ライフサイエンスコーパス: Alzheimer's

1 erlies neurodegenerative diseases, including Alzheimer's.

2 for enhanced stability and affinity for the Alzheimer's Abeta42 peptide.

3 s with neurodegenerative diseases, including Alzheimer's and Parkinson's disease, are thought to spre

4 ed to immune-to-brain communication, such as Alzheimer's and Parkinson's diseases.

5 nd to common neurodegenerative diseases like Alzheimer's and Parkinson's.

6 designed immunotherapy strategies to combat Alzheimer's and related neurodegenerative diseases.

7 differentiating between clinically diagnosed Alzheimer's and subcortical vascular cognitive impairmen

8 according to US National Institute on Aging-Alzheimer's Association neuropathological criteria, and

9 microglial proliferation in a mouse model of Alzheimer's beta-amyloidosis was increased threefold.

10 ired helical filament (PHF)-tau pathology in Alzheimer's brains.

11 h their associations with amyloid plaques in Alzheimer's brains: RTN3, but not RTN1, is abundantly en

12 tudy eligibility criteria, from the National Alzheimer's Coordinating Center (NACC) (n = 5,073, 158 A

13 or restoring cognitive function in aging and Alzheimer's dementia.

14 treatment may delay progression from MCI to Alzheimer's dementia.

15 ught to play an essential pathogenic role in Alzheimer s disease (AD).

16 d be categorised as stage 2 or 3 preclinical Alzheimer's disease (A+T+N-, A+T-N+, and A+T+N+; 86% at

17 STATEMENT Understanding how risk factors for Alzheimer's disease (AD) affect brain function and cogni

18 bustly accumulate within axonal swellings at Alzheimer's disease (AD) amyloid plaques.

19 Tauopathies, including Alzheimer's disease (AD) and other neurodegenerative con

20 nosis of neurodegenerative disorders such as Alzheimer's disease (AD) and related Dementias has been

21 ant post-translational modification (PTM) in Alzheimer's disease (AD) and related tauopathies.

22 l destruction methods.SIGNIFICANCE STATEMENT Alzheimer's disease (AD) and similar dementias are commo

23 ingulate cortex (PCC) predicts conversion to Alzheimer's disease (AD) and tracks disease progression,

24 The earliest stages of Alzheimer's disease (AD) are characterized by the format

25 The drugs currently used to treat Alzheimer's disease (AD) are limited in the benefits the

26 Most cases of Alzheimer's disease (AD) are sporadic, but a small perce

27 splant (KT) may develop post-KT dementia and Alzheimer's disease (AD) associated with their long-stan

28 laques, a potential biomarker present in the Alzheimer's disease (AD) brain is crucial for both clini

29 a-amyloid (Abeta) plaques are key lesions in Alzheimer's disease (AD) but both pathologies also occur

30 pse degeneration and cognitive impairment in Alzheimer's disease (AD) by reactivating expression of t

31 A genome-wide survival analysis of 14,406 Alzheimer's disease (AD) cases and 25,849 controls ident

32 proteinopathy patients while accounting for Alzheimer's disease (AD) copathology.

33 nterest on Tau protein is fast increasing in Alzheimer's disease (AD) diagnosis.

34 lot study on differentiating early stages of Alzheimer's disease (AD) from Dementia with Lewy Bodies

35 Many models of disease progression in Alzheimer's disease (AD) have been proposed to help guid

36 Pathological hallmarks of Alzheimer's disease (AD) include amyloid-beta (Abeta) pl

37 Alzheimer's disease (AD) is a detrimental neurodegenerat

38 SIGNIFICANCE STATEMENT: Alzheimer's disease (AD) is a devastating neurodegenerat

39 Alzheimer's disease (AD) is a prevalent neurodegenerativ

40 Alzheimer's disease (AD) is a type of dementia that caus

41 The pathological hallmark of Alzheimer's disease (AD) is accumulation of misfolded am

42 Elevated risk of developing Alzheimer's disease (AD) is associated with hypomorphic

43 Alzheimer's disease (AD) is characterized by deposition

44 Alzheimer's disease (AD) is characterized by extracellul

45 Alzheimer's disease (AD) is characterized by progressive

46 Alzheimer's disease (AD) is characterized by severe neur

47 Alzheimer's disease (AD) is characterized by the presenc

48 ein E-epsilon4 carriers, is a major risk for Alzheimer's disease (AD) is increasing steadily, with ov

49 A key molecular species in Alzheimer's disease (AD) is the Abeta42 alloform of Abet

50 Alzheimer's disease (AD) is the most common form of deme

51 current frontline symptomatic treatment for Alzheimer's disease (AD) is whole-body upregulation of c

52 y-Camacho et al. (2017) generate a humanized Alzheimer's disease (AD) model that reveals species-spec

53 FASS-LTP analysis in two well-characterized Alzheimer's disease (AD) mouse models (3xTg and Tg2576)

54 oinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by

55 inflammation can play a significant role in Alzheimer's disease (AD) pathogenesis.

