-
1
-
-
0030174981
-
The gene defects responsible for familial Alzheimer's disease
-
Tanzi RE, Kovacs DM, Kim T-W, Moir RD, Guenette SY, Wasco W: The gene defects responsible for familial Alzheimer's disease. Neurobiol Dis 1996, 3:159-168.
-
(1996)
Neurobiol Dis
, vol.3
, pp. 159-168
-
-
Tanzi, R.E.1
Kovacs, D.M.2
Kim, T.-W.3
Moir, R.D.4
Guenette, S.Y.5
Wasco, W.6
-
2
-
-
0029004341
-
Cloning of a novel gene bearing missense mutations in early onset familial Alzheimer disease
-
Sherrington R, Rogaev El, Liang Y, Rogaeva EA, Levesque G, Ikeda M, Chi H, Lin C, Li G, Holman K et al.: Cloning of a novel gene bearing missense mutations in early onset familial Alzheimer disease. Nature 1995, 375:754-760.
-
(1995)
Nature
, vol.375
, pp. 754-760
-
-
Sherrington, R.1
Rogaev, El.2
Liang, Y.3
Rogaeva, E.A.4
Levesque, G.5
Ikeda, M.6
Chi, H.7
Lin, C.8
Li, G.9
Holman, K.10
-
3
-
-
0029087026
-
Candidate gene for the chromosome 1 familial Alzheimer's disease locus
-
Levy-Lahad E, Wasco W, Poorkaj P, Romano DM, Oshima J, Pettingell WH, Yu CE, Jondro PD, Schmidt SD, Wang K et al.: Candidate gene for the chromosome 1 familial Alzheimer's disease locus. Science 1995, 269:973-977.
-
(1995)
Science
, vol.269
, pp. 973-977
-
-
Levy-Lahad, E.1
Wasco, W.2
Poorkaj, P.3
Romano, D.M.4
Oshima, J.5
Pettingell, W.H.6
Yu, C.E.7
Jondro, P.D.8
Schmidt, S.D.9
Wang, K.10
-
4
-
-
0029101491
-
Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene
-
Rogaev EI, Sherrington R, Rogaeva EA, Levesque G, Ikeda M, Liang Y, Chi H, Lin C, Hallman K, Tsuda T et al.: Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene. Nature 1995, 376:775-778.
-
(1995)
Nature
, vol.376
, pp. 775-778
-
-
Rogaev, E.I.1
Sherrington, R.2
Rogaeva, E.A.3
Levesque, G.4
Ikeda, M.5
Liang, Y.6
Chi, H.7
Lin, C.8
Hallman, K.9
Tsuda, T.10
-
5
-
-
0031052381
-
Amyloid, the presenilins and Alzheimer's disease
-
Hardy J: Amyloid, the presenilins and Alzheimer's disease. Trends Neurosci 1997, 20:154-159.
-
(1997)
Trends Neurosci
, vol.20
, pp. 154-159
-
-
Hardy, J.1
-
6
-
-
0030922421
-
Presenilins: Genes for life and death
-
Haass C: Presenilins: genes for life and death. Neuron 1997, 18:687-690.
-
(1997)
Neuron
, vol.18
, pp. 687-690
-
-
Haass, C.1
-
7
-
-
0001864568
-
The presenilin genes and their role in early-onset familial Alzheimer's disease
-
Tanzi RE, Kovacs DM, Kim T-W, Moir RD, Guenette SY, Wasco W: The presenilin genes and their role in early-onset familial Alzheimer's disease. Alzheimer Dis Rev 1996, 1:90-98.
-
(1996)
Alzheimer Dis Rev
, vol.1
, pp. 90-98
-
-
Tanzi, R.E.1
Kovacs, D.M.2
Kim, T.-W.3
Moir, R.D.4
Guenette, S.Y.5
Wasco, W.6
-
8
-
-
0342549411
-
Cell biology of presenilin 1
-
Thinakaran G: Cell biology of presenilin 1. Alzheimer Dis Rev 1996, 1:99-102.
-
(1996)
Alzheimer Dis Rev
, vol.1
, pp. 99-102
-
-
Thinakaran, G.1
-
9
-
-
15844425969
-
Endoproteolysis of presenilin 1 and accumulation of processed derivatives in vivo
-
Thinakaran G, Borchelt DR, Lee MK, Slunt HH, Spitzer L, Kim G, Ratovitsky T, Davenport F, Nordstedt C, Seeger M et al.: Endoproteolysis of presenilin 1 and accumulation of processed derivatives in vivo. Neuron 1996, 17:181-190. The first paper to describe the endoproteolysis and regulated accumulation of the proteolytic fragments of PS1. The authors reported the important findings that presenilin cleavage fragments may be the functional component of these proteins.
-
(1996)
Neuron
, vol.17
, pp. 181-190
-
-
Thinakaran, G.1
Borchelt, D.R.2
Lee, M.K.3
Slunt, H.H.4
Spitzer, L.5
Kim, G.6
Ratovitsky, T.7
Davenport, F.8
Nordstedt, C.9
Seeger, M.10
-
10
-
-
0030575338
-
Characterization of human presenilin 1 using N-terminal specific monoclonal antibodies: Evidence that Alzheimer mutations affect proteolytic processing
-
Mercken M, Takahashi H, Honda T, Sato K, Murayama M, Nakazato Y, Noguchi K, Imahori K, Takashima A: Characterization of human presenilin 1 using N-terminal specific monoclonal antibodies: evidence that Alzheimer mutations affect proteolytic processing. FEBS Lett 1996, 389:297-303.
