ライフサイエンスコーパス: Alzheimer disease

1 ars, 123 participants developed dementia (97 Alzheimer disease).

2 l tremor), probable DLB, and non-DLB (mainly Alzheimer disease).

3 with risk of dementia (all-cause dementia or Alzheimer disease).

4 effect comparable to their association with Alzheimer disease.

5 e an overview of the cardiovascular links to Alzheimer disease.

6 e the neurodegenerative pathology underlying Alzheimer disease.

7 ons between cerebrovascular risk factors and Alzheimer disease.

8 hic lateral sclerosis, Parkinson disease and Alzheimer disease.

9 cognitively intact older adults at risk for Alzheimer disease.

10 (BIIB037) in patients with prodromal or mild Alzheimer disease.

11 eral sclerosis, frontotemporal dementias and Alzheimer disease.

12 isease and 81,974 (7.9%) were diagnosed with Alzheimer disease.

13 The secondary outcome was a new diagnosis of Alzheimer disease.

14 lays an important role in the progression of Alzheimer disease.

15 tions in the amyloid burden in patients with Alzheimer disease.

16 s a major genetic risk factor for late-onset Alzheimer disease.

17 or detection of CSF clearance alterations in Alzheimer disease.

18 ostoperative delirium may indicate incipient Alzheimer disease.

19 entia, certain repeat expansion diseases and Alzheimer disease.

20 actors of CSPG4-type neural cell exosomes in Alzheimer disease.

21 y (ADT) and cognitive dysfunction, including Alzheimer disease.

22 try, including major depressive disorder and Alzheimer disease.

23 .5%) participants, including 194 (9.5%) with Alzheimer disease.

24 l CSF amyloid levels do not exclude incident Alzheimer disease.

25 ases such as frontotemporal degeneration and Alzheimer disease.

26 ns of future secondary prevention trials for Alzheimer disease.

27 to define neurodegeneration associated with Alzheimer disease.

28 eptors may contribute to the pathobiology of Alzheimer disease.

29 le of vascular disease in the development of Alzheimer disease.

30 ate of functional decline among persons with Alzheimer disease.

31 strongest genetic risk factor for late-onset Alzheimer disease.

32 ll be beneficial in arresting progression of Alzheimer disease.

33 strongest genetic risk factor for late-onset Alzheimer disease.

34 insights into the pathology and treatment of Alzheimer disease.

35 loss, and eventual cognitive dysfunction in Alzheimer disease.

36 d with cognitive decline in individuals with Alzheimer disease.

37 mechanism for sleep loss to increase risk of Alzheimer disease.

38 ng late mild cognitive impairment leading to Alzheimer disease.

39 t receive attention in Abeta mouse models of Alzheimer disease.

40 e brain, a core neuropathological feature of Alzheimer disease.

41 on 17 older adults with sporadic, late onset Alzheimer disease.

42 cardiovascular disorders, and Parkinson and Alzheimer diseases.

43 e dementia in the MI cohort was 9% (2.8% for Alzheimer disease, 1.6% for vascular dementia, and 4.5%

44 s, 20 HIV-negative patients with symptomatic Alzheimer disease, 15 cognitively normal HIV-positive in

45 edian: 12 y) of follow-up, 116 men developed Alzheimer disease, 64 men developed vascular dementia, a

46 algorithm developed for early prediction of Alzheimer disease achieved 82% specificity at 100% sensi

47 re significantly lower in patients with mild Alzheimer disease (AD) ( n = 24) than in age- and sex-ma

48 ficity of these alterations in patients with Alzheimer disease (AD) and behavioral-variant frontotemp

49 eta) plays a key role in the pathogenesis of Alzheimer disease (AD) and can be imaged in vivo using (

50 y acidic protein (GFAP) with common sporadic Alzheimer disease (AD) and cognitive decline is not esta

51 accumulation is essential for understanding Alzheimer disease (AD) and for design of antiamyloid dru

