ライフサイエンスコーパス: Alzheimer's disease

1 ar pathways related to cognitive decline and Alzheimer's disease.

2 shed neuroprotective genetic variant against Alzheimer's disease.

3 thological and clinical features compared to Alzheimer's disease.

4 n4 gene, those at highest risk of developing Alzheimer's disease.

5 ) accumulation in the brain is a hallmark of Alzheimer's Disease.

6 s the consideration of temporal processes of Alzheimer's disease.

7 onotherapy in patients with mild to moderate Alzheimer's disease.

8 has been identified in up to 75% of cases of Alzheimer's disease.

9 heral and central adaptive immune changes in Alzheimer's disease.

10 opportunity to reduce the risk of late-onset Alzheimer's disease.

11 rylated tau is a key pathological feature of Alzheimer's disease.

12 hed individuals and 21 patients with typical Alzheimer's disease.

13 o normal brain ageing from those specific to Alzheimer's disease.

14 lmark of numerous human disorders, including Alzheimer's disease.

15 important information for early diagnosis of Alzheimer's disease.

16 episodic memory is detectable in preclinical Alzheimer's disease.

17 in the cerebrospinal fluid of patients with Alzheimer's disease.

18 als that sustain microglial responses during Alzheimer's disease.

19 ity in samples from patients with late-onset Alzheimer's disease.

20 ation, as well as neurodegeneration found in Alzheimer's disease.

21 l cognitive decline with age as well as with Alzheimer's disease.

22 mine the safety and efficacy of nilotinib in Alzheimer's disease.

23 using a transgenic APP/PSEN1 mouse model of Alzheimer's disease.

24 ment of therapies halting the progression of Alzheimer's disease.

25 d pathophysiology in brain disorders such as Alzheimer's disease.

26 peptide, whose oligomers are associated with Alzheimer's disease.

27 ization and volume differences in ageing and Alzheimer's disease.

28 prevalent form of pre-senile dementia after Alzheimer's disease.

29 ragine endopeptidase (AEP) is upregulated in Alzheimer's disease.

30 cells derived from a mouse model relevant to Alzheimer's disease.

31 osphorylation of tau, which are hallmarks of Alzheimer's disease.

32 for preventing Abeta-related impairments in Alzheimer's disease.

33 ted with both familial and sporadic forms of Alzheimer's disease.

34 ipants with mild to moderate dementia due to Alzheimer's disease.

35 n of mild cognitive impairment into clinical Alzheimer's disease.

36 of primary age-related tauopathy compared to Alzheimer's disease.

37 biomarker of advanced Braak tau pathology in Alzheimer's disease.

38 ministered BACE inhibitor developed to treat Alzheimer's disease.

39 hromosome 17 (FTDP-17) and can contribute to Alzheimer's disease.

40 roughout the pathophysiological continuum of Alzheimer's disease.

41 g transcription factor (REST) to PD and also Alzheimer's disease.

42 ol for customized administration of drugs in Alzheimer's disease.

43 onsidered hallmarks of cognitive deficits in Alzheimer's disease.

44 pathogenic Abeta, a protein associated with Alzheimer's disease.

45 medial and lateral temporal lobe for typical Alzheimer's disease.

46 role in the pathogenesis and progression of Alzheimer's disease.

47 eta peptide plays a key role in the onset of Alzheimer's disease.

48 signations for identifying true non-amnestic Alzheimer's disease.

49 ta, which is critical in the pathogenesis of Alzheimer's disease.

50 th either behavioural variant FTD (bvFTD) or Alzheimer's disease.

51 ibrils derived from patients with Pick's and Alzheimer's diseases.

52 E (APOE4), the main susceptibility gene for Alzheimer's disease(11-14), leads to accelerated breakdo

53 -AA guidelines, 14 healthy controls, 14 mild Alzheimer's disease, 14 amyloid-positive mild cognitive

54 lzheimer's disease (18 with typical amnestic Alzheimer's disease, 17 with posterior cortical atrophy

55 g a cohort of 57 participants diagnosed with Alzheimer's disease (18 with typical amnestic Alzheimer'

56 tau368 was first evaluated in a pilot study (Alzheimer's disease = 20, control = 20), then in a secon

57 e the IWG-2 biomarker criteria were applied (Alzheimer's disease = 37, control = 45), and finally in

58 elation with 18F-GTP1 tau PET was evaluated (Alzheimer's disease = 38, control = 11).