-
(1996)
FEBS Lett
, vol.389
, pp. 297-303
-
-
Mercken, M.1
Takahashi, H.2
Honda, T.3
Sato, K.4
Murayama, M.5
Nakazato, Y.6
Noguchi, K.7
Imahori, K.8
Takashima, A.9
-
11
-
-
0030889220
-
Presenilin proteins undergo heterogenous endoproteolysis between Thr291 and Ala299 and occur as stable N- And C-terminal fragments in normal and Alzheimer brain tissue
-
Podlisny MB, Citron M, Amarante P, Sherrington R, Xia W, Zhang J, Diehl T, Levesque G, Fraser P, Haass C et al.: Presenilin proteins undergo heterogenous endoproteolysis between Thr291 and Ala299 and occur as stable N- and C-terminal fragments in normal and Alzheimer brain tissue. Neurobiol Dis 1997, 3:325-337.
-
(1997)
Neurobiol Dis
, vol.3
, pp. 325-337
-
-
Podlisny, M.B.1
Citron, M.2
Amarante, P.3
Sherrington, R.4
Xia, W.5
Zhang, J.6
Diehl, T.7
Levesque, G.8
Fraser, P.9
Haass, C.10
-
12
-
-
0030890399
-
Endoproteolytic processing and proteasomal degradation of presenilin 2 in transfected cells
-
Kim T-W, Pettingell WH, Hallmark OG, Moir RD, Wasco W, Tanzi RE: Endoproteolytic processing and proteasomal degradation of presenilin 2 in transfected cells. J Biol Chem 1997, 272:11006-11010. The first paper to report that PS2 undergoes endoproteolytic processing and is degraded via the ubiquitin-proteasome pathway. The authors raise the possibility that proteasomal degradation may be used to regulate the levels of full-length presenilins, thereby permitting regulated endoproteolytic cleavage.
-
(1997)
J Biol Chem
, vol.272
, pp. 11006-11010
-
-
Kim, T.-W.1
Pettingell, W.H.2
Hallmark, O.G.3
Moir, R.D.4
Wasco, W.5
Tanzi, R.E.6
-
13
-
-
0030293676
-
Familial Alzheimer's disease-linked presenilin 1 variants elevate Aβ1-42/1-40 ratio in vitro and in vivo
-
Borchelt DR, Thinakaran G, Eckman CB, Lee MK, Davenport F, Ratovitsky T, Prada C-M, Kim G, Seekins S, Yager D et al.: Familial Alzheimer's disease-linked presenilin 1 variants elevate Aβ1-42/1-40 ratio in vitro and in vivo. Neuron 1996, 17:1005-1013. One of three simultaneous reports (see [29•,30•]) demonstrating increases in the Aβ42 : Aβ40 ratio in transfected cells and transgenic mice expressing FAD mutant forms of the presenilins. The results in this paper are extremely similar and confirmatory findings to those described in [29•,30•].
-
(1996)
Neuron
, vol.17
, pp. 1005-1013
-
-
Borchelt, D.R.1
Thinakaran, G.2
Eckman, C.B.3
Lee, M.K.4
Davenport, F.5
Ratovitsky, T.6
Prada, C.-M.7
Kim, G.8
Seekins, S.9
Yager, D.10
-
14
-
-
0030868903
-
Alternative cleavage of Alzheimer-associated presenilins during apoptosis by a caspase-3 family protease
-
Kim T-W, Pettingell WH, Jung YK, Kovacs DM, Tanzi RE: Alternative cleavage of Alzheimer-associated presenilins during apoptosis by a caspase-3 family protease. Science 1997, 277:373-376. The first report showing that the presenilins undergo alternative endoproteolysis, which is mediated by an apoptosis-associated caspase-3 family protease and which is enhanced by the Asn141→lle FAD mutation. These findings suggest that the presenilins may be cell death substrates and that FAD mutations may lead to the enhanced activation of caspase-3 family proteases.
-
(1997)
Science
, vol.277
, pp. 373-376
-
-
Kim, T.-W.1
Pettingell, W.H.2
Jung, Y.K.3
Kovacs, D.M.4
Tanzi, R.E.5
-
15
-
-
12644290265
-
Evidence for phosphorylation and oligomeric assembly of presenilin 1
-
Seeger M, Nordstedt C, Petanceska S, Kovacs DM, Gouras GK, Hahne S, Fraser P, Levesque L, Czernik AJ, St George-Hyslop P et al.: Evidence for phosphorylation and oligomeric assembly of presenilin 1. Proc Natl Acad Sci USA 1997, 94:5090-5094. This report demonstrates the oligomeric association between amino- and carboxy-terminal PS1 endoproteolytic fragments and shows that the carboxyl terminus of PS1 can be phosphorylated (see also [16•]).