56 ilable on the effect of canola oil intake on Alzheimer's disease (AD) pathogenesis.

57 P) has long been appreciated for its role in Alzheimer's disease (AD) pathology.

58 igomeric amyloid-beta (Abetao) in triggering Alzheimer's disease (AD) pathophysiology.

59 emale CRF-OE mice were overrepresented in an Alzheimer's disease (AD) pathway.

60 protein (oAbeta) isolated from the brains of Alzheimer's disease (AD) patients have been shown experi

61 ormin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients.

62 in addition to local brain inflammation, in Alzheimer's disease (AD) progression.

63 al, and symptomatic heterogeneity underlying Alzheimer's disease (AD) requires a deep understanding o

64 Early intervention in Alzheimer's Disease (AD) requires novel biomarkers that

65 eference region differences between SVaD and Alzheimer's disease (AD) using Centiloid scores.

66 myloid-beta pathology early in the course of Alzheimer's disease (AD) with high sensitivity and speci

67 with frontotemporal dementia (FTD-ALS), and Alzheimer's disease (AD), and found profound apical dend

68 s upregulated in the brains of patients with Alzheimer's disease (AD), and its expression levels infl

69 ques are a key histopathological hallmark of Alzheimer's disease (AD), and soluble Abeta species are

70 s the most important genetic risk factor for Alzheimer's disease (AD), ApoE3 is neutral, and ApoE2 is

71 gate the effect of a genetic risk factor for Alzheimer's disease (AD), ApolipoproteinE epsilon4 (APOE

72 Serious brain disorders, such as the Alzheimer's Disease (AD), are associated with a marked d

73 at the intermediate and late Braak stages of Alzheimer's disease (AD), as well as in other neurodegen

74 eta) plays a key role in the pathogenesis of Alzheimer's disease (AD), but little is known about the

75 ne loss is recognized as an early feature of Alzheimer's disease (AD), but the underlying mechanisms

76 gomers is one of the earliest impairments in Alzheimer's Disease (AD), driving initial cognitive defi

77 of tau proteins, termed tauopathies, include Alzheimer's disease (AD), frontotemporal lobar degenerat

78 While SMD might be the earliest sign of Alzheimer's disease (AD), it also occurs in aging and va

79 been the central dogma in drug discovery for Alzheimer's disease (AD), leading to many small-molecule

80 rophy in seven neurodegenerative conditions (Alzheimer's disease (AD), Parkinson's disease (PD) and H

81 Alzheimer's disease (AD), via frontal compensatory proce

82 Age is, by far, the greatest risk factor for Alzheimer's disease (AD), yet few AD drug candidates hav

83 Alzheimer's disease (AD)-linked mutations in Presenilins

84 s in Amytrophic Lateral Sclerosis (ALS)- and Alzheimer's disease (AD)-linked neurons.

85 rils begin to accumulate in individuals with Alzheimer's disease (AD).

86 heir function in neurological diseases, like Alzheimer's disease (AD).

87 ansmission that is thought to be affected in Alzheimer's disease (AD).

88 iating the amyloid-beta and tau pathology in Alzheimer's disease (AD).

89 (CSF) and their potential as biomarkers for Alzheimer's disease (AD).

90 y for patients suffering from memory loss or Alzheimer's disease (AD).

91 in tauopathies, the most common of which is Alzheimer's disease (AD).

92 ate a cascade of neurodegenerative events in Alzheimer's disease (AD).

93 factors for cognitive decline and late onset Alzheimer's disease (AD).

94 as early detectable peripheral biomarkers in Alzheimer's disease (AD).

95 siderable contribution to risk of developing Alzheimer's disease (AD).

96 elates with reduced onset and progression of Alzheimer's disease (AD).

97 terations associated with the development of Alzheimer's disease (AD).

98 f the possible markers for the prediction of Alzheimer's disease (AD).