52 ents with mild cognitive impairment or early Alzheimer disease (AD) and found a 41% decrease in speci

53 Diabetes is a risk factor for Alzheimer disease (AD) and increases the risk of progres

54 an Americans have higher risks of developing Alzheimer disease (AD) and lower cerebrospinal fluid (CS

55 Alzheimer disease (AD) and other dementia syndromes are

56 aggregated tau, a key pathologic feature of Alzheimer disease (AD) and other neurodegenerative disor

57 bule-associated protein Tau is a hallmark of Alzheimer disease (AD) and other tauopathies.

58 l as in neurodegenerative disorders, such as Alzheimer disease (AD) and Parkinson disease (PD).

59 r most neurodegenerative diseases, including Alzheimer disease (AD) and Parkinson disease (PD).

60 The majority of people living with Alzheimer disease (AD) and related dementias are women.

61 amyloid fibrils, a histological hallmark of Alzheimer disease (AD) and two dozen related neurodegene

62 tural integrity as well as decreased risk of Alzheimer disease (AD) and vascular dementia (VaD).

63 nts with mild cognitive impairment (MCI) and Alzheimer disease (AD) are defective in phagocytosis and

64 positron emission tomography) biomarkers for Alzheimer disease (AD) are invasive or expensive.

65 , 50 million people live with dementia, with Alzheimer disease (AD) being responsible for two-thirds

66 myloid-beta (Abeta) burden are well known in Alzheimer disease (AD) but did not receive attention in

67 e (DS) show the neuropathological changes of Alzheimer disease (AD) by the age of 40 years.

68 k whole exome sequencing in 5,740 late-onset Alzheimer disease (AD) cases and 5,096 cognitively norma

69 ormal or MCI status to death, derived from 4 Alzheimer Disease (AD) Centers in the United States.

70 Deep gray matter structures in patients with Alzheimer disease (AD) contain higher brain iron concent

71 sted HR = 1.32 [95% CI = 1.10-1.57]) but not Alzheimer disease (AD) dementia (adjusted HR = 0.95 [95%

72 ation of new treatments for individuals with Alzheimer disease (AD) dementia and mild cognitive impai

73 Brain regions affected by Alzheimer disease (AD) display well-recognized early neu

74 targeting beta-amyloid peptides (Abeta) for Alzheimer disease (AD) failed for arguable reasons that

75 o identify older healthy persons at risk for Alzheimer disease (AD) for enrollment in AD prevention t

76 In a somewhat narrow diagnostic lens, Alzheimer disease (AD) has been considered a brain-speci

77 orphism in beta-amyloid (Abeta) plaques from Alzheimer disease (AD) has been recognized as an importa

78 e amyloid-beta (Abeta) cascade hypothesis of Alzheimer disease (AD) holds that brain accumulation of

79 e associated with a lower risk of late-onset Alzheimer disease (AD) in observational studies, suggest

80 Alzheimer disease (AD) is a chronic neurodegenerative di

81 Alzheimer disease (AD) is a heterogeneous disease with a

82 Alzheimer disease (AD) is a major cause of age-related d

83 There is growing evidence that Alzheimer disease (AD) is a pervasive metabolic disorder

84 Alzheimer disease (AD) is a progressive disorder that af

85 ion in cerebral amyloid angiopathy (CAA) and Alzheimer disease (AD) is arguably the clearest instance

86 The clinical progression of Alzheimer disease (AD) is associated with the accumulati

87 Alzheimer disease (AD) is characterized by beta-amyloid

88 Alzheimer disease (AD) is characterized by deterioration

89 individuals at elevated risk for developing Alzheimer disease (AD) is of clinical importance.

90 entifying individuals at risk for developing Alzheimer disease (AD) is of utmost importance.