-
(1997)
Proc Natl Acad Sci USA
, vol.94
, pp. 5090-5094
-
-
Seeger, M.1
Nordstedt, C.2
Petanceska, S.3
Kovacs, D.M.4
Gouras, G.K.5
Hahne, S.6
Fraser, P.7
Levesque, L.8
Czernik, A.J.9
St George-Hyslop, P.10
-
16
-
-
12644264304
-
Proteolytic processing of the Alzheimer disease-associated presenilin-1 gene generates an in vivo substrate for protein kinase C
-
Walter J, Grünberg J, Capell A, Pesold B, Schindzielorz A, Citron M, Mendla K, St George-Hyslop P, Multhaup G, Selkoe DJ, Haass C: Proteolytic processing of the Alzheimer disease-associated presenilin-1 gene generates an in vivo substrate for protein kinase C. Proc Natl Acad Sci USA 1997, 94:5349-5354. This report shows that the carboxy-terminal cleavage fragments of PS1 can be phosphorylated.
-
(1997)
Proc Natl Acad Sci USA
, vol.94
, pp. 5349-5354
-
-
Walter, J.1
Grünberg, J.2
Capell, A.3
Pesold, B.4
Schindzielorz, A.5
Citron, M.6
Mendla, K.7
St George-Hyslop, P.8
Multhaup, G.9
Selkoe, D.J.10
Haass, C.11
-
17
-
-
0029116848
-
Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimer's disease gene
-
Levitan D, Greenwald I: Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimer's disease gene. Nature 1995, 377:351-354.
-
(1995)
Nature
, vol.377
, pp. 351-354
-
-
Levitan, D.1
Greenwald, I.2
-
18
-
-
0029906585
-
Assessment of normal and mutant human presenilin function in Caenorhabditis elegans
-
Levitan D, Doyle TG, Brousseau D, Lee MK, Thinakaran G, Slunt HH, Sisodia SS, Greenwald I: Assessment of normal and mutant human presenilin function in Caenorhabditis elegans. Proc Natl Acad Sci USA 1996, 93:14940-14944. One of two reports (see [19•]) showing that human presenilins can rescue the sel-12 mutant phenotype.
-
(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 14940-14944
-
-
Levitan, D.1
Doyle, T.G.2
Brousseau, D.3
Lee, M.K.4
Thinakaran, G.5
Slunt, H.H.6
Sisodia, S.S.7
Greenwald, I.8
-
19
-
-
0031108103
-
The Sel-12 mutant phenotype of C. elegans is rescued independent of proteolytic processing by Wt but not mutant presenilin
-
Baumeister R, Leimer U, Zweckbronner J, Jakubek C, Gruenberg J, Haass C: The Sel-12 mutant phenotype of C. elegans is rescued independent of proteolytic processing by Wt but not mutant presenilin. Genes Function 1997, 1:149-159. One of two reports (see also [18•]) showing that human presenilins can rescue the sel-12 mutant phenotype.
-
(1997)
Genes Function
, vol.1
, pp. 149-159
-
-
Baumeister, R.1
Leimer, U.2
Zweckbronner, J.3
Jakubek, C.4
Gruenberg, J.5
Haass, C.6
-
20
-
-
17744401440
-
Presenilin 1 is required for Notch1 and DII1 expression in the paraxial mesoderm
-
Wong P, Zheng H, Chen H, Becher MW, Sirinathsinghji DJS, Trumbauer ME, Proce DL, Van der Ploeg LHT, Sisodia SS: Presenilin 1 is required for Notch1 and DII1 expression in the paraxial mesoderm. Nature 1997, 387:288-292. One of two reports (see [21••]) that were published simultaneously describing the phenotypes of the PS1 null mice. These data further suggest a role for PS1 in the Notch developmental pathway. PS1 expression may be required during development for proper temporal expression of Notch and Delta.
-
(1997)
Nature
, vol.387
, pp. 288-292
-
-
Wong, P.1
Zheng, H.2
Chen, H.3
Becher, M.W.4
Sirinathsinghji, D.J.S.5
Trumbauer, M.E.6
Proce, D.L.7
Van Der Ploeg, L.H.T.8
Sisodia, S.S.9
-
21
-
-
0030779784
-
Skeletal and CNS defects in presenilin-1-deficient mice
-
Shen J, Bronson RT, Chen DF, Xia W, Selkoe DJ, Tonegawa S: Skeletal and CNS defects in presenilin-1-deficient mice. Cell 1997, 89:629-639. One of two reports (see [20••]) that were published simultaneously describing the phenotypes of the PS1 null mice. In this paper, additional knock-out phenotype involving neuronal loss was observed.
-
(1997)
Cell
, vol.89
, pp. 629-639
-
-
Shen, J.1
Bronson, R.T.2
Chen, D.F.3
Xia, W.4
Selkoe, D.J.5
Tonegawa, S.6
-
22
-
-
0028989016
-
Notch1 is required for the coordinate segmentation of somites
-
Conlon RA, Reaume AG, Rossant J: Notch1 is required for the coordinate segmentation of somites. Development 1995, 121:1533-1545.
-
(1995)
Development
, vol.121
, pp. 1533-1545
-
-
Conlon, R.A.1
Reaume, A.G.2
Rossant, J.3
-
23
-
-
0030976083
-
Maintenance of somite borders in mice requires the Delta homologue DII1
-
Hrabe de Angelis M, McyIntyre J II, Gossler A: Maintenance of somite borders in mice requires the Delta homologue DII1. Nature 1997, 386:717-721.
