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Effect of aluminium on expression and processing of amyloid precursor protein
Author(s) -
Neill D.,
Leake A.,
Hughes D.,
Keith A.B.,
Taylor G.A.,
Allsop D.,
Rima B.K.,
Morris C.,
Candy J.M.,
Edwardson J.A.
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19961115)46:4<395::aid-jnr1>3.0.co;2-b
Subject(s) - aluminium , amyloid precursor protein , chemistry , messenger rna , β amyloid , microbiology and biotechnology , biochemistry , biophysics , biology , alzheimer's disease , medicine , gene , disease , organic chemistry
The environmental agent aluminium has been extensively investigated for a potential role in the aetiology of Alzheimer's disease. Despite many investigations there is at present no definite proof for any involvement. If aluminium is involved it is possible that its action is mediated through interaction with the synthesis or processing of amyloid precursor protein (APP). The present study compared aluminium loaded IMR‐32 neuroblastoma cells and rat brains with control cells and brains to determine if aluminium affected APP expression and/or processing. In the IMR‐32 model system aluminium had no effect on steady‐state APP mRNA levels or on the ratio of individual isoforms. It also had no quantitative or qualitative effect on APP‐immunoreactive bands detected in protein extracts from conditioned medium of these cells. In total cell extracts, aluminium reduced the intensity of APP‐immunoreactive bands between 120–105 kDa but had no effect on a 9 kDa band. In rat brains, aluminium had no effect on APP‐immunoreactive bands from soluble or insoluble‐membranous extracts. The results, in general, provide no evidence for any effect of aluminium on APP expression or processing. © 1996 Wiley‐Liss, Inc.