ライフサイエンスコーパス: Alzheimer's

1 ggregation and thus potential biomarkers for Alzheimer's (AD).

2 lipids has been observed in such diseases as Alzheimer's and chronic obstructive pulmonary disease.

3 +/- 4.628 years), from the population-based 'Alzheimer's and Families' study, with baseline MRI, CSF

4 obust predictor of brain pathology including Alzheimer's and other dementias.

5 aque deposits in the brain are indicative of Alzheimer's and other diseases.

6 ptional regulation, have also been linked to Alzheimer's and Parkinson's diseases.

7 ases such as diabetes, obesity, Parkinson's, Alzheimer's, and others.

8 generative diseases, including Huntington's, Alzheimer's, and prion diseases.

9 gions of interest reliably detected advanced Alzheimer's (Braak VI) pathology.

10 gham Heart Study (n = 102), and the National Alzheimer's Coordinating Center (NACC) (n = 582).

11 ological database maintained by the National Alzheimer's Coordinating Center (NACC).

12 Data were obtained from the National Alzheimer's Coordinating Center on participants with mil

13 g and non-human animal research assumes that Alzheimer's degeneration starts in the entorhinal cortic

14 healthy") controls (HC) and individuals with Alzheimer's dementia (AD).

15 ix patients (n = 12 with clinically probable Alzheimer's dementia and n = 14 with amyloid-positive mi

16 h late mild cognitive impairment and 71 with Alzheimer's dementia, age range 56-88 years), we investi

17 E2 allele is associated with a lower risk of Alzheimer's dementia, it is not yet known whether APOE2

18 ) allele is associated with a higher risk of Alzheimer's dementia, while the APOE2 allele is associat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 Alzheimer's disease is a progressive neurodegenerative d

161 Alzheimer's disease is an incurable neurodegenerative di

162 Alzheimer's disease is biologically heterogeneous, and d

163 Alzheimer's disease is characterized by the presence of

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

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

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

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

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

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

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

171 Alzheimer's disease neurodegeneration is thought to spre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 shed neuroprotective genetic variant against Alzheimer's disease.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

276 roughout the pathophysiological continuum of Alzheimer's disease.

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

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

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

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

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

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

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

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

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

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

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

288 iponectin knockout (APN(-/-)) mice developed Alzheimer's like pathologies, cerebral insulin resistanc

289 An Alzheimer's mouse model containing phospho-deficient PS1

290 Neurodegenerative diseases such as Alzheimer's or Parkinson's are associated with the prion

291 g and memory in health and are implicated in Alzheimer's pathogenesis.

292 New studies reveal that Alzheimer's pathologies now can be reliably quantified i

293 ites and small-molecules that were linked to Alzheimer's pathology in previous studies.

294 accompany or even precede the development of Alzheimer's pathology, raising the possibility that they

295 yndrome before the development of full-blown Alzheimer's pathology.

296 Abeta fibrils extracted from the brain of an Alzheimer's patient.

297 In clinical trials with early Alzheimer's patients, administration of anti-amyloid ant

298 : 1) AD diagnosis (International Genomics of Alzheimer's Project), 2) maternal family history of AD (

299 Our work has broad implications for anti-Alzheimer's research and drug development and the broade

300 National Institute for Health Research, and Alzheimer's Society.