ライフサイエンスコーパス: ADHD

1 ADHD effects were divided into those shared between twin

2 ADHD+ODD and ADHD-only showed volumetric reductions in t

3 ADHD+ODD and ADHD-only were associated with volumetric r

4 ADHD-related behaviour was assessed via maternal ratings

5 n a recent multi-site, mega-analysis of 1713 ADHD persons and 1529 controls.

6 daily smokers with (n=17) and without (n=20) ADHD completed fMRI scanning under each of three conditi

7 cheek swabs to obtain the genomic DNA of 200 ADHD male probands (mean age: 8.7 years), 192 patients'

8 HC (n = 47), children with AD-only (n = 42), ADHD-only (n = 34) and comorbid AD + ADHD (n = 31) had s

9 rface-based morphometry): ADHD+ODD (n = 67), ADHD-only (n = 243), and control subjects (n = 233).

10 A total of 58,912 ADHD cases (68.8% male) were identified and matched to 4

11 hout ADHD), ADHD-only (ie, without AD), AD + ADHD and healthy controls (HC; ie, no AD/no ADHD).

12 = 42), ADHD-only (n = 34) and comorbid AD + ADHD (n = 31) had significantly increased behavioural pr

13 osocial characteristics of children with AD, ADHD, comorbid AD/ADHD and age-matched healthy controls

14 stics of children with AD, ADHD, comorbid AD/ADHD and age-matched healthy controls and to investigate

15 aged 6-12 years: AD-only (ie, without ADHD), ADHD-only (ie, without AD), AD + ADHD and healthy contro

16 old in the weighted (to the 8.2% DSM-5/Adult ADHD Clinical Diagnostic Scale population prevalence) da

17 ,993,887 (47.2% female) adolescent and adult ADHD patients.

18 York University Langone Medical Center Adult ADHD Program (NYU Langone) and 2015-2016 primary care co

19 one respondents met DSM-5 criteria for adult ADHD in the semistructured diagnostic interview.

20 iagnosed has led to the development of adult ADHD screening scales for use in community, workplace, a

21 widely used World Health Organization Adult ADHD Self-Report Scale (ASRS) for screening.

22 duced decreases in activation observed among ADHD smokers compared with non-ADHD smokers.

23 and increased striatal activation only among ADHD smokers.

24 y and April), the cumulative incidence of an ADHD diagnosis was greatest for the youngest children (i

25 Using an ADHD rat model, we demonstrate that impulsive animals ar

26 We therefore investigated how ASD and ADHD co-aggregate in individuals and in families to test

27 ation between clinically ascertained ASD and ADHD in individuals and in families.

28 erlap between clinically ascertained ASD and ADHD remains largely unclear.

29 e presence of a genetic link between ASD and ADHD symptoms is supported by twin studies, but the gene

30 erlap between clinically ascertained ASD and ADHD, suggesting that genomic studies might have underes

31 rring neurodevelopmental conditions, ASD and ADHD, through both categorical and dimensional approache

32 fects related to both functional aspects and ADHD behaviour were also observed for DPP10 and TPH2.

33 Polygenic risk of autism and ADHD is associated with number of children.

34 e associations between maternal diseases and ADHD in offspring were analyzed using logistic regressio

35 e the familial coaggregation of epilepsy and ADHD and to estimate the contribution of genetic and env

36 Our findings suggest that epilepsy and ADHD may share less genetic risk as compared with other

37 stimate the association between epilepsy and ADHD within individual and across relatives.

38 lly complex association between epilepsy and ADHD, with shared familial factors and risk factors uniq

39 phenotypic correlation between epilepsy and ADHD, with the remaining variance largely explained by n

40 Assessments for Tourette syndrome, OCD, and ADHD symptoms were conducted in a discovery sample of 3,

41 associated with Tourette syndrome, OCD, and ADHD were estimated.

42 ADHD+ODD and ADHD-only showed volumetric reductions in total gray mat

43 ADHD+ODD and ADHD-only were associated with volumetric reductions in

44 h disinhibition, while Tourette syndrome and ADHD risk scores were not.

45 isk for neurodevelopmental disorders such as ADHD.