-
(1997)
Nature
, vol.386
, pp. 717-721
-
-
Hrabe De Angelis, M.1
McyIntyre J. II2
Gossler, A.3
-
24
-
-
10544229795
-
Expression of presenilin 1 and 2 (PS1 and PS2) in human and mouse tissues
-
Lee MK, Slunt HH, Martin LJ, Thinakaran G, Kim G, Gandy SE, Seeger M, Koo E, Price DL, Sisodia SS: Expression of presenilin 1 and 2 (PS1 and PS2) in human and mouse tissues. J Neurosci 1996, 16:7513-7525.
-
(1996)
J Neurosci
, vol.16
, pp. 7513-7525
-
-
Lee, M.K.1
Slunt, H.H.2
Martin, L.J.3
Thinakaran, G.4
Kim, G.5
Gandy, S.E.6
Seeger, M.7
Koo, E.8
Price, D.L.9
Sisodia, S.S.10
-
25
-
-
0030638153
-
Developmental regulation of presenilin mRNA expression parallels notch expression
-
Berezovska O, Xia M, Page K, Wasco W, Tanzi R, Hyman B: Developmental regulation of presenilin mRNA expression parallels notch expression. J Neuropath Exp Neurol 1997, 56:40-44.
-
(1997)
J Neuropath Exp Neurol
, vol.56
, pp. 40-44
-
-
Berezovska, O.1
Xia, M.2
Page, K.3
Wasco, W.4
Tanzi, R.5
Hyman, B.6
-
26
-
-
0030788767
-
Presenilin 1 interaction in the brain with a novel member of the Armadillo family
-
Zhou J, Liyanage U, Medina M, Ho C, Simmons AD, Lovett M, Kosik KS: Presenilin 1 interaction in the brain with a novel member of the Armadillo family. Neuroreport 1997, 8:1489-1494. This report shows that in the brain, PS1 interacts with δ-catenin, a putative novel mammalian homologue of the Drosophila Armadillo family, suggesting a role for PS1 in the Wingless signaling pathway.
-
(1997)
Neuroreport
, vol.8
, pp. 1489-1494
-
-
Zhou, J.1
Liyanage, U.2
Medina, M.3
Ho, C.4
Simmons, A.D.5
Lovett, M.6
Kosik, K.S.7
-
27
-
-
0029670476
-
Interaction between Wingless and Notch signaling pathways mediated by Dishevelled
-
Axelrod JD, Matsuno K, Artavanis-Tsakonas S, Perrimon N: Interaction between Wingless and Notch signaling pathways mediated by Dishevelled. Science 1996, 271:1826-1832.
-
(1996)
Science
, vol.271
, pp. 1826-1832
-
-
Axelrod, J.D.1
Matsuno, K.2
Artavanis-Tsakonas, S.3
Perrimon, N.4
-
28
-
-
16044373524
-
Aβ42(43) is increased in vivo by the PS1/2 and APP mutations linked to familial Alzheimer's disease
-
Scheuner D, Eckman C, Jensen M, Song X, Citron M, Suzuki N, Bird TD, Hardy J, Hutton M, Kukull W et al.: Aβ42(43) is increased in vivo by the PS1/2 and APP mutations linked to familial Alzheimer's disease. Nat Med 1996, 2:864-870. The first report to demonstrate increased Aβ42 in plasma and fibroblasts derived from FAD patients carrying PS1, PS2, or APP mutations. This seminar paper was the first to demonstrate a common phenotype for FAD mutations in APP and presenilins, causing a relative increase in the highly amyloidogenic peptide Aβ42.
-
(1996)
Nat Med
, vol.2
, pp. 864-870
-
-
Scheuner, D.1
Eckman, C.2
Jensen, M.3
Song, X.4
Citron, M.5
Suzuki, N.6
Bird, T.D.7
Hardy, J.8
Hutton, M.9
Kukull, W.10
-
29
-
-
16944362157
-
Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice
-
Citron M, Westaway D, Xia W, Carlson G, Diehl T, Levesque G, Johnson-Wood K, Lee M, Seubert P, Davis A, Kholodenko D et al.: Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice. Nat Med 1996, 3:67-72. One of three simultaneous reports (see [13•,30•]) demonstrating increases in the Aβ42 : Aβ40 ratio in transfected cells and transgenic mice expressing FAD mutant forms of the presenilins. The results in this paper are extremely similar and confirmatory findings to those described in [13•,30•].
-
(1996)
Nat Med
, vol.3
, pp. 67-72
-
-
Citron, M.1
Westaway, D.2
Xia, W.3
Carlson, G.4
Diehl, T.5
Levesque, G.6
Johnson-Wood, K.7
Lee, M.8
Seubert, P.9
Davis, A.10
Kholodenko, D.11
-
30
-
-
16044366039
-
Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1
-
Duff K, Eckman C, Zehr C, Yu X, Prada C-M, Perez-Tur J, Hutton M, Buee L, Harigaya Y, Yager D et al.: Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1. Nature 1996, 383:710-713. One of three simultaneous reports (see [13•,29•]) demonstrating increases in the Aβ42 : Aβ40 ratio in transfected cells and transgenic mice expressing FAD mutant forms of the presenilins. The results in this paper are extremely similar and confirmatory findings to those described in [13•,29•]. Uniquely, in this paper, increase of endogenous mouse Aβ42/Aβ40 is observed due to the expression of FAD mutant PS1 transgene.
