ライフサイエンスコーパス: familial Alzheimer's disease

1 n the presenilin genes are the main cause of familial Alzheimer's disease.

2 PS1), the protein most frequently mutated in familial Alzheimer's disease.

3 ttern of binding compared to late onset, non-familial Alzheimer's disease.

4 lated from rare individuals with early-onset familial Alzheimer's disease.

5 mbrane aspartyl protease, are known to cause familial Alzheimer's disease.

6 are elevated at the presymptomatic stages of familial Alzheimer's disease.

7 MRI scans that predate the clinical onset of familial Alzheimer's disease.

8 have been genetically linked to early-onset familial Alzheimer's disease.

9 responsible for the majority of early onset familial Alzheimer's disease.

10 senilins (PS) 1 and 2 are the major cause of familial Alzheimer's disease.

11 n of the loop has been demonstrated to cause familial Alzheimer's disease.

12 and amyloid precursor protein (APP) lead to familial Alzheimer's disease.

13 ncentrations) and mutations in PS1 linked to familial Alzheimer's disease.

14 a protein which carries mutations that cause familial Alzheimer's disease.

15 ecursor protein may mediate neurotoxicity in Familial Alzheimer's Disease.

16 s in Presenilin-1 (PS1) are a major cause of familial Alzheimer's disease.

17 association between PS1 and beta-catenin in familial Alzheimer's disease.

18 ggressive nature of presenilin-1 mutation in familial Alzheimer's disease.

19 mutated in most cases of autosomal dominant familial Alzheimer's disease.

20 te with the majority of early onset cases of familial Alzheimer's disease.

21 (APP) gene are associated with some forms of Familial Alzheimer's Disease.

22 which shows genetic linkage with late onset familial Alzheimer's disease.

23 enilin 1 and 2, account for most early-onset familial Alzheimer's disease.

24 mplicated in the pathogenesis of early-onset familial Alzheimer's disease.

25 unt for the majority of cases of early-onset familial Alzheimer's disease.

26 linked to about 25% of cases of early-onset familial Alzheimer's disease.

27 st common and aggressive form of early onset familial Alzheimer's disease.

28 families with early onset autosomal dominant familial Alzheimer's disease.

29 unt for the majority of early onset cases of familial Alzheimer's disease.

30 aggressive forms of early-onset (< 60 years) familial Alzheimer's disease.

31 o the earlier age of onset characteristic of familial Alzheimer's disease.

32 old but not in young Tg2576 mice, a model of familial Alzheimer's disease.

33 adiazine, as a GSM preclinical candidate for familial Alzheimer's disease.

34 ding in sporadic Alzheimer's disease but not familial Alzheimer's disease.

35 ry binding performance only in patients with familial Alzheimer's disease.

36 attern of amyloid-beta(4)(2) accumulation in familial Alzheimer's disease.

37 ) accumulation in cortical areas compared to familial Alzheimer's disease.

38 eta(4)(0)) accumulation in both sporadic and familial Alzheimer's disease.

39 the presymptomatic and symptomatic stages of familial Alzheimer's disease.

40 with Down syndrome (DS) that can also cause familial Alzheimer's disease.

41 participants) of APOE and hereditary CAA or familial Alzheimer's disease.

42 (APP) mutations associated with early-onset familial Alzheimer's disease.

43 rontotemporal dementia and both sporadic and familial Alzheimer's disease.

44 id-modifying treatments in the prevention of familial Alzheimer's disease.

45 precursor protein (APP) are associated with familial Alzheimer's disease.

46 presenilin 2 are rare causes of early onset familial Alzheimer's disease.

47 may not be as suitable a reference region in familial Alzheimer's disease.

48 ing deficits may be a preclinical marker for familial Alzheimer's disease.