46 em, associations with the Nogo-P3 as well as ADHD symptom severity were found suggesting that these s

47 vealed overlapping behavioral problems (ASD, ADHD, and anxiety disorders), hypotonia, broad-based gai

48 y relying on screening instruments to assess ADHD, not considering alternative causes of symptoms, or

49 We assessed ADHD-related behaviors at age 8 years using Conners' Tea

50 relative age within the school year, age at ADHD diagnosis, and year of diagnosis (1998-2003 vs 2004

51 ultations that result in a decision to begin ADHD treatment.

52 To examine the association between ADHD and both driver licensing and crash involvement and

53 oncurrent and long-term associations between ADHD medication treatment and substance-related events.

54 To explore associations between ADHD medication use and risk of MVCs in a large cohort o

55 Similar associations between ADHD medication use and test scores were detected in sen

56 ify whether the observed comorbidity between ADHD and BPD could be due to shared genetic risks.

57 lymorphism-based genetic correlation between ADHD and BPD in the full and age-restricted samples (rGf

58 lymorphism-based genetic correlation between ADHD and BPD is substantial, significant, and consistent

59 ith the existence of genetic overlap between ADHD and BPD, with potential differential genetic mechan

60 nd escalation are affected differentially by ADHD subtype and gender.

61 ight caudate anomalies reflected a childhood ADHD history and were present even among those who remit

62 ancing our therapeutic approach to childhood ADHD treatment.

63 METHOD: Individuals without childhood ADHD (N=239) were administered eight assessments from co

64 e with bipolar disorder suffer from comorbid ADHD.

65 the expression of genes in a set of curated ADHD candidate genes and five a priori selected, biologi

66 re two to three times more likely to develop ADHD.

67 that DNA methylation at birth differentiated ADHD trajectories across multiple genomic locations, inc

68 Attention-deficit/hyperactivity disorder (ADHD) affects 39 million people worldwide; in isolation,

69 Attention-deficit/hyperactivity disorder (ADHD) and anxiety-related disorders occur at rates 2-3 t

70 nd attention-deficit-hyperactivity disorder (ADHD) and between openness and schizophrenia and bipolar

71 Attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder (BPD) are frequently co-occur

72 ng attention-deficit/hyperactivity disorder (ADHD) and is currently the first-line pharmacological tr

73 at attention-deficit/hyperactivity disorder (ADHD) and off-label as a performance-enhancing agent in

74 ), attention deficit hyperactivity disorder (ADHD) and schizophrenia (SCZ).

75 ng attention deficit hyperactivity disorder (ADHD) and substance use disorders, are characterized by

76 en attention-deficit hyperactivity disorder (ADHD) and younger relative age in the school year.

77 th attention-deficit/hyperactivity disorder (ADHD) are at an increased risk of attempting suicide.

78 th attention-deficit/hyperactivity disorder (ADHD) are at greater risk for academic problems.

79 th attention-deficit/hyperactivity disorder (ADHD) are more likely to experience MVCs, but the effect

80 nd attention-deficit/hyperactivity disorder (ADHD) are strongly associated; however, the underlying f

81 od attention deficit hyperactivity disorder (ADHD) could guide novel interventions to improve its cli

82 Attention-deficit/hyperactivity disorder (ADHD) diagnosis is based on reported symptoms, which car

83 nd attention-deficit/hyperactivity disorder (ADHD) frequently co-occur.

84 Attention-deficit/hyperactivity disorder (ADHD) has an uncertain etiology, with potential contribu

85 of attention-deficit/hyperactivity disorder (ADHD) have most commonly reported volumetric abnormaliti

86 th attention-deficit/hyperactivity disorder (ADHD) in a recent multi-site, mega-analysis of 1713 ADHD

87 Attention-deficit hyperactivity disorder (ADHD) is a common childhood behavioural disorder.

88 Attention-deficit hyperactivity disorder (ADHD) is a prevalent and highly heritable disorder of ch

89 Attention-deficit/hyperactivity disorder (ADHD) is a prevalent developmental disorder, associated

90 Attention-deficit/hyperactivity disorder (ADHD) is associated with structural abnormalities in tot

91 lt attention-deficit/hyperactivity disorder (ADHD) is common, seriously impairing, and usually undiag

92 nd attention-deficit/hyperactivity disorder (ADHD) is increasingly appreciated, but the underlying br

93 Attention-deficit/hyperactivity disorder (ADHD) is the most common childhood neurodevelopmental di

94 th attention deficit hyperactivity disorder (ADHD) is unclear.