59 ACAT1 has also been implicated in Alzheimer's disease(4), atherosclerosis(5) and cancers(6

60 tauopathy has slower cognitive decline than Alzheimer's disease across multiple neuropsychological d

61 er neurodegenerative disorders, and identify Alzheimer's disease across the clinical continuum.

62 The neurodegenerative Alzheimer's disease (AD) affects more than 30 million pe

63 periodontal pathogens may alter the onset of Alzheimer's disease (AD) and all-cause dementia.

64 o representative neurodegenerative diseases, Alzheimer's disease (AD) and Down syndrome (DS), using D

65 in the differential diagnosis between FTLD, Alzheimer's disease (AD) and healthy ageing; their role

66 A hallmark feature of Alzheimer's disease (AD) and other tauopathies is the mi

67 n of amyloid Tau aggregates is implicated in Alzheimer's disease (AD) and other tauopathies.

68 ssociated protein that plays a major role in Alzheimer's disease (AD) and other tauopathies.

69 zed by reduced hippocampal volume, including Alzheimer's disease (AD) and schizophrenia.

70 Diabetes, obesity, and Alzheimer's disease (AD) are associated with vascular co

71 Tauopathies including Alzheimer's disease (AD) are marked by the accumulation

72 the early detection of peptides involved in Alzheimer's disease (AD) are required in order to prolon

73 Individuals afflicted with Alzheimer's disease (AD) can develop sleep problems even

74 Late-onset Alzheimer's disease (AD) can, in part, be considered a m

75 Alzheimer's disease (AD) causes unrelenting, progressive

76 al fluid (CSF) proteins with a connection to Alzheimer's disease (AD) demonstrated an association bet

77 We screen the 99% credible set of Alzheimer's disease (AD) GWAS variants identified at the

78 The interplay between viral infection and Alzheimer's disease (AD) has long been an area of intere

79 sensitive and specific plasma biomarkers for Alzheimer's disease (AD) have the potential to improve d

80 The incidence of Alzheimer's disease (AD) increases with age and is becom

81 Although Alzheimer's disease (AD) is a central nervous system dis

82 Alzheimer's disease (AD) is a neurodegenerative dementia

83 The lack of effective treatments for Alzheimer's disease (AD) is alarming, considering the nu

84 he most sensitive early cognitive markers of Alzheimer's disease (AD) is becoming increasingly import

85 One of the neuropathological hallmarks of Alzheimer's disease (AD) is cerebral deposition of amylo

86 Alzheimer's disease (AD) is characterized by amyloid pla

87 Alzheimer's disease (AD) is currently untreatable, and t

88 ippocampal neurogenesis (AHN) is impaired in Alzheimer's disease (AD) is essential for unravelling it

89 Prion-like transcellular spreading of tau in Alzheimer's Disease (AD) is mediated by tau binding to c

90 id-beta (Abeta) species and tau pathology in Alzheimer's disease (AD) is not fully understood.

91 ption in mild cognitive impairment (MCI) and Alzheimer's disease (AD) is poorly understood, particula

92 The pathogenesis of Alzheimer's disease (AD) is primarily driven by brain ac

93 A major characteristic of Alzheimer's disease (AD) is the accumulation of misfolde

94 Alzheimer's disease (AD) is the most common age-related

95 Alzheimer's disease (AD) is the most common neurodegener

96 the patients with Down syndrome (DS) develop Alzheimer's disease (AD) neuropathology by age 40.

97 istance contributes to neuroinflammation and Alzheimer's disease (AD) pathogenesis.

98 tion is implicated in cancer development and Alzheimer's disease (AD) pathogenesis.

99 of ceramides is deregulated in the brain of Alzheimer's disease (AD) patients and is associated with

100 major contributor of vascular dysfunction in Alzheimer's disease (AD) patients.