91 Alzheimer disease (AD) is one of several neurodegenerati

92 Alzheimer disease (AD) is the leading cause of dementia,

93 Alzheimer disease (AD) is the most common form of dement

94 Alzheimer disease (AD) is the most common form of neurod

95 Biomarker accuracy for Alzheimer disease (AD) is uncertain.

96 The global epidemic of Alzheimer disease (AD) is worsening, and no approved tre

97 as detected in the brains of multiple murine Alzheimer disease (AD) models, a phenomenon also observe

98 cium (Ca(2+)) signaling has been reported in Alzheimer disease (AD) models.

99 es cognitive function in a triple-transgenic Alzheimer disease (AD) mouse model.

100 to compare sex-specific rates of death with Alzheimer disease (AD) or dementia as the underlying or

101 The metabolic basis of Alzheimer disease (AD) pathology and expression of AD sy

102 To estimate regional Alzheimer disease (AD) pathology burden clinically, anal

103 Adults with Down syndrome (DS) develop Alzheimer disease (AD) pathology by their 5th decade.

104 emonstrated that cerebrovascular disease and Alzheimer disease (AD) pathology frequently co-occur in

105 inclusions in 40.5%, FTLD-tau in 40.5%, and Alzheimer disease (AD) pathology in 19% of cases.

106 ptides is a significant event that underpins Alzheimer disease (AD) pathology.

107 rmalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these chang

108 were found to be decreased in the brains of Alzheimer disease (AD) patients.

109 ntal net effects on the cognitive outcome of Alzheimer disease (AD) patients.

110 oE) colocalizes with amyloid-beta (Abeta) in Alzheimer disease (AD) plaques and in synapses, and evid

111 Current therapeutic approaches to Alzheimer disease (AD) remain disappointing and, hence,

112 the entire cortex and previously determined Alzheimer disease (AD) signature regions in the same pop

113 Methods: Three healthy controls (HCs) and 4 Alzheimer disease (AD) subjects underwent 2 dynamic PET

114 Methods: Three healthy controls (HC) and 4 Alzheimer disease (AD) subjects underwent two dynamic PE

115 1451 in cognitively healthy control (HC) and Alzheimer disease (AD) subjects, using reference region

116 YHV), 4 aged healthy volunteers (AHV), and 8 Alzheimer disease (AD) subjects.

117 the brain have a role in the pathogenesis of Alzheimer disease (AD) was proposed nearly 30 years ago.

118 The vast increase in Alzheimer disease (AD) worldwide has grave implications

119 delusions or hallucinations, are frequent in Alzheimer disease (AD), affecting 40 to 60% of individua

120 ants, 50% had neuropathological diagnoses of Alzheimer disease (AD), and 35% of vascular dementia (Va

121 effects in the molecular pathways underlying Alzheimer disease (AD), and even less is known about how

122 st important, common genetic determinant for Alzheimer disease (AD), and female APOE4 carriers presen

123 subjects, subjects with clinically probable Alzheimer disease (AD), and subjects with amnestic mild

124 the brain is 1 of 2 pathologic hallmarks of Alzheimer disease (AD), and the spatial distribution of

125 Cognitive impairment and dementia, including Alzheimer disease (AD), are common within the aging popu

126 principally responsible for neurotoxicity in Alzheimer disease (AD), but it is not known whether anti

127 aques implicated in the neurodegeneration of Alzheimer disease (AD), but therapies designed to reduce

128 hages (MHs) and amyloid beta accumulation in Alzheimer disease (AD), but to the knowledge of the auth

129 ommon neurodegenerative disorders, including Alzheimer disease (AD), dementia with Lewy bodies (DLB),

130 es and neurofibrillary tangles, hallmarks of Alzheimer disease (AD), enables monitoring of pathology

131 gorithm that predicts the final diagnosis of Alzheimer disease (AD), mild cognitive impairment, or ne

132 he impact of neurological disorders, such as Alzheimer disease (AD), on AMPK function and downstream

133 Motor slowing appears in preclinical Alzheimer disease (AD), progresses with AD progression,

134 major genetic risk determinant of late-onset Alzheimer disease (AD), with the APOE*epsilon4 allele co

135 e (Abeta) is a key player in the etiology of Alzheimer disease (AD), yet a systematic investigation o

136 ly, GGC repeat expansion was observed in two Alzheimer disease (AD)-affected families and three parki

137 e 1 (HSV1) in the pathogenesis of late-onset Alzheimer disease (AD).