95 Attention-deficit/hyperactivity disorder (ADHD) often persists into adolescence, when motor vehicl

96 od attention deficit hyperactivity disorder (ADHD) often present to clinics seeking stimulant medicat

97 Attention-deficit/hyperactivity disorder (ADHD) shows substantial heritability and is two to seven

98 Attention-deficit/hyperactivity disorder (ADHD) symptoms are most commonly treated with stimulant

99 od attention deficit hyperactivity disorder (ADHD) symptoms, both inattention and hyperactivity-impul

100 nd attention deficit hyperactivity disorder (ADHD) using genomic data from 150,656 Icelanders, exclud

101 y, attention deficit/hyperactivity disorder (ADHD), and autism spectrum disorder.

102 of attention-deficit/hyperactivity disorder (ADHD), we targeted the relationship of attentional, cogn

103 of attention deficit hyperactivity disorder (ADHD), which is a common childhood-onset psychiatric dis

104 th attention deficit hyperactivity disorder (ADHD), yet associations between pharmacological ADHD tre

105 th attention deficit hyperactivity disorder (ADHD).

106 of attention-deficit/hyperactivity disorder (ADHD).

107 or attention-deficit/hyperactivity disorder (ADHD).

108 nd attention-deficit/hyperactivity disorder (ADHD).

109 nd attention deficit hyperactivity disorder (ADHD).

110 as attention deficit/hyperactivity disorder (ADHD).

111 or attention-deficit/hyperactivity disorder (ADHD).

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

113 gh the formation of the international ENIGMA ADHD Working Group, we aimed to address weaknesses of pr

114 gs remained significant after accounting for ADHD symptom severity.

115 efrontal cortex structure is a biomarker for ADHD symptomatology.

116 reshold to meet full diagnostic criteria for ADHD.

117 The risk was somewhat elevated for ADHD with comorbid autism spectrum disorder (OR, 1.76; 9

118 nded multigenerational families enriched for ADHD (305 members with clinical phenotyping, 213 with DT

119 nded multigenerational families enriched for ADHD were evaluated.

120 implicate BDNF as a genetic risk factor for ADHD, potentially by virtue of its critical role in neur

121 mune components as possible risk factors for ADHD in offspring.

122 vity is a key pathophysiologic mechanism for ADHD, and identifying heritable phenotypes within these

123 res when patients were taking medication for ADHD were compared with scores when they were not taking

124 ervice system with low prescribing rates for ADHD, a younger relative age is associated with an incre

125 dentify subgroups of AD patients at risk for ADHD are poorly understood.

126 whether maternal PCOS increases the risk for ADHD in the offspring.

127 ls with ADHD are at higher familial risk for ADHD than the siblings of affected male individuals (odd

128 Nolan, and Pelham, and Version IV Scale for ADHD (SNAP-IV), and the neuropsychological function was

129 Medication approved solely for ADHD treatment.

130 C activity could be a treatment strategy for ADHD.

131 extend the brain maturation delay theory for ADHD to include subcortical structures and refute medica

132 ealth outcomes of schoolchildren treated for ADHD with their peers.

133 ochloride, are the most common treatment for ADHD, but the association between their therapeutic use

134 ntal cortical activity drives remission from ADHD, while anomalies in subcortical processes are "fixe

135 We monitored pupil size from ADHD and control subjects, during a visuo-spatial workin

136 duals with ASD were at higher risk of having ADHD compared with individuals who did not have ASD (odd

137 However, ADHD is still relatively under-recognised and underdiagn

138 ith ADHD, n-3 PUFAs supplementation improves ADHD clinical symptom scores (g=0.38, p<0.0001); and in

139 reviously reported striatal abnormalities in ADHD may be caused by comorbid conduct disorder rather t

140 variability of structural brain anomalies in ADHD can be explained, in part, by the differential vuln

141 iants largely do not explain the sex bias in ADHD prevalence.

142 hat pupil size could serve as a biomarker in ADHD.

143 with ADHD predict MPH-associated changes in ADHD inattentiveness and hyperactivity symptoms at 3 mon

144 are involved in response control deficits in ADHD.