101 tion.IMPORTANCE The "pathogen" hypothesis of Alzheimer's disease (AD) proposes that brain HSV-1 infec

102 Major depressive disorder (MDD) and Alzheimer's disease (AD) reciprocally elevate the risk f

103 TREM2 is an Alzheimer's disease (AD) risk gene expressed in microgli

104 Patients with Alzheimer's disease (AD) suffer from spatial memory impa

105 (CSF) is a central and relevant biomarker of Alzheimer's disease (AD) that correlates with the severi

106 ted 2 typical pathways from APOE genotype to Alzheimer's disease (AD) through gene expression enriche

107 Ageing is the major risk factor for Alzheimer's disease (AD), a condition involving brain hy

108 ssion tomography (PET) of tau pathologies in Alzheimer's disease (AD), although sensitive detection o

109 on of MSI1 and MSI2 in the brains tissues of Alzheimer's disease (AD), amyotrophic lateral sclerosis

110 is a promising strategy for the treatment of Alzheimer's disease (AD), and gold nanoparticles have pr

111 MT2 (or Kindlin-2), a genetic risk factor of Alzheimer's disease (AD), as a potential key modulator o

112 ils in the brain parenchyma is a hallmark of Alzheimer's disease (AD), but a mechanistic understandin

113 ontributes to the development of dementia in Alzheimer's disease (AD), but it has not been possible t

114 ed an association between sleep duration and Alzheimer's disease (AD), but it is unclear if sleep dur

115 rtical iron has been shown to be elevated in Alzheimer's disease (AD), but the impact of the directly

116 s high-affinity receptor TrkB are reduced in Alzheimer's disease (AD), contributing to progressive co

117 system (CNS) disorders, and in particular in Alzheimer's disease (AD), have paved the way to consider

118 In Alzheimer's disease (AD), human Tau is phosphorylated at

119 However, in Alzheimer's disease (AD), its reflection on regional neu

120 n cognitive performance and brain atrophy in Alzheimer's disease (AD), little is understood about how

121 ical processes, including the progression of Alzheimer's disease (AD), making nSMase2 a viable therap

122 Synaptic dysfunction plays a central role in Alzheimer's disease (AD), since it drives the cognitive

123 On the other hand, in conditions such as Alzheimer's disease (AD), stroke, Parkinson's disease, A

124 Several APP mutations cause familial Alzheimer's disease (AD), while the Icelandic APP mutati

125 genic factor in the onset and progression of Alzheimer's disease (AD).

126 profile the complex human brain proteome of Alzheimer's disease (AD).

127 ion in the brain parenchyma are hallmarks of Alzheimer's disease (AD).

128 omic datasets to study complex diseases like Alzheimer's disease (AD).

129 related neurodegenerative diseases including Alzheimer's disease (AD).

130 ry tangles likely cause neurodegeneration in Alzheimer's disease (AD).

131 esymptomatic individuals destined to develop Alzheimer's disease (AD).

132 s depleted in the cortex of individuals with Alzheimer's disease (AD).

133 sing disease-modifying interventions against Alzheimer's disease (AD).

134 yeloid cells 2 (TREM2) increases the risk of Alzheimer's disease (AD).

135 myloid (Abeta) deposits, hallmark lesions of Alzheimer's disease (AD).

136 a) and are potential therapeutic targets for Alzheimer's disease (AD).

137 cerebral hypoperfusion is characteristic of Alzheimer's disease (AD).

138 ding amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD).

139 ) has been suggested to be a risk factor for Alzheimer's disease (AD).

140 looxygenase2 (COX2) in neurons in a model of Alzheimer's disease (AD).

141 almost all neurological diseases, including Alzheimer's disease (AD).

142 ially important for complex diseases such as Alzheimer's disease (AD).

143 tive ability observed in the early stages of Alzheimer's disease (AD).

144 y tangle (NFT) pathology during the onset of Alzheimer's disease (AD).

145 degeneration at the pre-symptomatic stage of Alzheimer's disease (AD).

146 , and with cognition in SCZ and pathology in Alzheimer's disease (AD).

147 myloid (Abeta) metabolism and progression of Alzheimer's disease (AD).

148 ogenesis of cardiovascular disease (CVD) and Alzheimer's disease (AD).

149 HR 1.59 (95% CI, 1.38-1.83); P < 0.0001] or Alzheimer's disease [adjusted HR 1.50 (95% CI, 1.26-1.78

150 l subtypes had an excess of genetic risk for Alzheimer's disease (all P > 0.01).

151 In Alzheimer's disease, amyloid deposits along the brain va

152 crobiome alterations in Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and

153 ay be a hallmark for the early prediction of Alzheimer's disease and a predictor of cognitive decline

154 most common neurodegenerative disease after Alzheimer's disease and affects 1% of the population abo

155 mary, plasma p-tau217 increases during early Alzheimer's disease and can be used to monitor disease p

156 eatment of diseases such as atherosclerosis, Alzheimer's disease and cancer(2-7).

157 e whose aberrant activity is associated with Alzheimer's disease and cancer.