49 A sample of 19 patients with familial Alzheimer's disease, 18 asymptomatic carriers a

50 Additionally, in vivo studies in the familial Alzheimer's disease 5xFAD murine model revealed

51 etected with PET and FDG in Huntington's and familial Alzheimer's diseases 7 and 5 y, respectively, b

52 In familial Alzheimer's disease, Abeta is excessively produ

53 enilin (PSEN1 and PSEN2) genes are linked to familial Alzheimer's disease (AD) and cause loss of its

54 Most early onset cases of familial Alzheimer's disease (AD) are caused by mutation

55 e amyloid precursor protein gene (APP) cause familial Alzheimer's disease (AD) by increasing generati

56 The majority of familial Alzheimer's disease (AD) cases are caused by mu

57 Greater than 90% of familial Alzheimer's disease (AD) is linked to mutations

58 ursor protein (APP) and presenilin (PSEN) to familial Alzheimer's disease (AD) is well established.

59 P) gene alter APP processing, either causing familial Alzheimer's disease (AD) or protecting against

60 al, and occipital neocortices in 40 cases of familial Alzheimer's disease (AD) or sporadic (idiopathi

61 Both sporadic and familial Alzheimer's disease (AD) patients exhibit incre

62 myloid (Abeta) precursor protein (APP) cause familial Alzheimer's disease (AD) probably by enhancing

63 ptide) is invariably elevated in early-onset familial Alzheimer's disease (AD), and it is also increa

64 idues 21-23, which are linked to early onset familial Alzheimer's disease (AD), are primarily associa

65 es (PS-1 and PS-2) are linked to early onset familial Alzheimer's disease (AD), but the mechanisms by

66 (ASYN) in neurodegenerative disease such as familial Alzheimer's disease (AD), dementia with Lewy bo

67 cidation of the genetic basis of early-onset familial Alzheimer's disease (AD), the etiology of spora

68 ly APP and not the APLPs have been linked to familial Alzheimer's disease (AD), this data should help

69 dence and earlier age of onset of late onset familial Alzheimer's disease (AD), whereas apoE2 may hav

70 ns that alter gamma-secretase activity cause familial Alzheimer's disease (AD), whereas ApoE4, an apo

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

72 s in the Abeta precursor protein (APP) cause familial Alzheimer's disease (AD).

73 cursor protein (APP) are the major causes of familial Alzheimer's disease (AD).

74 in human PS1 and PS2 homologs are a cause of familial Alzheimer's disease (AD).

75 ilin-1 (PS1) gene is a cause of early- onset familial Alzheimer's disease (AD).

76 lineate non-cell autonomous contributions to familial Alzheimer's disease (AD).

77 n genes that process APP are correlated with familial Alzheimer's disease (AD).

78 Autosomal dominant familial Alzheimer's disease (ADAD) is a rare disorder w

79 mutations in symptomatic autosomal dominant familial Alzheimer's disease (ADAD).

80 Mutations in the presenilins that cause familial Alzheimer's disease alter the activity of these

81 presenilin-1 and -2 gene are associated with familial Alzheimer's disease and are thought to alter ga

82 wa mutation, is associated with early onset, familial Alzheimer's disease and cerebral amyloid angiop

83 resenilin-1 (PSEN1) gene are associated with familial Alzheimer's disease and frontotemporal dementia

84 ntribute to the understanding of preclinical familial Alzheimer's disease and help set the stage for

85 esent a viable strategy for the treatment of familial Alzheimer's disease and other monogenic disease

86 Mutant human presenilins cause early-onset familial Alzheimer's disease and render cells susceptibl

87 Presenilin mutations give rise to familial Alzheimer's disease and result in elevated prod

88 loid-beta1-40 concentrations were similar in familial Alzheimer's disease and sporadic Alzheimer's di

89 ization to the neuropathology in early-onset familial Alzheimer's disease and sporadic Alzheimers' di

90 lobes are vulnerable to the early stages of familial Alzheimer's disease and their damage is associa