138 y regulate inflammation and neurotoxicity in Alzheimer disease (AD).

139 e strongest genetic risk factor for sporadic Alzheimer disease (AD).

140 ve plateaus at an early symptomatic stage of Alzheimer disease (AD).

141 plaques and tangles is a central feature of Alzheimer disease (AD).

142 oid-beta (Abeta) oligomers are implicated in Alzheimer disease (AD).

143 V45 visualized by PET is a key biomarker for Alzheimer disease (AD).

144 f many neurodegenerative diseases, including Alzheimer disease (AD).

145 the primary toxic agents in the etiology of Alzheimer disease (AD).

146 m those with normal cognition and those with Alzheimer disease (AD).

147 making them a promising physiologic model of Alzheimer disease (AD).

148 omal dysfunction is considered pathogenic in Alzheimer disease (AD).

149 sion from mild cognitive impairment (MCI) to Alzheimer disease (AD).

150 t research has been predominantly focused on Alzheimer disease (AD).

151 o neuronal dysfunction and loss that lead to Alzheimer disease (AD).

152 ers of cytotoxicity and neuroinflammation in Alzheimer disease (AD).

153 arker for pathologic changes associated with Alzheimer disease (AD).

154 easingly been associated to neurotoxicity in Alzheimer disease (AD).

155 in current diagnostic testing approaches for Alzheimer disease (AD).

156 d and used to advance biomedical research in Alzheimer disease (AD).

157 the most influential genetic risk factor for Alzheimer disease (AD).

158 important known risk factors for developing Alzheimer disease (AD).

159 that are occurring during the progression of Alzheimer disease (AD).

160 ied an association between periodontitis and Alzheimer disease (AD); however, the nature of this asso

161 einker syndrome (GSS)) n = 4), patients with Alzheimer disease (AD, n = 14) and age-matched controls

162 kinson disease (PD; n = 179), FTD (n = 179), Alzheimer disease (AD; n = 300), memory-predominant mild

163 generated from individuals with and without Alzheimer disease (AD; n(control) = 13; n(AD) = 83) from

164 B-PET and CSF Abeta in 37 autosomal dominant Alzheimer disease (ADAD) mutation carriers.

165 Risk of Alzheimer disease (aHR, 0.92; 95% CI, 0.88-0.95) and oth

166 ded proteins such as amyloid-beta and tau in Alzheimer disease, alpha-synuclein in Parkinson disease,

167 in some neurodegenerative diseases, such as Alzheimer disease, amyotrophic lateral sclerosis and eve

168 c variants on seven neurological phenotypes (Alzheimer disease, amyotrophic lateral sclerosis, depres

169 diseases, included 6 3 with typical amnesic Alzheimer disease and 3 with atypical variants (posterio

170 We repeated analyses for Alzheimer disease and accounting for stroke.

171 tenuated inversion recovery in subjects with Alzheimer disease and amyotrophic lateral sclerosis.

172 s CA1 subfield oxidative stress in models of Alzheimer disease and Angelman syndrome.

173 n vivo will lead to new diagnostic tools for Alzheimer disease and better understanding of its neurob

174 Association between Alzheimer disease and genetic variants and genes was mea

175 erstand the complex cellular interactions in Alzheimer disease and how these change throughout the co

176 umulation is important in studying aging and Alzheimer disease and is only as accurate as the signal-

177 The tau protein aggregates in aging and Alzheimer disease and may lead to memory loss through di

178 evalent feature, such as multiple sclerosis, Alzheimer disease and motor neuron disease.