145 mode network and dopaminergic dysfunction in ADHD.

146 se variations contribute to heterogeneity in ADHD.

147 velopment), ZNF544 (previously implicated in ADHD), ST3GAL3 (linked to intellectual disability) and P

148 association study of executive inhibition in ADHD in Han Chinese.

149 er, the potential role of DNA methylation in ADHD symptoms is currently unclear.

150 larger motivational effect on performance in ADHD already at this relatively young age.

151 la, accumbens, and hippocampus reductions in ADHD.

152 Epigenetic mechanisms may play a role in ADHD-associated deficits but findings need to be replica

153 he degree to which geographic variability in ADHD is independent of, or explained by, risk factors ma

154 ated determinants of geographic variation in ADHD-related behaviors among children living near the po

155 ing loss and behavioral disorders, including ADHD and anxiety-related disorders.

156 ge and sex displayed significantly increased ADHD-related behavior among children whose mothers resid

157 was significantly associated with increased ADHD symptoms (OR 1.88; 95% CI 1.04-3.39).

158 A methylation at birth associates with later ADHD trajectories; and then followed up at age 7 to inve

159 sonance imaging (surface-based morphometry): ADHD+ODD (n = 67), ADHD-only (n = 243), and control subj

160 The new ADHD screening scale is short, easily scored, detects th

161 ADHD and healthy controls (HC; ie, no AD/no ADHD).

162 bserved among ADHD smokers compared with non-ADHD smokers.

163 The association of ADHD symptoms with daily smoking, number of cigarettes p

164 the neuronal circuits and molecular basis of ADHD and its potential treatment using SHR.

165 analysis did not support a higher burden of ADHD common risk variants in female cases (odds ratio [c

166 tions between brain structural correlates of ADHD symptomatology and maps of dopaminergic gene expres

167 sociated with brain structural correlates of ADHD symptomatology.

168 lar processes tied to the clinical course of ADHD are separated from the subcortical processes that a

169 efined as an ICD-coded register diagnosis of ADHD and/or registered prescription of medications to tr

170 served 61640 individuals with a diagnosis of ADHD from January 1, 2006, to December 31, 2013.

171 Even if the clinical diagnosis of ADHD is excluded, children with AD show increased levels

172 elihood of receiving a clinical diagnosis of ADHD.

173 likely to experience MVCs, but the effect of ADHD medication treatment on the risk of MVCs remains un

174 olecular components influence the effects of ADHD treatment.

175 enhance our understanding of the etiology of ADHD.

176 Exclusion of ADHD cases with comorbid autism spectrum disorder attenu

177 A sub group of ADHD children performed the task twice, with and without

178 plain only a fraction of the heritability of ADHD.

179 el insights into the epigenetic landscape of ADHD symptoms, highlighting the potential importance of

180 d AD symptoms were unrelated to the level of ADHD symptoms.

181 h AD-only had significantly higher levels of ADHD symptoms than HC.

182 d, children with AD show increased levels of ADHD symptoms.

183 relationship between dimensional measures of ADHD symptomatology, brain structure, and reaction time

184 ex structure and multi-informant measures of ADHD symptoms in a large population-based sample of adol

185 n of AMPAR function and the normalization of ADHD-like behaviors in SHR.

186 The outcome of ADHD was defined as an ICD-coded register diagnosis of A

187 activity that underpins the adult outcome of ADHD was pinpointed.

188 account when considering the possibility of ADHD in a child or encountering a child with a pre-exist

189 Considering the high prevalence of ADHD and its association with MVCs, these findings warra

190 e community and administrative prevalence of ADHD in children and adolescents, an overview of barrier

191 Parent ratings of ADHD symptoms (Development and Well-Being Assessment and

192 Parent ratings of ADHD symptoms were obtained using the Development and We

193 essment and SDQ), adolescent self-reports of ADHD symptoms on the SDQ, and reaction time variability

194 Self-reports of ADHD symptoms were assessed using the youth version of t

195 tilized parent, teacher, and self-reports of ADHD symptoms, impairment, substance use, and other ment

196 statistically significant increased risk of ADHD (odds ratio [OR] = 3.47, 95% confidence interval [C

197 individuals with ASD were at higher risk of ADHD compared with relatives of individuals without ASD.

