In situ hybridization analysis of presenilin 1 mRNA in Alzheimer disease and in lesioned rat brain

被引:47
作者
Page, K [1 ]
Hollister, R [1 ]
Tanzi, RE [1 ]
Hyman, BT [1 ]
机构
[1] HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GENET & AGING LAB,BOSTON,MA 02114
关键词
hippocampal formation; excitotoxic lesion;
D O I
10.1073/pnas.93.24.14020
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Presenilin-1 (PS-1) gene mutations are responsible for the majority of the early onset familial forms of Alzheimer disease (AD), Neither PS-1's anatomic distribution in brain nor expression in AD have been reported, Using in situ hybridization in the rat forebrain, we show that PS-1 mRNA expression is primarily in cortical and hippocampal neurons, with less expression in subcortical structures, In a regional pattern similar to APP695, Excitotoxic lesions lead to loss of PS-1 signal, A neuronal pattern of expression of PS-1 mRNA was also observed in the human hippocampal formation, AD and control levels did not differ, PS-1 is expressed in brain areas vulnerable to AD changes more so than in areas spared in AD; however, PS-1 expression is not sufficient to mark vulnerable regions, Collectively, these data suggest that the neuropathogenic process consequent to PS-1 mutations begins in neuronal cell populations.
引用
收藏
页码:14020 / 14024
页数:5
相关论文
共 28 条
[1]   INDUCTION OF AMYLOID PRECURSOR PROTEIN MESSENGER-RNA AFTER HEAT-SHOCK IN CULTURED HUMAN LYMPHOBLASTOID-CELLS [J].
ABE, K ;
STGEORGEHYSLOP, PH ;
TANZI, RE ;
KOGURE, K .
NEUROSCIENCE LETTERS, 1991, 125 (02) :169-171
[2]  
*ALZH DIS COLL GRO, 1995, NAT GENET, V11, P219
[3]   The Topographical and Neuroanatomical Distribution of Neurofibrillary Tangles and Neuritic Plaques in the Cerebral Cortex of Patients with Alzheimer's Disease [J].
Arnold, Steven E. ;
Hyman, Bradley T. ;
Flory, Jill ;
Damasio, Antonio R. ;
Van Hoesen, Gary W. .
CEREBRAL CORTEX, 1991, 1 (01) :103-116
[4]   NEUROFIBRILLARY TANGLES BUT NOT SENILE PLAQUES PARALLEL DURATION AND SEVERITY OF ALZHEIMERS-DISEASE [J].
ARRIAGADA, PV ;
GROWDON, JH ;
HEDLEYWHYTE, ET ;
HYMAN, BT .
NEUROLOGY, 1992, 42 (03) :631-639
[5]   INFLAMMATORY PROCESSES INDUCE BETA-AMYLOID PRECURSOR PROTEIN-CHANGES IN MOUSE-BRAIN [J].
BRUGG, B ;
DUBREUIL, YL ;
HUBER, G ;
WOLLMAN, EE ;
DELHAYEBOUCHAUD, N ;
MARIANI, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (07) :3032-3035
[6]   MUTATIONS OF THE PRESENILIN-I GENE IN FAMILIES WITH EARLY-ONSET ALZHEIMERS-DISEASE [J].
CAMPION, D ;
FLAMAN, JM ;
BRICE, A ;
HANNEQUIN, D ;
DUBOIS, B ;
MARTIN, C ;
MOREAU, V ;
CHARBONNIER, F ;
DIDIERJEAN, O ;
TARDIEU, S ;
PENET, C ;
PUEL, M ;
PASQUIER, F ;
LEDOZE, F ;
BELLIS, G ;
CALENDA, A ;
HEILIG, R ;
MARTINEZ, M ;
MALLET, J ;
BELLIS, M ;
CLERGETDARPOUX, F ;
AGID, Y ;
FREBOURG, T .
HUMAN MOLECULAR GENETICS, 1995, 4 (12) :2373-2377
[7]   MOLECULAR-GENETIC ANALYSIS OF FAMILIAL EARLY-ONSET ALZHEIMERS-DISEASE LINKED TO CHROMOSOME 14Q24.3 [J].
CRUTS, M ;
BACKHOVENS, H ;
WANG, SY ;
VANGASSEN, G ;
THEUNS, J ;
DEJONGHE, C ;
WEHNERT, A ;
DEVOECHT, J ;
DEWINTER, G ;
CRAS, P ;
BRUYLAND, M ;
DATSON, N ;
WEISSENBACH, J ;
DENDUNNEN, JT ;
MARTIN, JJ ;
HENDRIKS, L ;
Van Broeckhoven, C .
HUMAN MOLECULAR GENETICS, 1995, 4 (12) :2363-2371
[8]   SEGREGATION OF A MISSENSE MUTATION IN THE AMYLOID PRECURSOR PROTEIN GENE WITH FAMILIAL ALZHEIMERS-DISEASE [J].
GOATE, A ;
CHARTIERHARLIN, MC ;
MULLAN, M ;
BROWN, J ;
CRAWFORD, F ;
FIDANI, L ;
GIUFFRA, L ;
HAYNES, A ;
IRVING, N ;
JAMES, L ;
MANT, R ;
NEWTON, P ;
ROOKE, K ;
ROQUES, P ;
TALBOT, C ;
PERICAKVANCE, M ;
ROSES, A ;
WILLIAMSON, R ;
ROSSOR, M ;
OWEN, M ;
HARDY, J .
NATURE, 1991, 349 (6311) :704-706
[9]   ALZHEIMERS-DISEASE - CELL-SPECIFIC PATHOLOGY ISOLATES THE HIPPOCAMPAL-FORMATION [J].
HYMAN, BT ;
VANHOESEN, GW ;
DAMASIO, AR ;
BARNES, CL .
SCIENCE, 1984, 225 (4667) :1168-1170
[10]   RELATION OF NEURONAL APP-751/APP-695 MESSENGER-RNA RATIO AND NEURITIC PLAQUE DENSITY IN ALZHEIMERS-DISEASE [J].
JOHNSON, SA ;
MCNEILL, T ;
CORDELL, B ;
FINCH, CE .
SCIENCE, 1990, 248 (4957) :854-857