91 Nine sporadic Alzheimer's disease, three familial Alzheimer's disease and three non-Alzheimer's d

92 deletion in exon 9) that is associated with familial Alzheimer's disease and which does not require

93 lar Abeta peptide as well as mutants causing familial Alzheimer's disease, and find that all but one

94 s of familial amyotrophic lateral sclerosis, familial Alzheimer's disease, and Huntington's disease a

95 ons in the PSEN genes are the major cause of familial Alzheimer's disease, and presenilin (PS) is the

96 However, rare forms of familial Alzheimer's disease are associated with mutatio

97 Most cases of early-onset familial Alzheimer's disease are caused by mutations in

98 Most cases of autosomal-dominant familial Alzheimer's disease are linked to mutations in

99 ) and presenilin-2 (PS2), the major genes of familial Alzheimer's disease, are homologous to sel-12,

100 rom cases with dementia with Lewy bodies and familial Alzheimer's disease associated with known PSEN1

101 Familial Alzheimer's disease-associated mutations in pre

102 event that also occurs in the absence of the familial Alzheimer's disease-associated mutations in PS2

103 fragment are associated with the presence of familial Alzheimer's disease-associated mutations.

104 The familial Alzheimer's disease-associated protein Presenil

105 A familial Alzheimer's disease-associated PS-1 mutant, PS-

106 Several familial Alzheimer's disease-associated PS1 mutations ha

107 rocedures) for sporadic Alzheimer's disease, familial Alzheimer's disease, autism spectrum disorder a

108 dence of genetic heterogeneity in late-onset familial Alzheimer's disease, based on sex of affected p

109 d primary fibroblasts from two patients with familial Alzheimer's disease, both caused by a duplicati

110 ations in presenilins are the major cause of familial Alzheimer's disease, but the pathogenic mechani

111 dividuals with sporadic Alzheimer's disease, familial Alzheimer's disease (carrying PSEN1 and PSEN2 v

112 amples of frontal neocortex from early-onset familial Alzheimer's disease cases (PS1 and PS2), late-o

113 ears of age) of autopsy-confirmed late-onset familial Alzheimer's disease cases and 90 age-matched co

114 plaques were present in the neocortex of all familial Alzheimer's disease cases and one sporadic Alzh

115 cortex, the superior temporal sulcus, of 30 familial Alzheimer's disease cases carrying 10 different

116 The majority of familial Alzheimer's disease cases have been attributed

117 five sporadic Alzheimer's disease and three familial Alzheimer's disease cases were analysed for 3H-

118 st-mortem amyloid-beta plaque load; however, familial Alzheimer's disease cases with abundant cotton

119 sease case, in the caudate nucleus from four familial Alzheimer's disease cases, but not in the cereb

120 of 72 individuals affected with early-onset familial Alzheimer's disease caused by an autosomal domi

121 kindred with early-onset autosomal dominant familial Alzheimer's disease caused by an intronic prese

122 Twenty two patients with familial Alzheimer's disease caused by the E280A single

123 with 85Dbo transgenic mice, which coexpress familial Alzheimer's disease-causing amyloid precursor p

124 amma-secretase complex frequently mutated in familial Alzheimer's disease, clear from glutamatergic t

125 These findings imply that in familial Alzheimer's disease cognitive decline predates

126 etween Aug 1 and Dec 6, 2011, members of the familial Alzheimer's disease Colombian kindred aged 18-6

127 nd longitudinal cohort study, members of the familial Alzheimer's disease Colombian kindred aged 8-75

128 cal signs and symptoms were more frequent in familial Alzheimer's disease compared with sporadic Alzh

129 r of mutations in the Abeta sequence lead to familial Alzheimer's disease, congophilic amyloid angiop

130 tion and other neuropathological features in familial Alzheimer's disease due to autosomal dominant m

131 Individuals with familial Alzheimer's disease due to PSEN1 mutations deve

132 sporadic Alzheimer's disease, 12 cases with familial Alzheimer's disease due to PSEN1 mutations, two

133 e affected in patients who meet criteria for familial Alzheimer's disease due to the mutation E280A o

134 utations in the PSEN1 gene cause early-onset familial Alzheimer's disease (eFAD) and increase the pro

135 rain is increased in 54 cases of early-onset familial Alzheimer's disease, encompassing 25 mutations

136 EN1 and PSEN2) cause a subset of early-onset familial Alzheimer's disease (EO-FAD).

137 ble use in primary prevention of early-onset familial Alzheimer's disease (EOFAD).