158 of three-repeat (3R) tau isoforms) and from Alzheimer's disease and chronic traumatic encephalopathy

159 rates of neurodegenerative diseases such as Alzheimer's disease and chronic traumatic encephalopathy

160 model was trained using clinically diagnosed Alzheimer's disease and cognitively normal subjects from

161 nction is associated with the development of Alzheimer's disease and familial acne inversa in humans.

162 ve emerged as a preclinical manifestation of Alzheimer's disease and frontotemporal dementia, disease

163 tic PLD3 variants previously associated with Alzheimer's disease and investigated each variant's effe

164 The amyloid-beta peptide is correlated with Alzheimer's disease and is assumed to cause toxicity by

165 rative diseases such as Parkinson's disease, Alzheimer's disease and multiple sclerosis.

166 Our data suggest an association between Alzheimer's disease and NPH changes, supporting the rece

167 le promise to push forward efforts to combat Alzheimer's disease and other neurodegenerative disorder

168 d tau protein are a pathological hallmark of Alzheimer's disease and other tauopathy conditions.

169 ed with early or late hippocampal atrophy in Alzheimer's disease and primary age-related tauopathy, w

170 For patients with Alzheimer's disease and primary age-related tauopathy, w

171 es of hippocampal and neocortical atrophy in Alzheimer's disease and primary age-related tauopathy.

172 ide range of serious human diseases, such as Alzheimer's disease and prion diseases.

173 onse in the blood and cerebrospinal fluid in Alzheimer's disease and provide evidence of clonal, anti

174 ven approaches to examining heterogeneity in Alzheimer's disease and related dementias, with a princi

175 egeneration in the detection and tracking of Alzheimer's disease and the evaluation of disease-modify

176 wn syndrome are at increased genetic risk of Alzheimer's disease and therefore develop the spectrum o

177 s 5108 participants from a clinical trial of Alzheimer's disease and three longitudinal cohort studie

178 We determined incident dementia including Alzheimer's disease and vascular dementia, analyzing dat

179 of patients suffering from type 2 diabetes, Alzheimer's disease, and diabetes-induced dementia, ther

180 hemorrhagic stroke, traumatic brain injury, Alzheimer's disease, and multiple sclerosis, and evaluat

181 novel druggable target for the treatment of Alzheimer's disease, and possibly other neurodegenerativ

182 not differ between amnestic and non-amnestic Alzheimer's disease, and receiver operating characterist

183 pir and atrophy mirror clinical phenotype in Alzheimer's disease, and whether optimal longitudinal ne

184 a-amyloid (Abeta) fibrils and Tau tangles in Alzheimer's disease are accessible only via invasive cer

185 kers for future clinical treatment trials in Alzheimer's disease are different for MRI and tau-PET an

186 e mini-mental state examination (K-MMSE) and Alzheimer's disease assessment scale-cognitive subscale

187 ting role of increased neuroanatomic risk of Alzheimer's disease associated with exposure.

188 more, neither the variant with the strongest Alzheimer's disease association nor the nearest gene are

189 (Abeta) peptide, a key pathogenic factor in Alzheimer's disease, attenuates the increase in cerebral

190 ) for sporadic Alzheimer's disease, familial Alzheimer's disease, autism spectrum disorder and multip

191 -psychiatric diseases such as schizophrenia, Alzheimer's disease, autism spectrum disorder, and bipol

192 ons not only for the genetic underpinning of Alzheimer's disease but also for how we estimate sex-dep

193 cognitive, and neuropsychiatric symptoms in Alzheimer's disease', by Tetreault etal.

194 Many cellular functions perturbed in Alzheimer's disease can be recapitulated using iPSC-deri

195 with the burdens of chronic diseases such as Alzheimer's disease, cardiovascular disease, and diabete

196 localizes to pathological tau aggregates in Alzheimer's disease cases, and that it is continuously r

197 specific regions of interest associated with Alzheimer's disease, clinical depression, and other diso

198 l variability at the single-subject level in Alzheimer's disease, complicating our understanding of b

199 p-tau181 showed gradual increases along the Alzheimer's disease continuum, from the lowest concentra

200 au pathology or neurodegeneration across the Alzheimer's disease continuum.