-
(1996)
Nature
, vol.383
, pp. 710-713
-
-
Duff, K.1
Eckman, C.2
Zehr, C.3
Yu, X.4
Prada, C.-M.5
Perez-Tur, J.6
Hutton, M.7
Buee, L.8
Harigaya, Y.9
Yager, D.10
-
31
-
-
12644258498
-
The presenilin 2 mutation (N141I) linked to familial Alzheimer disease (Volga German families) increases the secretion of amyloid β protein ending at the 42nd (or 43rd) residue
-
Tomita T, Maruyama K, Saido TC, Kume H, Shinozaki K, Tokuhiro S, Capell A, Walter J, Grünberg J, Haass C et al.: The presenilin 2 mutation (N141I) linked to familial Alzheimer disease (Volga German families) increases the secretion of amyloid β protein ending at the 42nd (or 43rd) residue. Proc Natl Acad Sci USA 1997, 94:2025-2030.
-
(1997)
Proc Natl Acad Sci USA
, vol.94
, pp. 2025-2030
-
-
Tomita, T.1
Maruyama, K.2
Saido, T.C.3
Kume, H.4
Shinozaki, K.5
Tokuhiro, S.6
Capell, A.7
Walter, J.8
Grünberg, J.9
Haass, C.10
-
32
-
-
16944365745
-
Enhanced production and oligomerization of the 42-residue amyloid beta protein by Chinese hamster ovary cells stably expressing mutant presenilins
-
Xia W, Zhang J, Kholodenko D, Citron M, Podlisny MB, Teplow DB, Haass C, Seubert P, Koo EH, Selkoe DJ: Enhanced production and oligomerization of the 42-residue amyloid beta protein by Chinese hamster ovary cells stably expressing mutant presenilins. J Biol Chem 1997, 272:7977-7982.
-
(1997)
J Biol Chem
, vol.272
, pp. 7977-7982
-
-
Xia, W.1
Zhang, J.2
Kholodenko, D.3
Citron, M.4
Podlisny, M.B.5
Teplow, D.B.6
Haass, C.7
Seubert, P.8
Koo, E.H.9
Selkoe, D.J.10
-
33
-
-
16044365171
-
The E280A presenilin 1 Alzheimer mutation produces increased Aβ42 deposition and severe cerebellar pathology
-
Lemere CA, Lopera F, Kosik KS, Lendon CL, Ossa J, Saido TC, Yamaguchi H, Ruiz A, Martinez A, Madrigal L et al.: The E280A presenilin 1 Alzheimer mutation produces increased Aβ42 deposition and severe cerebellar pathology. Nat Med 1996, 2:1146-1150.
-
(1996)
Nat Med
, vol.2
, pp. 1146-1150
-
-
Lemere, C.A.1
Lopera, F.2
Kosik, K.S.3
Lendon, C.L.4
Ossa, J.5
Saido, T.C.6
Yamaguchi, H.7
Ruiz, A.8
Martinez, A.9
Madrigal, L.10
-
34
-
-
15144345926
-
Novel presenilin 1 gene mutation: Increased β-amyloid and neurofibrillary changes
-
Gomez-Isla T, Wasco W, Pettingell WP, Garubhagavatula S, Schmidt DD, Jondro PD, McNamara M, Rodes LA, DiBlasi T, Growdon WB et al.: Novel presenilin 1 gene mutation: increased β-amyloid and neurofibrillary changes. Ann Neurol 1997, 41:809-813.
-
(1997)
Ann Neurol
, vol.41
, pp. 809-813
-
-
Gomez-Isla, T.1
Wasco, W.2
Pettingell, W.P.3
Garubhagavatula, S.4
Schmidt, D.D.5
Jondro, P.D.6
McNamara, M.7
Rodes, L.A.8
Diblasi, T.9
Growdon, W.B.10
-
35
-
-
9444276544
-
Amyloid β protein (Aβ) deposition in chromosome 14-linked Alzheimer's disease: Predominance of Aβ42(43)
-
Mann DMA, Iwatsubo T, Cairns NJ, Lantos PL, Nochlin D, Sumi SM, Bird TD, Poorkaj P, Hardy J, Hutton M et al.: Amyloid β protein (Aβ) deposition in chromosome 14-linked Alzheimer's disease: predominance of Aβ42(43). Ann Neurol 1996, 40:149-156.
-
(1996)
Ann Neurol
, vol.40
, pp. 149-156
-
-
Dma, M.1
Iwatsubo, T.2
Cairns, N.J.3
Lantos, P.L.4
Nochlin, D.5
Sumi, S.M.6
Bird, T.D.7
Poorkaj, P.8
Hardy, J.9
Hutton, M.10
-
36
-
-
0030614569
-
Amyloid (Aβ) deposition in chromosome 1-linked Alzheimer's disease: The Volga German families
-
Mann DMA, Iwatsubo T, Nochlin D, Sumi SM, Levy-Lahad E, Bird TD: Amyloid (Aβ) deposition in chromosome 1-linked Alzheimer's disease: the Volga German families. Ann Neurol 1997, 41:52-57.
-
(1997)
Ann Neurol
, vol.41
, pp. 52-57
-
-
Mann, D.M.A.1
Iwatsubo, T.2
Nochlin, D.3
Sumi, S.M.4
Levy-Lahad, E.5
Bird, T.D.6
-
37
-
-
0031054505
-
Formation of stable complexes between two Alzheimer's disease gene products: Presenilin-2 and β-amyloid precursor protein
-
Weidemann A, Paliga K, Dürrwang U, Czech C, Evin G, Masters CL, Beyreuther K: Formation of stable complexes between two Alzheimer's disease gene products: presenilin-2 and β-amyloid precursor protein. Nat Med 1997, 3:328-332.