138 otype identified from a Swedish kindred with familial Alzheimer's disease, evaluation of the cellular

139 ) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer's disease (FAD) and alter proteolytic

140 the most common form of dominant early-onset familial Alzheimer's disease (FAD) and are associated wi

141 senilin 1 (PS1) are linked to early onset of familial Alzheimer's disease (FAD) and are shown to fost

142 s in presenilins (PS) are the major cause of familial Alzheimer's disease (FAD) and have been associa

143 Autosomal dominant forms of familial Alzheimer's disease (FAD) are associated with i

144 The vast majority of pedigrees with familial Alzheimer's disease (FAD) are caused by inherit

145 Most cases of early-onset familial Alzheimer's disease (FAD) are caused by mutatio

146 ial, early-onset autosomal dominant forms of familial Alzheimer's disease (FAD) are caused by mutatio

147 The majority of early-onset cases of familial Alzheimer's disease (FAD) are linked to mutatio

148 precursor (APP) associated with early-onset familial Alzheimer's disease (FAD) can alter the ratio o

149 te with a small subset of autosomal dominant familial Alzheimer's disease (FAD) cases wherein deposit

150 t are mutated in the majority of early onset familial Alzheimer's disease (FAD) cases.

151 PS2) account for the majority of early-onset familial Alzheimer's disease (FAD) cases.

152 Recently it was proposed that the familial Alzheimer's disease (FAD) causing presenilin (P

153 Fifty-two individuals from a familial Alzheimer's disease (FAD) cohort (9 symptomatic

154 s simplex virus (HSV) vectors expressing the familial Alzheimer's disease (FAD) gene presenilin-1 (PS

155 gh an association between the product of the familial Alzheimer's disease (FAD) gene, presenilin 1 (P

156 amyloid precursor protein (APP) genes cause familial Alzheimer's disease (FAD) in a nearly fully pen

157 -protein precursor (APP) mutations linked to familial Alzheimer's disease (FAD) increase the extracel

158 Familial Alzheimer's disease (FAD) is characterized by a

159 Familial Alzheimer's disease (FAD) is frequently associa

160 inking presenilin-1 (PS-1) gene mutations to familial Alzheimer's disease (FAD) is uncertain, but has

161 Here we found that, in the late-stage familial Alzheimer's disease (FAD) mouse model, repressi

162 red in Alzheimer's disease (AD) patients and familial Alzheimer's disease (FAD) mouse models.

163 tic (E22G), Dutch (E22Q), and Flemish (A21G) familial Alzheimer's disease (FAD) mutants for any chang

164 tor, upregulation of Abeta42 production by a familial Alzheimer's disease (FAD) mutation in the APP g

165 lin-1 (Psen1) knockin (KI) mice carrying the familial Alzheimer's disease (FAD) mutation L435F or C41

166 Familial Alzheimer's disease (fAD) mutations alter amylo

167 Mouse models with familial Alzheimer's disease (FAD) mutations exhibit amy

168 Familial Alzheimer's disease (FAD) mutations in APP caus

169 ess human PS1 variants linked to early-onset familial Alzheimer's disease (FAD) neither exhibit EE-in

170 regate with approximately 25% of early onset familial Alzheimer's disease (FAD) pedigrees.

171 ected members of the majority of early-onset familial Alzheimer's disease (FAD) pedigrees.

172 ), cause dementia in a subset of early-onset familial Alzheimer's disease (FAD) pedigrees.