201 Ageing and Alzheimer's disease contributed additive effects on grey

202 ors by which APOE and its variants influence Alzheimer's disease could have a major impact on the und

203 mild cognitive impairment (3.0 +/- 5.3%) and Alzheimer's disease dementia (2.9 +/- 5.7%), respectivel

204 e impairment patients who later converted to Alzheimer's disease dementia (n = 40) had accelerated p-

205 icipants were aged 55-85 years with probable Alzheimer's disease dementia and a Mini Mental State Exa

206 ange over time of participants who developed Alzheimer's disease dementia during follow-up were compa

207 paired, 88 cognitively impaired (MCI n = 67, Alzheimer's disease dementia n = 21), data accessed Octo

208 paired, 42 cognitively impaired (MCI n = 16, Alzheimer's disease dementia n = 26), data obtained Nove

209 with a lower risk of developing all-cause or Alzheimer's disease dementia, adjusted hazard ratio (HR)

210 cognitive impairment who did not convert to Alzheimer's disease dementia.

211 developed dementia, including 374 cases with Alzheimer's disease dementia.

212 rongly associated with risk of all-cause and Alzheimer's disease dementia.

213 ial functioning, and language at the time of Alzheimer's disease diagnosis.

214 rimental to cognitive decline in preclinical Alzheimer's disease during late middle-age.

215 Familial forms of Alzheimer's disease (FAD) are caused by mutations in the

216 Familial Alzheimer's disease (fAD) mutations alter amyloid precur

217 red using identical procedures) for sporadic Alzheimer's disease, familial Alzheimer's disease, autis

218 and amyloid beta pathologies, differentiate Alzheimer's disease from other neurodegenerative disorde

219 entified in the human brain that affects the Alzheimer's disease gene, amyloid precursor protein (APP

220 this does not equate to the discovery of 40 Alzheimer's disease genes.

221 rations in the amyloid beta-positive MCI and Alzheimer's disease groups (p<0.001, Alzheimer's disease

222 Three new Alzheimer's disease GWAS published in 2018 and 2019, whi

223 ta peptide (Abeta) is a causative process in Alzheimer's disease, has driven many therapeutic efforts

224 brain diseases, including schizophrenia and Alzheimer's disease, have also been identified using mac

225 E) are known to increase risk for developing Alzheimer's disease, however there is controversy from h

226 alysis discovered 19 susceptibility loci for Alzheimer's disease in populations of European ancestry.

227 pecific genes and molecular pathways driving Alzheimer's disease, including the splicing factor PTBP1

228 ntributor to age-related dementia, including Alzheimer's disease, inextricably linked to disease onse

229 has been studied in people with epilepsy or Alzheimer's disease, intending to enhance memory perform

230 Alzheimer's disease is a progressive neurodegenerative d

231 Alzheimer's disease is an incurable neurodegenerative di

232 Alzheimer's disease is biologically heterogeneous, and d

233 Alzheimer's disease is characterized by the presence of

234 indicate that concomitant LATE pathology in Alzheimer's disease is not associated with greater neuro

235 ns that phosphorylated tau interacts with in Alzheimer's disease is surprisingly limited.

236 neuroinflammation via IFITM3 and the risk of Alzheimer's disease is thereby increased.

237 tures and PTMs of tau filaments from CBD and Alzheimer's disease, it is found that ubiquitination of

238 Age being the main risk factor for Alzheimer's disease, it is particularly challenging to d

239 stin et al. is interesting, particularly for Alzheimer's disease, it may benefit from incorporating t

240 and novel therapeutic targets of late-onset Alzheimer's Disease (LOAD), we performed an integrative

241 me-wide significant risk loci for late-onset Alzheimer's disease (LOAD).

242 ongoing and have validated several genes at Alzheimer's disease loci, but greater sample sizes and c

243 uggests that many individuals diagnosed with Alzheimer's disease may actually suffer from a mixed dem

244 elated processes common to those observed in Alzheimer's disease may contribute to cognitive impairme

245 g therapeutics have shown efficacy in rodent Alzheimer's disease models yet failed to benefit human p

246 pply the method to brain homogenates from an Alzheimer's disease mouse model.

247 on (n = 431; age range 55-90 years) and with Alzheimer's disease (n = 50 with late mild cognitive imp

248 ents with svPPA (n = 70), bvFTD (n = 70) and Alzheimer's disease (n = 70).

249 Alzheimer's disease neurodegeneration is thought to spre

250 ase and cognitively normal subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI) datas

251 diagnosis of major depression (LLD) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) Depre

252 Here, we extracted data from Alzheimer's Disease Neuroimaging Initiative (ADNI) parti

253 disease using two independent samples of the Alzheimer's Disease Neuroimaging Initiative (n1 = 284; n

254 t cross-sectional samples, obtained from the Alzheimer's Disease Neuroimaging Initiative project.