179 The risk of Alzheimer disease and other dementias was not higher in

180 in the pathogenesis of small vessel disease, Alzheimer disease and other neurodegenerative and inflam

181 pathology, the other major proteinopathy of Alzheimer disease and other tauopathies, or tau-mediated

182 sis of neurodegenerative diseases, including Alzheimer disease and Parkinson disease.

183 ciations of flavonoid intake and the risk of Alzheimer disease and related dementias (ADRD) are incon

184 udies suggest that one strategy for treating Alzheimer disease and related tauopathies may be inhibit

185 gs for treatment of cognitive impairments in Alzheimer disease and schizophrenia.

186 gations are a hallmark of amyloid-associated Alzheimer disease and some forms of non-amyloid-associat

187 niversal occurrence of the histopathology of Alzheimer disease and the high prevalence of dementia in

188 implicated in neurologic disorders including Alzheimer disease and traumatic brain injury (TBI).

189 Diagnoses of Alzheimer disease and vascular dementia were secondary o

190 in diagnosis (from Alzheimer disease to non-Alzheimer disease and vice versa) between pre- and post-

191 meostasis regulation, with high relevance in Alzheimers disease and type 2 diabetes interlink.

192 such as CTSH (which was also associated with Alzheimer disease) and SARM1 may make worthwhile therape

193 Diabetes, Alzheimer disease, and heart disease caused the most non

194 knowledge, no effective treatments exist for Alzheimer disease, and new molecules are years away.

195 lude neurodegenerative conditions, including Alzheimer disease, and of hormones to include cytokines,

196 potential drug target for neuropathic pain, Alzheimer disease, and prostate cancer.

197 ion into plaques is a pathologic hallmark of Alzheimer disease appearing years before the onset of sy

198 cal diseases, such as Huntington disease and Alzheimer disease, are well-characterized proteinopathie

199 seases, including cardiovascular disease and Alzheimer disease, as well as all-cause mortality.

200 work demonstrating CSF clearance deficits in Alzheimer disease associated with amyloid-beta deposits

201 A major constituent of drusen deposits are Alzheimer disease-associated amyloid beta (Abeta) peptid

202 " The main outcome was incident diagnosis of Alzheimer disease based on the International Classificat

203 F-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue studies assessing binding

204 ques and neurofibrillary tangles co-occur in Alzheimer disease, but with different topological and te

205 g asymptomatic as well as clinical stages of Alzheimer disease calls for precise localization and qua

206 alth and Science University Layton Aging and Alzheimer Disease Center and Oregon Brain Bank.

207 onducted in 31 National Institute on Aging's Alzheimer Disease Centers.

208 ted tau proteins are closely associated with Alzheimer disease clinical phenotype and neurodegenerati

209 Alzheimer disease currently affects 5.8 million persons

210 beta) may contribute to cognitive decline of Alzheimer disease, defining the most critical forms has

211 orks during progression from normal aging to Alzheimer disease dementia (AD) has also been observed.

212 The antemortem clinical diagnoses were Alzheimer disease dementia (n = 6), probable dementia wi

213 le dementia with Lewy bodies (n = 12), mixed Alzheimer disease dementia and probable dementia with Le

214 ion of cognitively unimpaired elderly versus Alzheimer disease dementia, ROC curves based on visual A

215 Dementia and Alzheimer disease diagnoses were retrieved from Finnish

216 ries from 2006 to 2013 and compared rates of Alzheimer disease diagnosis for 399 979 statin users 65

217 s associated with a reduced risk of incident Alzheimer disease diagnosis for white women (HR, 0.84, 9

218 Medications approved to treat Alzheimer disease (donepezil, galantamine, rivastigmine,

219 ssessed by a composite outcome that included Alzheimer disease drug therapy, other drug therapy, and