173 cosegregate with the majority of early-onset familial Alzheimer's disease (FAD) pedigrees.

174 penetrant genetic alterations that result in familial Alzheimer's disease (FAD) provides a unique mod

175 tivity, and APP with mutations linked to the familial Alzheimer's disease (FAD) provides substantiall

176 atic activity is reduced in cells expressing familial Alzheimer's disease (FAD) PS1 mutations compare

177 Familial Alzheimer's disease (fAD) results from mutation

178 e mutations with autosomal dominant forms of familial Alzheimer's disease (FAD) suggest important rol

179 ilin genes (PS1 and PS2) causing early-onset familial Alzheimer's disease (FAD) was assessed in a pop

180 nilin mutations are the most common cause of familial Alzheimer's disease (FAD), but the mechanisms b

181 senilin-1 (PS1) are the predominant cause of familial Alzheimer's disease (FAD), but the underlying m

182 S2), the leading cause of autosomal dominant familial Alzheimer's disease (FAD), cause highly specifi

183 an early onset inherited disorder that, like familial Alzheimer's disease (FAD), is characterized by

184 In familial Alzheimer's disease (FAD), missense point mutat

185 APP, whose mutations cause familial Alzheimer's disease (FAD), modulates neurotrans

186 In dominantly inherited familial Alzheimer's disease (FAD), point mutations V642

187 Here we show that PS1, a protein involved in familial Alzheimer's disease (FAD), promotes cell surviv

188 e the development of a prion disorder and of familial Alzheimer's disease (fAD), respectively.

189 In familial Alzheimer's disease (FAD), three mutations V642

190 Here we report that familial Alzheimer's disease (FAD)-associated presenilin

191 Familial Alzheimer's disease (FAD)-causing mutant presen

192 ximal phenotype observed in cells expressing familial Alzheimer's disease (FAD)-causing mutant presen

193 s of wild type and transgenic mice harboring familial Alzheimer's disease (FAD)-linked APPswe/PS1Delt

194 In contrast, familial Alzheimer's disease (FAD)-linked mutant PS1 or

195 Familial Alzheimer's disease (FAD)-linked mutations in t

196 vesicles containing beta APP is impaired in familial Alzheimer's disease (FAD)-linked PS1 mutant cel

197 in genes encoding presenilin 1 (PS1) causes familial Alzheimer's disease (FAD).

198 ne are the most commonly recognized cause of familial Alzheimer's disease (FAD).

199 ction of beta-amyloid 42 (Abeta42) and cause familial Alzheimer's disease (FAD).

200 n (PS) gene mutations that cause early-onset familial Alzheimer's disease (FAD).

201 S1 molecule are linked to autosomal dominant familial Alzheimer's disease (FAD).

202 S1), the molecule most frequently mutated in familial Alzheimer's Disease (FAD).

203 n presenilin genes are linked to early onset familial Alzheimer's disease (FAD).

204 account for approximately 50% of early-onset familial Alzheimer's disease (FAD).

205 s the major gene responsible for early-onset familial Alzheimer's disease (FAD).

206 , are the major association with early-onset familial Alzheimer's disease (FAD).

207 lead to dominant-inheritance of early-onset familial Alzheimer's disease (FAD).

208 nd PS2, cause a major portion of early onset familial Alzheimer's disease (FAD).

209 ed to the majority of cases with early-onset familial Alzheimer's disease (FAD).

210 14, and 21 cause autosomal dominant forms of familial Alzheimer's disease (FAD).

211 appear to cause the majority of early-onset familial Alzheimer's disease (FAD).

212 N2) genes are the major cause of early-onset familial Alzheimer's disease (FAD).

213 enilin-1 (PSEN1) gene are the major cause of familial Alzheimer's disease (FAD).

214 (PS1) mutations are the most common cause of familial Alzheimer's disease (FAD).