255 he analyses of PET-imaging outcomes from the Alzheimer's Disease Neuroimaging Initiative study, and t

256 t has been suggested that the combination of Alzheimer's disease neuropathological change (ADNC) and

257 o-pathologies in the presence and absence of Alzheimer's disease neuropathology.

258 ric was genetically correlated with clinical Alzheimer's disease (P-values > 0.42) nor associated wit

259 bility of late-onset human diseases, such as Alzheimer's disease, Parkinson's disease, and type 2 dia

260 treatment of various brain maladies such as Alzheimer's disease, Parkinson's disease, brain lymphoma

261 have increased long-term risks of dementia, Alzheimer's disease, Parkinson's disease, motor neuron d

262 d the associations between LNB and dementia, Alzheimer's disease, Parkinson's disease, motor neuron d

263 ed no long-term increased risks of dementia, Alzheimer's disease, Parkinson's disease, motor neuron d

264 -beta (Abeta) likely plays a primary role in Alzheimer's disease pathogenesis, but longitudinal Abeta

265 ovide evidence of the presence or absence of Alzheimer's disease pathological hallmarks: amyloid plaq

266 tress kinases involved in the development of Alzheimer's disease pathology were significantly activat

267 ietal regions characteristically affected by Alzheimer's disease pathology.

268 gitudinal cognitive changes in patients with Alzheimer's disease pathology.

269 ase (AD) through gene expression enriched in Alzheimer's disease pathway.

270 maps by comparing cortical thickness in each Alzheimer's disease patient versus a group of age-matche

271 brain regions functionally connected to each Alzheimer's disease patient's location of atrophy using

272 Post-mortem temporal cortex samples from Alzheimer's disease patients (n = 9) were used as positi

273 jects across two independent datasets (total Alzheimer's disease patients = 330).

274 No more than 42% of Alzheimer's disease patients had atrophy at any given lo

275 alian tauopathies, including brains of human Alzheimer's disease patients.

276 ute to the cognitive impairments observed in Alzheimer's disease patients.

277 esult in misclassifications for non-amnestic Alzheimer's disease patients.

278 drug for leukemia, indicates improvement in Alzheimer's disease phenotypes.

279 tween cases, but distinct from those seen in Alzheimer's disease, Pick's disease and CTE(17-19).

280 his to a range of tau pathologies, including Alzheimer's disease, primary age-related tauopathy, agei

281 e expectancy, and increases vulnerability to Alzheimer's disease-related dementias.

282 ed dementia, and therapeutics targeting only Alzheimer's disease-related processes may have severely

283 Many gaps in our understanding of Alzheimer's disease remain despite intense research effo

284 Development of tau-based therapies for Alzheimer's disease requires an understanding of the tim

285 ecise, intuitive visualization of individual Alzheimer's disease risk en route to accurate diagnosis.

286 ging importance of polygenic predictions for Alzheimer's disease, sex-dependent polygenic effects hav

287 s differed between amnestic and non-amnestic Alzheimer's disease; standard cut-offs for phosphorylate

288 appears to be distinct from that of clinical Alzheimer's disease, suggesting that a shift in focus to

289 provides better sensitivity to non-amnestic Alzheimer's disease than either the ATN framework or the

290 ed several gene risk factors associated with Alzheimer's disease that are specifically or highly expr

291 d the number of known susceptibility loci in Alzheimer's disease to 40.

292 eta-analysed with data from GWAS of clinical Alzheimer's disease to attain sample sizes of 388 324 an

293 ther studies used parental family history of Alzheimer's disease to define proxy cases and controls i

294 se longitudinal patterns differ from typical Alzheimer's disease, to what degree flortaucipir and atr

295 ssed the sequence of pathological staging in Alzheimer's disease using two independent samples of the

296 MCI and Alzheimer's disease groups (p<0.001, Alzheimer's disease vs all other groups).

297 osis, frontotemporal lobar degeneration, and Alzheimer's disease, were found to be highly prone to ph

298 aps in patients with a clinical diagnosis of Alzheimer's disease will also localize to syndrome-speci

299 racterisation of the genetic architecture of Alzheimer's disease, with the identification of 40 susce

300 ts exhibit the neuropathological features of Alzheimer's disease without signs of cognitive impairmen