220 in APP, PSEN1, and PSEN2 lead to early-onset Alzheimer disease (EOAD) but account for only approximat

221 in neurodegenerative disease with a focus on Alzheimer disease, for which the evidence is most compel

222 ly different between the nonimpaired and the Alzheimer disease groups (eg, neuroticism: beta = 0.00;

223 Individuals with symptomatic Alzheimer disease had elevated tau PET SUVRs.

224 ational monitoring of four miRNAs related to Alzheimer disease (has-miR-143-3p, has-miR-18b-5p, has-m

225 of having mild cognitive impairment (MCI) or Alzheimer disease have been reported.

226 ic risk score analysis for the prediction of Alzheimer disease have given area under the curve (AUC)

227 ts were similar when excluding patients with Alzheimer disease (hazard ratio, 2.32; 95% CI, 1.73-3.12

228 ptica spectrum disorders, Parkinson disease, Alzheimer disease, Huntington disease, and amyotrophic l

229 3%-25.9%]) and from non-Alzheimer disease to Alzheimer disease in 1201 of 11 409 (10.5% [95% CI, 10.0

230 gnosis changed from Alzheimer disease to non-Alzheimer disease in 2860 of 11 409 patients (25.1% [95%

231 For Alzheimer disease in particular, genome-wide association

232 workgroup proposed a research framework for Alzheimer disease in which biomarker classification of r

233 peptide (Abeta), a key pathogenic factor in Alzheimer disease, induces profound alterations in neuro

234 Alzheimer disease is associated with deposition of the a

235 hat accumulate in the brain of patients with Alzheimer disease, is abundant in platelets, but its phy

236 of clinical progression among patients with Alzheimer disease leads to difficulty in providing clini

237 ives from an individually varying mixture of Alzheimer disease, Lewy body disease, and vascular brain

238 tion to the use of biomarkers for predicting Alzheimer disease, little information is available at th

239 strong genetic covariance between late-onset Alzheimer disease (LOAD) and amyotrophic lateral scleros

240 Late onset Alzheimer disease (LOAD) is traditionally considered as

241 RV-NPL was applied to analyze 107 late-onset Alzheimer disease (LOAD) pedigrees of Caribbean Hispanic

242 Sporadic late-onset Alzheimer disease (LOAD) preceded by mild cognitive impa

243 PET imaging of tau pathology in Alzheimer disease may benefit from the use of white matt

244 initially associated with increased risk of Alzheimer disease, may potentially influence other compl

245 isks of congenital abnormalities, cancer, or Alzheimer disease.Meta-analysis results indicate an infl

246 Subjects with a clinical diagnosis of Alzheimer disease, mild cognitive impairment, or normal

247 s of 544 MCI patients were obtained from the Alzheimer Disease Neuroimaging Initiative database and a

248 tudy included 319 patients with MCI from the Alzheimer Disease Neuroimaging Initiative database.

249 imaging in 35 healthy participants from the Alzheimer Disease Neuroimaging Initiative database.

250 rker that links a specific type of molecular Alzheimer disease neuropathologic condition with clinica

251 nual cognitive and clinical evaluations, and Alzheimer disease neuropathology was quantified after de

252 In the United States, Alzheimer disease, one cause of dementia, affects 5.8 mi

253 deviation decrease, 1.07-1.61), similar for Alzheimer disease only, and unaltered by accounting for

254 is a biomarker for cardiovascular diseases, Alzheimer disease, pancreatitis and diabetes.

255 he glymphatic system, which are important in Alzheimer disease pathogenesis, may also be involved in

256 le earlier identification of subjects in the Alzheimer Disease pathologic continuum, as well as a fin

257 se cognitive outcomes and is associated with Alzheimer disease pathology in the brain.

258 cts lead to cognitive impairment and promote Alzheimer disease pathology is not well understood.