198 omponents were found to increase the risk of ADHD in offspring.

199 first child whereas higher polygenic risk of ADHD is associated with having more children.

200 and their relatives are at increased risk of ADHD.

201 Total severity of ADHD-traits was not significantly related to DTI metrics

202 next-generation targeted sequencing study of ADHD in 152 child and adolescent cases and 188 controls

203 n group of the Multimodal Treatment Study of ADHD.

204 7 (n=892, 50% male) and (2) trajectories of ADHD symptoms (7-15 years).

205 vestigate the association between the use of ADHD medication and performance on higher education entr

206 aternal PCOS increased the odds of offspring ADHD by 42% after adjustment for confounders (odds ratio

207 There was no evidence for adult-onset ADHD independent of a complex psychiatric history.

208 tom checklists were excluded from late-onset ADHD diagnosis.

209 Individuals seeking treatment for late-onset ADHD may be valid cases; however, more commonly, symptom

210 Among individuals with impairing late-onset ADHD symptoms, the most common reason for diagnostic exc

211 seeking stimulant medication for late-onset ADHD symptoms.

212 ort studies support the notion of late-onset ADHD, but these investigations are limited by relying on

213 nged with additional adjustment for parental ADHD, infant birth weight, and gestational age.

214 ood, contrasting remitted against persistent ADHD.

215 METHOD: Adult participants (persistent ADHD, N=35; remit-ted ADHD, N=47; never affected, N=99)

216 The persistent ADHD group showed under-activation, whereas the remitted

217 D), yet associations between pharmacological ADHD treatment and substance-related problems remain unc

218 sex, licensing age, and/or being prescribed ADHD medication at licensure.

219 to periods in which patients did not receive ADHD medication, male patients had 35% lower odds of con

220 were lower during periods when they received ADHD medication.

221 Individuals receiving ADHD medication during the years 2004-2012 were defined

222 hese results provide evidence that receiving ADHD medication is unlikely to be associated with greate

223 lower risk of MVCs in months when receiving ADHD medication compared with months when not receiving

224 lower risk of MVCs in months when receiving ADHD medication.

225 howed under-activation, whereas the remitted ADHD group did not differ significantly from the never-a

226 Adolescents who had more severe ADHD symptoms as children were more likely to initiate s

227 lopment of fundamental therapies that target ADHD pathophysiology.

228 rticipants (persistent ADHD, N=35; remit-ted ADHD, N=47; never affected, N=99) were scanned with func

229 These findings suggest that ADHD medications may help ameliorate educationally relev

230 , for those born between May and August, the ADHD incidence ratio was 1.37 (95% CI 1.24-1.53; p<0.000

231 Saliva samples were collected from the ADHD patients to analyze DHEA and DHEA-S levels.

232 uctions of frontal lobes were largest in the ADHD+ODD group, possibly underlying observed larger impa

233 nections that are heritable and pertinent to ADHD.

234 eases with immune components were related to ADHD in offspring: multiple sclerosis (adjusted odds rat

235 and to investigate aspects of AD related to ADHD symptoms.

236 d to investigate disease patterns related to ADHD symptoms.

237 nidate (a psychostimulant drug used to treat ADHD), which blocks dopamine transporters and norepineph

238 istered prescription of medications to treat ADHD.

239 multiple entrance tests (n = 2524) and used ADHD medications intermittently, the test scores were a

240 understand the specific mechanisms by which ADHD influences crash risk.

241 ls with a driver's license, 764 of 1785 with ADHD (42.8%) and 4715 of 13221 without ADHD (35.7%) cras

242 nd cognition in children and adolescent with ADHD; and (2) case-control studies assessing the levels

243 We know little about when adolescents with ADHD get licensed and, once they do, the extent to which

244 Adolescents with ADHD get licensed less often and at an older age.

245 Moreover, children and adolescents with ADHD have lower levels of DHA (seven studies, n=412, g=-

246 erformances in children and adolescents with ADHD, and that these youth have a deficiency in n-3 PUFA

247 cal tissues of children and adolescents with ADHD.

248 ural differences in children and adults with ADHD compared with those without this diagnosis.

249 urotrophic factor (BDNF) was associated with ADHD at Bonferroni corrected levels.