-
(1997)
Nat Med
, vol.3
, pp. 328-332
-
-
Weidemann, A.1
Paliga, K.2
Dürrwang, U.3
Czech, C.4
Evin, G.5
Masters, C.L.6
Beyreuther, K.7
-
38
-
-
0030753089
-
In vivo interaction between amyloid precursor protein and presenilins in mammalian cells: Implication for the pathogenesis of Alzheimer's disease
-
Xia W, Zhang J, Koo EH, Selkoe DJ: In vivo interaction between amyloid precursor protein and presenilins in mammalian cells: implication for the pathogenesis of Alzheimer's disease. Proc Natl Acad Sci USA 1997, 94:8208-8213.
-
(1997)
Proc Natl Acad Sci USA
, vol.94
, pp. 8208-8213
-
-
Xia, W.1
Zhang, J.2
Koo, E.H.3
Selkoe, D.J.4
-
39
-
-
0030293854
-
Protein topology of presenilin 1
-
Doan A, Thinakaran G, Borchelt DR, Slunt HH, Ratovitsky T, Podlisny M, Selkoe DJ, Seeger M, Gandy SE, Price DL, Sisodia SS: Protein topology of presenilin 1. Neuron 1996, 17:1023-1030. The first study to describe the topology of PS1 and to show that the amino terminus, large hydrophilic loop, and carboxyl terminus are all cytoplasmic.
-
(1996)
Neuron
, vol.17
, pp. 1023-1030
-
-
Doan, A.1
Thinakaran, G.2
Borchelt, D.R.3
Slunt, H.H.4
Ratovitsky, T.5
Podlisny, M.6
Selkoe, D.J.7
Seeger, M.8
Gandy, S.E.9
Price, D.L.10
Sisodia, S.S.11
-
40
-
-
0030922146
-
Evidence for a six-transmembrane domain structure of presenilin 1
-
Lehmann S, Chiesa R, Harris DA: Evidence for a six-transmembrane domain structure of presenilin 1. J Biol Chem 1997, 272:12047-12051.
-
(1997)
J Biol Chem
, vol.272
, pp. 12047-12051
-
-
Lehmann, S.1
Chiesa, R.2
Harris, D.A.3
-
41
-
-
0030952217
-
Intracellular generation and accumulation of amyloid β-peptide terminating at amino acid 42
-
Wild-Bode C, Yamazaki T, Capell A, Leimer U, Steiner H, Ihara Y, Haass C: Intracellular generation and accumulation of amyloid β-peptide terminating at amino acid 42. J Biol Chem 1997, 272:16085-16088. This report demonstrates that Aβ42 is generated primarily in the endoplasmic reticulum. The generation of intracellular Aβ could be an initial step in AD neuropathogenesis.
-
(1997)
J Biol Chem
, vol.272
, pp. 16085-16088
-
-
Wild-Bode, C.1
Yamazaki, T.2
Capell, A.3
Leimer, U.4
Steiner, H.5
Ihara, Y.6
Haass, C.7
-
42
-
-
0030769092
-
Alzheimer's Aβ(1-42) is generated in the endoplasmic reticulum/intermediate compartment of NT2N cells
-
Cook DG, Forman MS, Sung JC, Leight S, Kolson DL, Iwatsubo T, Lee VM-Y, Doms RW: Alzheimer's Aβ(1-42) is generated in the endoplasmic reticulum/intermediate compartment of NT2N cells. Nat Med 1997, 3:1021-1023. This paper definitely shows that Aβ42, primary component of senile plaques in AD, can be generated in the endoplasmic reticulum, suggesting that this may be the initial site of AD pathogenesis. See also annotation [43••].
-
(1997)
Nat Med
, vol.3
, pp. 1021-1023
-
-
Cook, D.G.1
Forman, M.S.2
Sung, J.C.3
Leight, S.4
Kolson, D.L.5
Iwatsubo, T.6
Lee, V.M.-Y.7
Doms, R.W.8
-
43
-
-
0030769091
-
Distinct sites of intracellular production of Alzheimer's disease Aβ40/42 amyloid peptides
-
Hartmann T, Bieger SC, Brühl B, Tienari PJ, Ida N, Allsop D, Roberts GW, Masters CL, Dotti CG, Unsicker K, Beyreuther K: Distinct sites of intracellular production of Alzheimer's disease Aβ40/42 amyloid peptides. Nat Med 1997, 3:1016-1020. This is the first report to show that while Aβ42 is mainly localized in the endoplasmic reticulum, Aβ40 is present in the Golgi and cell surface. Along with other reports [41••,42••], these data point to the endoplasmic reticulum as an initial cellular compartment of AD neuropathogenesis.
-
(1997)
Nat Med
, vol.3
, pp. 1016-1020
-
-
Hartmann, T.1
Bieger, S.C.2
Brühl, B.3
Tienari, P.J.4
Ida, N.5
Allsop, D.6
Roberts, G.W.7
Masters, C.L.8
Dotti, C.G.9
Unsicker, K.10
Beyreuther, K.11
-
44
-
-
0029784838
-
Amyloid β-protein and the genetics of Alzheimer's disease
-
Selkoe DJ: Amyloid β-protein and the genetics of Alzheimer's disease. J Biol Chem 1996, 271:18295-18298.