99 nephrine to the forebrain and degenerates in Alzheimer's disease (AD).

100 amma-secretase underlies the pathogenesis of Alzheimer's disease (AD).

101 mal network (ELN) are a signature feature of Alzheimer's disease (AD).

102 tion, and neurodegenerative diseases such as Alzheimer's disease (AD).

103 d to the pathologic and clinical features of Alzheimer's disease (AD).

104 in tauopathies, the most common of which is Alzheimer's disease (AD).

105 maintain cognitive function in patients with Alzheimer's disease (AD).

106 beta peptide (Abeta42) is a pivotal event in Alzheimer's disease (AD).

107 is considered central to the pathogenesis of Alzheimer's disease (AD).

108 is an initiating step in the pathogenesis of Alzheimer's disease (AD).

109 ) in fresh brain samples of a mouse model of Alzheimer's disease (AD).

110 ology of neurodegenerative disorders such as Alzheimer's disease (AD).

111 roglia is known to play an important role in Alzheimer's disease (AD).

112 nervous system-related pathologies, such as Alzheimer's disease (AD).

113 rogress in unraveling the pathophysiology of Alzheimer's disease (AD).

114 ippocampal area of patients with early-stage Alzheimer's disease (AD).

115 sent the two major pathological hallmarks of Alzheimer's disease (AD).

116 Alzheimer's disease (AD; n = 164) was identified with 70

117 d the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) battery (Word List Learning,

118 contributing mechanism underlying late-onset Alzheimer's disease (LOAD).

119 are also associated with increased risk for Alzheimer's disease (rg=-0.155).

120 d with aging and many human diseases such as Alzheimer's disease [1-3].

121 Cog]) and self-reported QoL (Quality of Life Alzheimer's Disease [QoL-AD]) for the person with dement

122 ociated with type 2 diabetes (T2D), with the Alzheimer's disease amyloid-beta (Abeta) peptide modulat

123 onstitute the histopathological hallmarks of Alzheimer's disease and are prominent targets for novel

124 ed the relationship between genetic risk for Alzheimer's disease and cortical thickness, such that in

125 e more clearly detected by PBB3 in brains of Alzheimer's disease and diffuse neurofibrillary tangles

126 ementia with Lewy bodies, five patients with Alzheimer's disease and five healthy control subjects to

127 to investigate pathological states including Alzheimer's disease and HIV-associated neurocognitive di

128 participants, but not those of patients with Alzheimer's disease and MCI, possess effective phagocyto

129 The innate immune system of patients with Alzheimer's disease and mild cognitive impairment (MCI)

130 Prion diseases, like Alzheimer's disease and Parkinson disease, are rapidly p

131 unction ranging from severe loss, as seen in Alzheimer's disease and Parkinson's disease, to relative

132 ens for neurodegenerative diseases including Alzheimer's disease and Parkinson's disease.

133 eases associated with hippocampal pathology (Alzheimer's disease and schizophrenia) are more enriched

134 s, including addiction, Parkinson's disease, Alzheimer's disease and schizophrenia.

135 Alzheimer's Disease trial, 180 patients with Alzheimer's disease and symptoms of agitation or psychos

136 Tau-mediated neurodegeneration in Alzheimer's disease and tauopathies is generally assumed

137 However, rare forms of familial Alzheimer's disease are associated with mutations in APP

138 e decline (greater impairment on the 11-item Alzheimer's Disease Assessment Scale cognitive subscale

139 Primary outcomes were cognition (Alzheimer's Disease Assessment Scale-cognitive [ADAS-Cog

140 ipants who received IVIG performed better on Alzheimer's Disease Assessment Scale-cognitive subscale

141 ssessed by Mini-Mental State Examination and Alzheimer's Disease Assessment Scale.

142 ect of sleep modulates amyloid-beta or other Alzheimer's disease biomarkers.

143 relevance not only to the pathophysiology of Alzheimer's disease but also diet-associated obesity.

144 ll function is implicated in the etiology of Alzheimer's disease by human genetics.

145 polyneuropathy, and Abeta42 associated with Alzheimer's disease by stabilizing their respective prot

146 ocortical, limbic and subcortical areas from Alzheimer's disease cases (n = 19), neurologically norma

147 dividuals with mild cognitive impairment and Alzheimer's disease clinical diagnoses can display signi

148 We applied this tool to the analysis of Alzheimer's disease data from three datasets CHS, FHS an

149 re achieved at very low amisulpride doses in Alzheimer's disease due to higher than anticipated occup

150 o be actively involved in the development of Alzheimer's disease due to its ability to seed the aggre

151 ion and the role of environmental factors in Alzheimer's disease etiology.