215 )variants causes autosomal dominant forms of familial Alzheimer's disease (FAD).

216 alytic subunit of gamma-secretase, result in familial Alzheimer's disease (FAD).

217 resenilins (PS) account for most early-onset familial Alzheimer's disease (FAD).

218 Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in

219 The familial Alzheimer's disease gene product amyloid beta p

220 The familial Alzheimer's disease gene product amyloid beta p

221 The familial Alzheimer's disease gene product beta-amyloid (

222 The familial Alzheimer's disease gene products, presenilin-1

223 ALG-3, a truncated form of the familial Alzheimer's disease gene PS2, confers resistanc

224 runcated mouse homologue of the chromosome 1 familial Alzheimer's disease gene PS2, rescues T hybrido

225 complementary DNA that is homologous to the familial Alzheimer's disease gene STM2, rescues a T cell

226 PS2, the chromosome 1 familial Alzheimer's disease gene, has been shown to be

227 asing amyloid-beta ('TASTPM', transgenic for familial Alzheimer's disease genes APP/PSEN1).

228 with ageing and in mouse models that express familial Alzheimer's disease genes.

229 We observed that familial Alzheimer's disease had disproportionate amyloi

230 Familial Alzheimer's disease had greater striatal tau pa

231 e, three non-demented individuals at risk of familial Alzheimer's disease had scans 6-14 months apart

232 The majority of cases with early onset familial Alzheimer's disease have been attributed to mut

233 The four genes so far implicated in familial Alzheimer's disease have each been shown to ele

234 Amyloid imaging studies of presymptomatic familial Alzheimer's disease have revealed the striatum

235 e significantly altered in both sporadic and familial Alzheimer's disease; however, such changes were

236 (APP) gene are associated with rare cases of familial Alzheimer's disease; however, the normal functi

237 Mutations in PS1 that are associated with familial Alzheimer's disease impair the ability of PS1 t

238 oter in CNS neurons that causes early onset, familial Alzheimer's disease in humans.

239 We discuss a pathogenic pathway for familial Alzheimer's disease in which defective presenil

240 and PS2 that are associated with early-onset familial Alzheimer's disease increase the production of

241 that expression of APP mutations that cause familial Alzheimer's disease increases the intracellular

242 ecursor protein (APP), whose mutations cause familial Alzheimer's disease, interacts with the synapti

243 Early-onset familial Alzheimer's disease is caused in part by pathog

244 The most common cause of familial Alzheimer's disease is mutation of the genes en

245 Early-onset familial Alzheimer's disease is the most aggressive form

246 1 (PS1), mutated in pedigrees of early-onset familial Alzheimer's disease, is a polytopic integral me

247 nse mutation of APP, implicated in a form of familial Alzheimer's disease, is adjacent to this latter

248 lar in sporadic Alzheimer's disease while in familial Alzheimer's disease it was lower in the neocort

249 hich was discovered in a Swedish family with familial Alzheimer's disease, leads to increased beta-se

250 ocytic abnormalities distinguish subtypes of familial Alzheimer's disease linked to APP mutations fro

251 A beta alloforms, including those containing familial Alzheimer's disease-linked amino acid substitut

252 requirements for "replacement" we expressed familial Alzheimer's disease-linked and experimental del

253 ralleling the observation that expression of familial Alzheimer's disease-linked mutant PS1 compromis

254 Transgene expression of familial Alzheimer's disease-linked mutants of beta-amyl

255 ostasis is a common molecular consequence of familial Alzheimer's disease-linked presenilin mutations

256 this report, we examine the activity of two familial Alzheimer's disease-linked PS1 variants on the

257 esenilin 1 (Psen1(-/-) mice) or expressing a familial Alzheimer's disease-linked Psen1 mutation (Psen

258 rge family-based and case-control late-onset familial Alzheimer's disease (LOAD) samples of SOX5 vari

259 a(4)(2) accumulation in subcortical areas in familial Alzheimer's disease may be driven by APP and it

260 oidosis and improved cognitive function in a familial Alzheimer's disease mouse model.