-
(1996)
J Biol Chem
, vol.271
, pp. 18295-18298
-
-
Selkoe, D.J.1
-
45
-
-
13344282063
-
Alzheimer associated presenilins 1 and 2: Neuronal expression in brain and localization to intracellular membranes in mammalian cells
-
Kovacs DM, Fausett HJ, Page KJ, Kim T-W, Moir RD, Merriam DE, Hollister RD, Hallmark OG, Mancini R, Felsenstein KM et al.: Alzheimer associated presenilins 1 and 2: neuronal expression in brain and localization to intracellular membranes in mammalian cells. Nat Med 1996, 2:224-229. The first report to demonstrate the predominant neuronal expression of the presenilins in brain and their subcellular localization in the endoplasmic reticulum and Golgi of mammalian cells.
-
(1996)
Nat Med
, vol.2
, pp. 224-229
-
-
Kovacs, D.M.1
Fausett, H.J.2
Page, K.J.3
Kim, T.-W.4
Moir, R.D.5
Merriam, D.E.6
Hollister, R.D.7
Hallmark, O.G.8
Mancini, R.9
Felsenstein, K.M.10
-
46
-
-
8044231311
-
The Alzheimer's disease-associated presenilins are differentially phosphorylated proteins located predominantly within the endoplasmic reticulum
-
Walter J, Capell A, Grünberg J, Pesold B, Schindzielorz A, Prior R, Podlisny MB, Fraser P, St George Hyslop P, Selkoe DJ, Haass C: The Alzheimer's disease-associated presenilins are differentially phosphorylated proteins located predominantly within the endoplasmic reticulum. Mol Med 1997, 2:673-691.
-
(1997)
Mol Med
, vol.2
, pp. 673-691
-
-
Walter, J.1
Capell, A.2
Grünberg, J.3
Pesold, B.4
Schindzielorz, A.5
Prior, R.6
Podlisny, M.B.7
Fraser, P.8
St George Hyslop, P.9
Selkoe, D.J.10
Haass, C.11
-
47
-
-
0029812077
-
Expression and analysis of presenilin 1 in a human neuronal system: Localization in cell bodies and dendrites
-
Cook DG, Sung JC, Golde TE, Felsenstein KM, Wojczk BS, Tanzi RE, Trojanowski JQ, Lee VM-Y, Doms RW: Expression and analysis of presenilin 1 in a human neuronal system: localization in cell bodies and dendrites. Proc Natl Acad Sci USA 1996, 93:9223-9228.
-
(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 9223-9228
-
-
Cook, D.G.1
Sung, J.C.2
Golde, T.E.3
Felsenstein, K.M.4
Wojczk, B.S.5
Tanzi, R.E.6
Trojanowski, J.Q.7
Lee, V.M.-Y.8
Doms, R.W.9
-
48
-
-
15444341611
-
Phosphorylation, subcellular localization, and membrane orientation of the Alzheimer's disease-associated presenilins
-
Strooper BD, Beullens M, Contreras B, Levesque L, Craessaerts K, Cordell B, Moechars D, Bollen M, Fraser P, St George-Hyslop P, Van Leuven F: Phosphorylation, subcellular localization, and membrane orientation of the Alzheimer's disease-associated presenilins. J Biol Chem 1997, 272:3590-3598.
-
(1997)
J Biol Chem
, vol.272
, pp. 3590-3598
-
-
Strooper, B.D.1
Beullens, M.2
Contreras, B.3
Levesque, L.4
Craessaerts, K.5
Cordell, B.6
Moechars, D.7
Bollen, M.8
Fraser, P.9
St George-Hyslop, P.10
Van Leuven, F.11
-
49
-
-
0028577208
-
Immunohistochemical evidence for apoptosis in Alzheimer's disease
-
Su J, Anderson A, Cummings B, Cotman C: Immunohistochemical evidence for apoptosis in Alzheimer's disease. Neuroreport 1994, 5:2529-2533.
-
(1994)
Neuroreport
, vol.5
, pp. 2529-2533
-
-
Su, J.1
Anderson, A.2
Cummings, B.3
Cotman, C.4
-
50
-
-
0028019105
-
Possible role of neuronal apoptosis in Alzheimer's disease
-
Johnson EM: Possible role of neuronal apoptosis in Alzheimer's disease. Neurobiol Aging 1994, 15:5187-5189.
-
(1994)
Neurobiol Aging
, vol.15
, pp. 5187-5189
-
-
Johnson, E.M.1
-
51
-
-
0029245289
-
A potential role for apoptosis in neurodegeneration and Alzheimer's disease
-
Cotman CW, Anderson AJ: A potential role for apoptosis in neurodegeneration and Alzheimer's disease. Mol Neurobiol 1995, 10:19-45.
-
(1995)
Mol Neurobiol
, vol.10
, pp. 19-45
-
-
Cotman, C.W.1
Anderson, A.J.2
-
52
-
-
0001796872
-
Apoptosis and Alzheimer's disease
-
Edited by Wasco W, Tanzi RE. Totowa, New Jersey: Humana Press
-
LeBlanc A: Apoptosis and Alzheimer's disease. In Molecular Mechanism of Dementia. Edited by Wasco W, Tanzi RE. Totowa, New Jersey: Humana Press; 1996:57-71.