152 8F-AV-1451) associated with well-established Alzheimer's disease factors in a cohort including cognit

153 duals (5,728 AD, 5,653 CN controls) from the Alzheimer's Disease Genetics Consortium (ADGC), a Nation

154 and 9,386 older controls from Phase 1 of the Alzheimer's Disease Genetics Consortium (ADGC), providin

155 ols (age at examination, >65 years) from the Alzheimer's Disease Genetics Consortium.

156 ntified rare coding variants associated with Alzheimer's disease in a three-stage case-control study

157 tor for frontotemporal dementia spectrum and Alzheimer's disease in an initial case-control study.

158 on of induced neuron-based model of sporadic Alzheimer's disease in mice and humans, and used this sy

159 l features of neurodegeneration occurring in Alzheimer's disease including age-dependent cortical atr

160 Memory impairment in Alzheimer's disease is a manifestation of brain patholog

161 tion of AbetaOs in AD.SIGNIFICANCE STATEMENT Alzheimer's disease is characterized by progressive cogn

162 Alzheimer's disease is characterized by the self-assembl

163 Alzheimer's disease is one of the most devastating neuro

164 One of the main research topics related to Alzheimer's disease is the aggregation of the amyloid-be

165 on as seen in neurological disorders such as Alzheimer's disease may contribute to neurovascular dysf

166 ed loss of synapses and cognitive decline in Alzheimer's disease mice.

167 th mitochondrial dysfunction in the brain of Alzheimer's disease mouse model CRND8 as early as 3 mont

168 nd improved cognitive function in a familial Alzheimer's disease mouse model.

169 External validation in Alzheimer's Disease Neuroimaging Initiative 2 showed tha

170 , and 180 patients with AD dementia from the Alzheimer's Disease Neuroimaging Initiative.

171 ease neuropathology, 56 (26%) with low-level Alzheimer's disease neuropathology, 45 (21%) with interm

172 thy, we identified 49 (23%) patients with no Alzheimer's disease neuropathology, 56 (26%) with low-le

173 opathology, 45 (21%) with intermediate-level Alzheimer's disease neuropathology, and 63 (30%) with hi

174 neuropathology, and 63 (30%) with high-level Alzheimer's disease neuropathology.

175 including cognitive decline associated with Alzheimer's disease or schizophrenia.

176 al in groups with varying levels of comorbid Alzheimer's disease pathology according to US National I

177 's component features.SIGNIFICANCE STATEMENT Alzheimer's disease pathology appears earliest in brain

178 ociated with dementia that is independent of Alzheimer's disease pathology or larger infarcts (ie, la

179 e in late-life depression is associated with Alzheimer's disease pathology.

180 inhibits glutamatergic synaptic function in Alzheimer's disease patients.

181 ure in vivo may correlate with variations in Alzheimer's disease phenotype, in analogy to distinct pr

182 dysfunction may be a critical early step in Alzheimer's disease progression.

183 genic mechanisms resulting from the sporadic Alzheimer's disease risk factor apolipoprotein E (APOE)

184 ction between APOE varepsilon3/4 and another Alzheimer's disease risk factor, desmoglein 2 (DSG2).

185 stributions of autoradiographic labelling of Alzheimer's disease slices with 11C-PBB3 and 18F-AV-1451

186 athology and cognitive impairment across the Alzheimer's disease spectrum.

187 icroglial activation was increased by 36% in Alzheimer's disease subjects compared with controls.

188 activation in mild cognitive impairment and Alzheimer's disease subjects.

189 Moreover, studies in mouse models of Alzheimer's disease suggest that certain classes of AEDs

190 Of particular interest, the ATP7B(K832R) Alzheimer's disease susceptibility allele was found, for

191 alterations in mild cognitive impairment and Alzheimer's disease that can complement existing dimensi

192 ent a previously unrecognized contributor to Alzheimer's disease that is independent of neuronal hypo

193 d beta precursor protein), a major player in Alzheimer's disease that is known to have immune and inf

194 In Alzheimer's disease the amyloid-beta peptide (Abeta) mis

195 he Abeta peptides, which are associated with Alzheimer's disease through their presence in amyloid pl

