, or ADHD and 1,072 controls.

214 ns of genetic correlation of ADHD with other ADHD-related datasets and different traits and disorders

215 onments is a promising candidate to overcome ADHD related memory problems.

216 enome-wide association studies on persistent ADHD in adults and ADHD in childhood separately and join

217 These findings confirm that persistent ADHD in adults is a neurodevelopmental disorder and exte

218 on (ADHD-I), and ADHD-combined presentation (ADHD-C).

219 disabilities, ADHD-inattentive presentation (ADHD-I), and ADHD-combined presentation (ADHD-C).

220 The high-priority ADHD candidate genes were significantly coexpressed in t

221 f which they classified 432 as high-priority ADHD candidate genes.

222 n modules were found among the high-priority ADHD genes.

223 dentified or replicated, and novel recurrent ADHD-associated SV loci were discovered.

224 DHD-RS inattention subscale and the CTRS-R:S ADHD index and hyperactivity subscale also deteriorated

225 od but can persist into adult life; the same ADHD genetic loading appears to contribute across the li

226 ation of gene expression related to specific ADHD phenotypes.

227 firming the role of MDD, we demonstrate that ADHD and schizophrenia likely play a role in the aetiolo

228 We hypothesized that ADHD participants would make more exploratory decisions

229 Our analyses indicate that ADHD-associated alleles are enriched in loss of function

230 cent longitudinal studies have observed that ADHD symptoms may emerge later during adolescence and ad

231 The cumulative body of data showed that ADHD medications cause modest elevations in resting hear

232 randomization approach we found support that ADHD is causal for lifetime cannabis use, with an odds r

233 The ADHD cases included 116 African Americans (AA) and 89 of

234 The ADHD incidence rate was 3.41 per 1,000 person-years in t

235 The ADHD PRS associated with impulsivity symptoms (b = 0.006

236 The ADHD-RS inattention subscale and the CTRS-R:S ADHD index

237 tic resonance imaging (MRI) results from the ADHD ENIGMA Consortium (subcortical MRI n = 3242; cortic

238 Signal test was specifically related to the ADHD trait, delayed discounting and working memory were

239 rain structure is specifically associated to ADHD or CD symptoms in a general population of adolescen

240 ngulate cortex were negatively associated to ADHD symptoms when controlling for CD symptoms while ros

241 ked to intellectual disability contribute to ADHD risk through common genetic variants.

242 ctual disability-related genes contribute to ADHD risk through effects of common alleles.

243 uggests that TRAPPC9 and MEF2C contribute to ADHD-related behavior through distinct neural substrates

244 ronal brain function, and highly relevant to ADHD pathogenesis and regulation of gene expression rela

245 d contribution of common genetic variants to ADHD in children and adults.

246 ve, and behavioral functioning that underlie ADHD and other existing psychiatric categories to create

247 of a shared genetic architecture underlying ADHD and different traits to a lifespan perspective.

248 ght into the molecular mechanisms underlying ADHD and allows prioritization of genes for functional v

249 olved in the biological processes underlying ADHD that can be targeted by pharmacological agents.

250 rough gene set and gene-wide analyses, using ADHD meta-analytic data from the Psychiatric Genomics Co

251 s of neural activity among adolescents whose ADHD has improved.

252 ed in an independent cohort (N=231; 132 with ADHD; age range, 7-18 years).

253 participated (mean 21 years, 212 (39%) with ADHD), most with cognitive assessments, neuroanatomic im

254 Children and adolescents with ADHD also had smaller intracranial volume than control s

255 nsolidation in children and adolescents with ADHD.

256 erns of psychiatric disorders in adults with ADHD (n = 38,636; 2.3%), ASD (n = 7528; 0.4%), and both

257 nt to which genetic variants associated with ADHD also influence broader psychopathology dimensions r

258 ntified the genetic variants associated with ADHD and ASD that likely act through gene regulation.

259 romosomes 1 and 17 that were associated with ADHD and ASD, respectively, through pleiotropy at shared

260 top-down regulatory systems associated with ADHD and CD symptoms.

261 re characteristics typically associated with ADHD and should represent a valuable model to investigat

262 sure to PFOS or PFOA was not associated with ADHD during childhood [odds ratios (ORs) ranging from 0.

263 le SVs and target genes that associated with ADHD from previous studies were identified or replicated

264 at the frequency of variants associated with ADHD has steadily decreased since Paleolithic times, par

265 dentified by GWAS studies as associated with ADHD in humans are significantly altered in our mouse mo

266 tal Tdap vaccination was not associated with ADHD risk in offspring, supporting recommendations to va

267 y gene set was significantly associated with ADHD risk in the discovery and replication data sets.

268 common genetic risk variants associated with ADHD, and captured by PRS, also influence a general gene

269 ntified common gene variants associated with ADHD, but most of the genetic architecture remains unkno

270 ility genes were tested for association with ADHD risk through gene set and gene-wide analyses, using

271 le suggested more specific associations with ADHD and learning disorders than the literature currentl

272 effects of methylphenidate in children with ADHD and ID.

273 of acute aerobic exercise for children with ADHD as a potential means to facilitate brain health.

274 Children with ADHD compared with those with OCD had smaller hippocampa

275 However, children with ADHD vary considerably in their symptom profiles, sympto

276 ol are sustained for 60 min in children with ADHD.

277 ng of over 20,000 individuals diagnosed with ADHD and 35,000 controls, to assess the evolution of ADH

278 disruptive mood dysregulation disorder, with ADHD, or without psychopathology.

279 l types of EDs was found in individuals with ADHD (any ED: odds ratio [OR] = 3.97, 95% confidence int

280 variation studies in 6,176 individuals with ADHD and 25,026 control subjects and prioritized genes b

281 of 7.9 for cannabis use in individuals with ADHD in comparison to individuals without ADHD (95% CI (

282 ria including recurrence in individuals with ADHD, absence in control subjects, complete coverage in

283 ader clinical needs of many individuals with ADHD, especially over the longer term.

284 e identified a large cohort of patients with ADHD (N = 3,874,728, 47.8% female patients) using data f

285 ol subjects (N=5,827) and from patients with ADHD (N=2,271), ASD (N=1,777), and OCD (N=2,323) from 15

286 34 patients with ADHD and 34 typically developing participants (age 9-15

287 associations evaluated in the patients with ADHD compared with the controls were: P_D=0.41 vs 0.44;

288 relevant subgroups, including patients with ADHD with preexisting depression or substance use disord

289 ed risk of suicide attempts in patients with ADHD, and nonstimulant medication is unlikely to increas

290 ts, which was not the case for patients with ADHD.

291 Other adverse effects reported with ADHD stimulants included arrhythmia, nonischemic cardiom

292 s revealed that this variant segregated with ADHD and delayed sleep phase disorder (DSPD) in the affe

293 significantly higher among non-smokers with ADHD, and their choices of nicotine were not influenced

294 with washout, to five boys (8-15 years) with ADHD.

295 Within ADHD, cognitive (neuropsychological) and temperament/per

296 en children and adolescents with and without ADHD suggests that behavioral tagging might only be able

297 ne exposure in young adults with and without ADHD using a novel paradigm of exposure to model initial

298 rences between young adults with and without ADHD with respect to the initial subjective and reinforc

299 th ADHD in comparison to individuals without ADHD (95% CI (3.72, 15.51), P = 5.88 x 10(-5)).

300 relatives compared with individuals without ADHD and their relatives.