250 gate whether relative age is associated with ADHD diagnosis in a country where prescribing rates are

251 significantly heritable and associated with ADHD.

252 in the SULT2A1 gene were not associated with ADHD.

253 Association with ADHD symptoms was found in several tracts, most strongly

254 Heritability and association with ADHD symptoms were estimated in 24 extended multigenerat

255 these probes maintained an association with ADHD trajectories at age 7.

256 Thirty-one children with ADHD and thirty age- and IQ-matched typically developing

257 function network is altered in children with ADHD and whether COMT polymorphism is associated with th

258 en while receiving medication, children with ADHD fare worse than their peers across a wide range of

259 , 1998, and Dec 31, 2011, 6136 children with ADHD were identified.

260 Children with ADHD were more likely to require hospitalization overall

261 ere strong and significant for children with ADHD, but not for adults.

262 ipants were children with ASD, children with ADHD, or typically developing children.

263 y recognition and treatment of children with ADHD-type difficulties provides an opportunity to improv

264 e data were also obtained from children with ADHD.

265 pathways were significantly correlated with ADHD-associated volumetric reductions: apoptosis, oxidat

266 arly likely to show genetic covariation with ADHD.

267 1, and Dec 31, 2004, who were diagnosed with ADHD from age 7 years onwards (age of starting school).

268 first MPH dose in boys newly diagnosed with ADHD predict MPH-associated changes in ADHD inattentiven

269 imulant drug-naive boys newly diagnosed with ADHD while they performed the AX version of the continuo

270 for first crash among licensed drivers with ADHD was 1.36 times higher than for those without ADHD (

271 Among 2 319 450 patients identified with ADHD, the mean (SD) age was 32.5 (12.8) years, and 51.7%

272 Only 129 individuals with ADHD (12.1%) were prescribed medication in the 30 days b

273 he licensing probability of individuals with ADHD 6 months after eligibility was 35% lower (for males

274 that the siblings of female individuals with ADHD are at higher familial risk for ADHD than the sibli

275 e (d=-0.10) were smaller in individuals with ADHD compared with controls in the mega-analysis.

276 ith harmonised protocols of individuals with ADHD compared with those who do not have this diagnosis.

277 ever, indicated that female individuals with ADHD may be at especially high risk for certain comorbid

278 ata were available for 4609 individuals with ADHD, 9650 individuals with BPD (5167 thereof with early

279 education entrance tests in individuals with ADHD.

280 smoking vulnerability among individuals with ADHD.

281 onally relevant outcomes in individuals with ADHD.

282 w- and high-functioning ASD in the link with ADHD.

283 Our sample comprised 1713 participants with ADHD and 1529 controls from 23 sites with a median age o

284 study, a US national cohort of patients with ADHD (n = 2 319 450) was identified from commercial heal

285 ears 2004-2012 were defined as patients with ADHD (N = 47,944), and all remaining individuals (N = 2,

286 hat up to 22.1% of the MVCs in patients with ADHD could have been avoided if they had received medica

287 thin-individual analyses, male patients with ADHD had a 38% (odds ratio, 0.62; 95% CI, 0.56-0.67) low

288 Among patients with ADHD, rates of MVCs were lower during periods when they

289 k of MVCs in a large cohort of patients with ADHD.

290 5) and thalamus (p=0.39) between people with ADHD and controls.

291 the association of pregnancy residence with ADHD-related behaviors and assess whether prenatal organ

292 during smoking withdrawal among smokers with ADHD.

293 RCTs, totalling n=534 randomized youth with ADHD, n-3 PUFAs supplementation improves ADHD clinical s

294 RCTs, totalling n=214 randomized youth with ADHD, n-3 PUFAs supplementation improves cognitive measu

295 with ADHD (42.8%) and 4715 of 13221 without ADHD (35.7%) crashed during the study period.

296 crash risk compared with adolescents without ADHD.

297 Periods with and without ADHD medication use.

298 ildren aged 6-12 years: AD-only (ie, without ADHD), ADHD-only (ie, without AD), AD + ADHD and healthy

299 Compared with individuals without ADHD, the licensing probability of individuals with ADHD

300 was 1.36 times higher than for those without ADHD (95% CI, 1.25-1.48) and did not vary by sex, licens