196 HOD: In the Antipsychotic Discontinuation in Alzheimer's Disease trial, 180 patients with Alzheimer's

197 existing dimensional approaches for staging Alzheimer's disease using a variety of biomarkers, which

198 s toxicity of amyloid-beta species linked to Alzheimer's disease was initially treated with scepticis

199 Alzheimer's disease was uncommon (6%) among patients who

200 oteins related to amyloid-beta metabolism or Alzheimer's disease were quantified by enzyme-linked imm

201 has an important role in the pathogenesis of Alzheimer's disease with its three isoforms having disti

202 atment of clinical seizures in patients with Alzheimer's disease with select antiepileptic drugs (AED

203 N = 14), controls (N = 14) and "asymptomatic Alzheimer's disease" (ASYMAD), i.e., individuals with si

204 unity on neurodegenerative disorders such as Alzheimer's disease, amyotrophic lateral sclerosis, Park

205 unction leads to such disorders as epilepsy, Alzheimer's disease, and autism.

206 (Abeta) plays a crucial synaptotoxic role in Alzheimer's disease, and hyperphosphorylated tau facilit

207 he second most common form of dementia after Alzheimer's disease, and there is increasing awareness t

208 oid precursor protein (APP), a key player in Alzheimer's disease, belongs to the family of synaptic a

209 ds have a greater role for AMD compared with Alzheimer's disease, but a lesser role than for CAD.

210 Bryostatin is in clinical trials for Alzheimer's disease, cancer, and HIV/AIDS eradication.

211 Alzheimer's disease, dementia with Lewy bodies and genet

212 s, with known revised diagnosis in over 25% (Alzheimer's disease, dementia with Lewy bodies, and prog

213 In patients with Alzheimer's disease, deposition of amyloid-beta is accom

214 k1A might be an ideal therapeutic target for Alzheimer's disease, especially for Down syndrome and EG

215 mation of amyloid beta fibrils implicated in Alzheimer's disease, gamma-secretase is an important tar

216 or protein, BACE1 is a therapeutic target in Alzheimer's disease, however, consistent with its role i

217 and PTEN dysregulation and suggest that, in Alzheimer's disease, impairment of brain insulin signali

218 ith an increased risk of dementia, including Alzheimer's disease, in patients with prostate cancer.

219 n are associated with the pathophysiology of Alzheimer's disease, it is clear that amyloid precursor

220 alogs for the management of type 2 diabetes, Alzheimer's disease, or other diseases related to IAPP d

221 hology in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington

222 such as anxiety, depression, schizophrenia, Alzheimer's disease, Parkinson's disease, and pain, prov

223 y of developing age-related diseases such as Alzheimer's disease, Parkinson's disease, multiple scler

224 litating protein deposition diseases such as Alzheimer's disease, prion diseases, and type II diabete

225 various neurodegenerative diseases including Alzheimer's disease, progressive supranuclear palsy and

226 ought to result in neurodegeneration causing Alzheimer's disease, progressive supranuclear palsy, chr

227 m antipsychotic prescribing for psychosis in Alzheimer's disease, the mechanisms underpinning antipsy

228 the brain increases with the progression of Alzheimer's disease, thus classifying BChE as a promisin

229 ker of neurodegenerative diseases, including Alzheimer's disease, where olfactory deficits precede de

230 erm memory performance and is reminiscent of Alzheimer's disease, which is characterized by degenerat

231 rformance in individuals at genetic risk for Alzheimer's disease, with the caveat that the order of c

232 -AD mouse brain slice culture model with key Alzheimer's disease-like changes.

233 Those with Alzheimer's disease-related cognitive impairment were yo

234 d BACE1 is accumulated in the distal axon of Alzheimer's disease-related mutant human APP transgenic

235 In this regard, new evidence linking Alzheimer's disease-related pathology and neuronal stem

236 pt of cognitive aging to include evidence of Alzheimer's disease-related protein aggregation as an un

237 ckness, suggesting that cortical thinning in Alzheimer's disease-vulnerable brain regions is a mechan

238 ic risk showed reduced cortical thickness in Alzheimer's disease-vulnerable regions.

239 eper understanding of the molecular basis of Alzheimer's disease.

240 autism spectrum disorder, schizophrenia, and Alzheimer's disease.

241 ergic hypofunction in patients with advanced Alzheimer's disease.

242 y amyloid-beta proteotoxic diseases, such as Alzheimer's disease.

243 n-specific manner to cognitive impairment in Alzheimer's disease.