-
(1996)
Molecular Mechanism of Dementia
, pp. 57-71
-
-
LeBlanc, A.1
-
53
-
-
0029671219
-
2+-binding protein ALG-2 and Alzheimer's disease gene ALG-3
-
2+-binding protein ALG-2 and Alzheimer's disease gene ALG-3. Science 1996, 271:521-524.
-
(1996)
Science
, vol.271
, pp. 521-524
-
-
Vito, P.1
Lancana, E.2
D'Adamio, L.3
-
54
-
-
10544224542
-
PS2 participates in cellular apoptosis: Constitutive activity conferred by Alzheimer mutation
-
Wolozin B, Iwasaki K, Vito P, Ganjei K, Lacana E, Sunderland T, Zhao B, Kusiak JW, Wasco W, D'Adamio L: PS2 participates in cellular apoptosis: constitutive activity conferred by Alzheimer mutation. Science 1996, 274:1710-1713.
-
(1996)
Science
, vol.274
, pp. 1710-1713
-
-
Wolozin, B.1
Iwasaki, K.2
Vito, P.3
Ganjei, K.4
Lacana, E.5
Sunderland, T.6
Zhao, B.7
Kusiak, J.W.8
Wasco, W.9
D'Adamio, L.10
-
55
-
-
0030580281
-
Alzheimer-associated presenilin-2 confers increased sensitivity to apoptosis in PC12 cells
-
Deng G, Pike CJ, Cotman CW: Alzheimer-associated presenilin-2 confers increased sensitivity to apoptosis in PC12 cells. FEBS Lett 1996, 397:50-54.
-
(1996)
FEBS Lett
, vol.397
, pp. 50-54
-
-
Deng, G.1
Pike, C.J.2
Cotman, C.W.3
-
56
-
-
0030891662
-
Alzheimer's PS-1 mutation perturbs calcium homeostasis and sensitizes PC12 cells to death induced by amyloid β-peptide
-
Guo Q, Furukawa K, Sopher BL, Pham DG, Xie J, Robinson N, Martin GM, Mattson MP: Alzheimer's PS-1 mutation perturbs calcium homeostasis and sensitizes PC12 cells to death induced by amyloid β-peptide. Neuroreport 1996, 8:379-383.
-
(1996)
Neuroreport
, vol.8
, pp. 379-383
-
-
Guo, Q.1
Furukawa, K.2
Sopher, B.L.3
Pham, D.G.4
Xie, J.5
Robinson, N.6
Martin, G.M.7
Mattson, M.P.8
-
57
-
-
9344227302
-
Cleavage of huntingtin by apopain, proapoptotic cysteine protease, is modulated by the polyglutamine tract
-
Goldberg YP, Nicholson DW, Rasper DM, Kalchman MA, Koide HB, Graham RK, Bromm M, Kazemi-Esfarjani P, Thornberry NA, Vailancourt JP, Hyden MR: Cleavage of huntingtin by apopain, proapoptotic cysteine protease, is modulated by the polyglutamine tract. Nat Genet 1996, 13:442-449.
-
(1996)
Nat Genet
, vol.13
, pp. 442-449
-
-
Goldberg, Y.P.1
Nicholson, D.W.2
Rasper, D.M.3
Ma, K.4
Koide, H.B.5
Graham, R.K.6
Bromm, M.7
Kazemi-Esfarjani, P.8
Thornberry, N.A.9
Vailancourt, J.P.10
Hyden, M.R.11
-
58
-
-
0029554875
-
A mutation in Alzheimer's disease destroying a splice acceptor site in the presenilin-1 gene
-
Perez-Tur J, Froelich S, Prihar G, Crook R, Baker M, Duff K, Wragg M, Busfield F, Lendon C, Clark RF et al.: A mutation in Alzheimer's disease destroying a splice acceptor site in the presenilin-1 gene. Neuroreport 1996, 7:297-301.
-
(1996)
Neuroreport
, vol.7
, pp. 297-301
-
-
Perez-Tur, J.1
Froelich, S.2
Prihar, G.3
Crook, R.4
Baker, M.5
Duff, K.6
Wragg, M.7
Busfield, F.8
Lendon, C.9
Clark, R.F.10
-
59
-
-
0031004532
-
Developmental regulation of presenilin-1 processing in the brain suggests a role in neuronal differentiation
-
Hartmann H, Busciglio J, Baumann K-H, Staufenbiel M, Yankner BA: Developmental regulation of presenilin-1 processing in the brain suggests a role in neuronal differentiation. J Biol Chem 1997, 272:14505-14508.
-
(1997)
J Biol Chem
, vol.272
, pp. 14505-14508
-
-
Hartmann, H.1
Busciglio, J.2
Baumann, K.-H.3
Staufenbiel, M.4
Yankner, B.A.5
-
60
-
-
0030657665
-
Cellular expression and proteolytic processing of presenilin proteins is developmentally regulated during neuronal differentiation
-
in press
-
Capell A, Saffrich R, Olivo J-C, Meyn L, Walter J, Grünberg J, Dotti C, Haass C: Cellular expression and proteolytic processing of presenilin proteins is developmentally regulated during neuronal differentiation. J Neurochem 1997, in press.
-
(1997)
J Neurochem
-
-
Capell, A.1
Saffrich, R.2
Olivo, J.-C.3
Meyn, L.4
Walter, J.5
Grünberg, J.6
Dotti, C.7
Haass, C.8
|