259 nal mixed effects model, postmortem markers (Alzheimer disease pathology, Lewy bodies, transactive re

260 ined associations between scam awareness and Alzheimer disease pathology, particularly beta-amyloid b

261 iated by amyloid-beta (Abeta) and downstream Alzheimer disease pathology.

262 nction and may find potential application in Alzheimer disease patients to noninvasively evaluate str

263 myloid, which is accumulated in the brain of Alzheimer disease patients.

264 d resting heart rate (P = 0.020) compared to Alzheimer disease patients.

265 were found to be decreased in the brains of Alzheimer disease patients.

266 In conclusion, therapeutic Alzheimer disease prevention strategies aimed at decreas

267 mortem brain tissue from PD cases but not in Alzheimer disease, progressive supranuclear palsy, or mu

268 58; P < .001; and 3 patients with nonamnesic Alzheimer disease, r = -0.51; P < .001; r = -0.63; P < .

269 18F]AV-1451 binding (3 patients with amnesic Alzheimer disease, r = -0.82; P < .001; r = -0.70; P < .

270 The symptoms of Alzheimer disease reflect a loss of neural circuit integ

271 n(control) = 13; n(AD) = 83) from the Knight Alzheimer Disease Research Center (Knight ADRC).

272 th neurodegenerative syndromes from the Mayo Alzheimer Disease Research Center and Mayo Clinic Study

273 and instrumental activities of daily living (Alzheimer Disease Research Center IADLs), pain (geriatri

274 dministered formal neuropsychiatric testing (Alzheimer Disease Research Center UDS battery), basic an

275 based study of cognitive ageing, or the Mayo Alzheimer Disease Research Center, a longitudinal study

276 iated with a statistically significant lower Alzheimer disease risk among black men.

277 nd rosuvastatin were associated with reduced Alzheimer disease risk for white women only (HR, 0.82, 9

278 Because statins may affect Alzheimer disease risk, physicians should consider which

279 cerebral amyloid accumulation and subsequent Alzheimer disease risk.

280 est that research on preclinical markers for Alzheimer disease should take the continuum of CSF amylo

281 Growing evidence from Alzheimer disease supports a potentially beneficial role

282 cortical regions was higher in patients with Alzheimer disease than in healthy control participants.

283 cerebral microcirculation may play a role in Alzheimer disease, the leading cause of late-life dement

284 ension has more recently been linked also to Alzheimer disease-the major cause of dementia in older p

285 cated in cancers, arrhythmia, and late-onset Alzheimer disease, these findings may trigger research d

286 For Alzheimer disease, this includes an acetylcholinesterase

287 s (25.1% [95% CI, 24.3%-25.9%]) and from non-Alzheimer disease to Alzheimer disease in 1201 of 11 409

288 nome sequence data from families affected by Alzheimer disease to illustrate the application of the R

289 the proportion of changes in diagnosis (from Alzheimer disease to non-Alzheimer disease and vice vers

290 The etiologic diagnosis changed from Alzheimer disease to non-Alzheimer disease in 2860 of 11

291 nson disease (PD) and related parkinsonisms, Alzheimer disease, traumatic brain injury, and even in n

292 h mild cognitive impairment due to suspected Alzheimer disease) underwent dynamic PET imaging for up

293 the genetic risk for the most severe form of Alzheimer disease unexplained.

294 es healthy controls (HCs) from subjects with Alzheimer disease, variability exists in the cortical si

295 tiology of cognitive impairment was unknown, Alzheimer disease was a diagnostic consideration, and kn

296 in the prefrontal cortex of individuals with Alzheimer disease were significantly enriched with genes

297 er - a problem that is best characterized in Alzheimer disease, where it begins presymptomatically.

298 trations have been reported in patients with Alzheimer disease while higher serum PK concentrations h

299 for amyloid-beta pathology with symptomatic Alzheimer disease who usually have tau pathology, epsilo

300 ted with more than 1 neuropathology, usually Alzheimer disease with cerebrovascular pathology.