244 esent a new therapeutic avenue for combating Alzheimer's disease.

245 led states is central to the pathogenesis of Alzheimer's disease.

246 degenerative neurological illnesses, such as Alzheimer's disease.

247 xic effect of Abeta(1-40) and Abeta(1-42) in Alzheimer's disease.

248 s the risk for the development of late-onset Alzheimer's disease.

249 cated in reducing the severity of stroke and Alzheimer's disease.

250 as autism spectrum disorder, depression and Alzheimer's disease.

251 ing TLR4-TLR6 dimerization as a treatment of Alzheimer's disease.

252 Ser367 should be useful in the treatment of Alzheimer's disease.

253 a with Lewy bodies, Parkinson's disease, and Alzheimer's disease.

254 d individuals at early symptomatic stages of Alzheimer's disease.

255 ntribute to the loss of synaptic function in Alzheimer's disease.

256 umerous neuropsychiatric disorders including Alzheimer's disease.

257 t target for developing therapeutics against Alzheimer's disease.

258 e contributes directly to the development of Alzheimer's disease.

259 sion is associated with an increased risk of Alzheimer's disease.

260 plays a central role in the pathogenesis of Alzheimer's disease.

261 id and fcMRI in individuals with preclinical Alzheimer's disease.

262 ein 43 (TDP-43) is another protein linked to Alzheimer's disease.

263 regates in the brain tissue of patients with Alzheimer's disease.

264 higher in dementia with Lewy bodies than in Alzheimer's disease.

265 r of neural circuit defects in patients with Alzheimer's disease.

266 oup of community-dwelling veterans with mild Alzheimer's disease.

267 community-dwelling veterans (N=60) with mild Alzheimer's disease.

268 isk of side effects including angioedema and Alzheimer's disease.

269 BChE as a promising drug target in advanced Alzheimer's disease.

270 ggests a new link between RBFOX proteins and Alzheimer's disease.

271 treat psychosis, agitation and aggression in Alzheimer's disease.

272 loid fibrils is a defining characteristic of Alzheimer's disease.

273 hat are able to slow down the progression of Alzheimer's disease.

274 logical disorders, such as schizophrenia and Alzheimer's disease.

275 ousal and in pathological conditions such as Alzheimer's disease.

276 is, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease.

277 in other neurodegenerative disorders such as Alzheimer's disease.

278 ant for managing diseases such as cancer and Alzheimer's disease.

279 cluding multiple sclerosis (MS), stroke, and Alzheimer's disease.

280 nd aging and in models of brain ischemia and Alzheimer's disease.

281 on is an important modifiable risk factor in Alzheimer's disease.

282 well-known amyloid-beta peptide involved in Alzheimer's disease.

283 tiple neurodegenerative disorders, including Alzheimer's disease.

284 upancy for optimal treatment of psychosis in Alzheimer's disease.

285 suggesting a link between mRNA stability and Alzheimer's disease."

286 Herpes simplex virus type 1 and Alzheimer's disease: possible mechanisms and signposts.

287 is a dominant feature in the pathogenesis of Alzheimer's disease; however, it is not clear how indivi

288 eptic activity is frequently associated with Alzheimer's disease; this association has therapeutic im

289 re common disorders, such as Parkinson's and Alzheimer's diseases.

290 ritical to the neurodegenerative pathways of Alzheimer's, Huntington's, and Parkinson's diseases and

291 associated with degenerative diseases (i.e., Alzheimer's, Huntington's, and Parkinson's diseases), ca

292 NMNAT2 is significantly reduced in Alzheimer's, Huntington's, Parkinson's diseases.

293 Abeta) aggregation in vitro and suppress the Alzheimer's-like phenotypes in a transgenic mouse model

294 s in several neurodegenerative diseases like Alzheimer's, Parkinson's, prion diseases, etc.

295 s, the peptides and proteins associated with Alzheimer's, Parkinson's, type 2 diabetes and prion dise

296 s in episodic memory and the accumulation of Alzheimer's pathology are common in cognitively normal o

297 d 51% at age 80 years) or with suspected non-Alzheimer's pathophysiology (A-T+N-, A-T-N+, and A-T+N+;

298 usative factors underlying memory defects in Alzheimer's patients.

299 obtained from the International Genomics of Alzheimer's Project (17,008 AD cases and 37,154 controls

300 controls from the International Genomics of Alzheimer's Project (IGAP Stage 1), we identified AD-ass