261 overexpressing either wild-type PSEN1 or the Familial Alzheimer's disease mutant PSEN1-Delta9 (PS1-mu

262 Neuronal expression of familial Alzheimer's disease-mutant human amyloid precur

263 ta-catenin (PS1Deltacat) or by two different familial Alzheimer's disease mutants.

264 s and acceleration of disease progression in familial Alzheimer's disease mutation carriers.

265 Furthermore, we show that the PS1M146V familial Alzheimer's disease mutation exhibits a partial

266 amyloid precursor protein and had the P264L familial Alzheimer's disease mutation in presenilin-1.

267 ition in transgenic mice that coexpress five familial Alzheimer's disease mutations (5XFAD mice).

268 in mouse model that incorporates the Swedish familial Alzheimer's disease mutations and converts mous

269 Familial Alzheimer's disease mutations in APP-CTFs did n

270 Familial Alzheimer's disease mutations in the presenilin

271 mer's disease, carry the Swedish and Indiana familial Alzheimer's disease mutations of the human amyl

272 ockets to investigate the mechanism by which familial Alzheimer's disease mutations within APP increa

273 del (containing the humanized APP with three familial Alzheimer's disease mutations) and the APP(WT)

274 to residue 23 of Abeta, thus differing from familial Alzheimer's disease mutations, which occur outs

275 de (Abeta) domain and expressing the Swedish familial Alzheimer's disease mutations.

276 eta42:Abeta40 ratios shown to correlate with familial Alzheimer's disease mutations.

277 ubcortical areas, from post-mortem brains of familial Alzheimer's disease (n = 10; age at death: 50.0

278 rtue of fully penetrant genetic alterations (familial Alzheimer's disease or FAD) provide a model in

279 e subjects in our centre who have late onset familial Alzheimer's disease or mutations in presenilin

280 Relative to controls, patients with familial Alzheimer's disease performed poorly on both me

281 ippocampal and whole-brain volumes change as familial Alzheimer's disease progresses from the presymp

282 Recent advances in the genetics of familial Alzheimer's disease provide direction for thera

283 in cell lines expressing well characterized familial Alzheimer's disease PSEN1 mutations, L166P and

284 esenilin proteins, which are associated with familial Alzheimer's disease, regulate Notch signaling.

285 city and spatial memory in mice that express familial Alzheimer's disease-related mutations in APP an

286 mutant forms of presenilin-1 (PS1) found in familial Alzheimer's disease resulted in a characteristi

287 nonical full-length PSEN2 transcripts versus familial Alzheimer's disease samples and controls.

288 sAD patient exhibited the phenotypes seen in familial Alzheimer's disease samples.

289 e of mutant presenilin or betaAPP alleles in familial Alzheimer's disease subjects.

290 Enhanced aggregation in Abeta with familial Alzheimer's disease substitutions may result fr

291 roups, while 3H-PiB binding was lower in the familial Alzheimer's disease than the sporadic Alzheimer

292 me that has been extensively investigated in familial Alzheimer's disease) to have an integral role i

293 ease required both PrP(C) and Fyn, and human familial Alzheimer's disease transgene-induced convulsiv

294 A PS2 mutation associated with familial Alzheimer's disease was found to generate a mol

295 ic individuals at risk of autosomal dominant familial Alzheimer's disease was performed to assess the

296 hort-term memory binding is also impaired in familial Alzheimer's disease, whether this impairment ex

297 42/Abeta40 production ratio is a hallmark of familial Alzheimer's disease, which can be caused by mut

298 ration at the early presymptomatic stages of familial Alzheimer's disease, which supports its potenti

299 The causes of phenotypic heterogeneity in familial Alzheimer's disease with autosomal dominant inh

300 ssociated with dementia with Lewy bodies and familial Alzheimer's disease with concomitant alpha-synu