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Expression of APP pathway mRNAs and proteins in Alzheimer’s disease

Matsui, Toshifumi, Ingelsson, Martin, Fukumoto, Hiroaki, Ramasamy, Karunya, Kowa, Hisatomo, Frosch, Matthew P., Irizarry, Michael C., Hyman, Bradley T.·2007·Brain Research

Abstract

In both trisomy 21 and rare cases of triplication of amyloid precursor protein (APP) Alzheimer's disease (AD) pathological changes are believed to be secondary to increased expression of APP. We hypothesized that sporadic AD may also be associated with changes in transcription of APP or its metabolic partners. To address this issue, temporal neocortex of 27 AD and 21 non-demented control brains was examined to assess mRNA levels of APP isoforms (total APP, APP containing the Kunitz protease inhibitor domain [APP-KPI] and APP770) and APP metabolic enzymatic partners (the APP cleaving enzymes beta-secretase [BACE] and presenilin-1 [PS-1], and putative clearance molecules, low-density lipoprotein receptor protein [LRP] and apolipoprotein E [apoE]). Furthermore, we evaluated how changes in APP at the mRNA level affect the amount of Tris buffer extractable APP protein and Abeta40 and 42 peptides in AD and control brains. As assessed by quantitative PCR, APP-KPI (p=0.007), APP770 (p=0.004), PS-1 (p=0.004), LRP (p=0.003), apoE (p=0.0002) and GFAP (p<0.0001) mRNA levels all increased in AD, and there was a shift from APP695 (a neuronal isoform) towards KPI containing isoforms that are present in glia as well. APP-KPI mRNA levels correlated with soluble APPalpha-KPI protein (sAPPalpha-KPI) levels measured by ELISA (tau=0.33, p=0.015 by Kendall's rank correlation); in turn, soluble APPalpha-KPI protein levels positively correlated with Tris-extractable, soluble Abeta40 (p=0.046) and 42…

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Research works printed but not linked: 42

  1. Aldea, 2002, Rapid detection of herpes simplex virus DNA in genital ulcers by real-time PCR using SYBR green I dye as the detection signal, J. Clin. Microbiol., 40, 1060, 10.1128/JCM.40.3.1060-1062.2002 · DOI
  2. Altschul, 1990, Basic local alignment search tool, J. Mol. Biol., 215, 403, 10.1016/S0022-2836(05)80360-2 · DOI · Paper page
  3. Arelin, 2002, LRP and senile plaques in Alzheimer’s disease: colocalization with apolipoprotein E and with activated astrocytes, Brain Res. Mol. Brain Res., 104, 38, 10.1016/S0169-328X(02)00203-6 · DOI
  4. Blacker, 1998, The genetics of Alzheimer disease: current status and future prospects, Arch. Neurol., 55, 294, 10.1001/archneur.55.3.294 · DOI
  5. Braak, 1991, Demonstration of amyloid deposits and neurofibrillary changes in whole brain sections, Brain Pathol., 1, 213, 10.1111/j.1750-3639.1991.tb00661.x · DOI · Paper page
  6. Cataldo, 2000, Endocytic pathway abnormalities precede amyloid beta deposition in sporadic Alzheimer’s disease and Down syndrome: differential effects of APOE genotype and presenilin mutations, Am. J. Pathol., 157, 277, 10.1016/S0002-9440(10)64538-5 · DOI · Paper page
  7. Fink, 1998, Real-time quantitative RT-PCR after laser-assisted cell picking, Nat. Med., 4, 1329, 10.1038/3327 · DOI
  8. Fukumoto, 1999, Primary cultures of neuronal and non-neuronal rat brain cells secrete similar proportions of amyloid beta peptides ending at A beta40 and A beta42, NeuroReport, 10, 2965, 10.1097/00001756-199909290-00017 · DOI
  9. Giulian, 1996, Specific domains of beta-amyloid from Alzheimer plaque elicit neuron killing in human microglia, J. Neurosci., 16, 6021, 10.1523/JNEUROSCI.16-19-06021.1996 · DOI
  10. Gutala, 2004, The use of real-time PCR analysis in a gene expression study of Alzheimer’s disease post-mortem brains, J. Neurosci. Methods, 132, 101, 10.1016/j.jneumeth.2003.09.005 · DOI
  11. Harrison, 1996, Amyloid precursor protein mRNAs in Alzheimer’s disease, Neurodegeneration, 5, 409, 10.1006/neur.1996.0055 · DOI
  12. Huse, 2000, Maturation and endosomal targeting of beta-site amyloid precursor protein-cleaving enzyme. The Alzheimer’s disease beta-secretase, J. Biol. Chem., 275, 33729, 10.1074/jbc.M004175200 · DOI · Paper page
  13. Ingelsson, 2004, Early Abeta accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain, Neurology, 62, 925, 10.1212/01.WNL.0000115115.98960.37 · DOI · Paper page
  14. Ingelsson, 2006, No alteration in tau exon 10 alternative splicing in tangle-bearing neurons of the Alzheimer’s disease brain, Acta Neuropathol. (Berl.), 112, 439, 10.1007/s00401-006-0095-3 · DOI
  15. Iwata, 2000, Identification of the major Abeta1-42-degrading catabolic pathway in brain parenchyma: suppression leads to biochemical and pathological deposition, Nat. Med., 6, 143, 10.1038/77399 · DOI
  16. Iwata, 2001, Metabolic regulation of brain Abeta by neprilysin, Science, 292, 1550, 10.1126/science.1059946 · DOI
  17. Jacobsen, 1991, Quantitative measurement of alternatively spliced amyloid precursor protein mRNA expression in Alzheimer’s disease and normal brain by S1 nuclease protection analysis, Neurobiol. Aging, 12, 585, 10.1016/0197-4580(91)90090-7 · DOI
  18. Johnston, 1996, Quantification of APP and APLP2 mRNA in APOE genotyped Alzheimer’s disease brains, Brain Res. Mol. Brain Res., 43, 85, 10.1016/S0169-328X(96)00161-1 · DOI
  19. Kim, 2000, Neuroendocrine-specific protein C, a marker of neuronal differentiation, is reduced in brain of patients with Down syndrome and Alzheimer’s disease, Biochem. Biophys. Res. Commun., 276, 329, 10.1006/bbrc.2000.3464 · DOI
  20. Kinoshita, 2001, Demonstration by fluorescence resonance energy transfer of two sites of interaction between the low-density lipoprotein receptor-related protein and the amyloid precursor protein: role of the intracellular adapter protein Fe65, J. Neurosci., 21, 8354, 10.1523/JNEUROSCI.21-21-08354.2001 · DOI · Paper page
  21. Koo, 1994, Evidence that production and release of amyloid beta-protein involves the endocytic pathway, J. Biol. Chem., 269, 17386, 10.1016/S0021-9258(17)32449-3 · DOI · Paper page
  22. Lopes, 1994, Expression of alpha 2-macroglobulin receptor/low density lipoprotein receptor-related protein is increased in reactive and neoplastic glial cells, FEBS Lett., 338, 301, 10.1016/0014-5793(94)80288-2 · DOI · Paper page
  23. Matsui, 2006, Coodinated expression of caspase 8, 3 and 7 mRNA in temporal cortex of Alzheimer Disease: relationship to formic acid extractable Ab42 levels, J. Neuropathol. Exp. Neurol., 65, 508, 10.1097/01.jnen.0000229238.05748.12 · DOI
  24. Miller, 1988, A simple salting out procedure for extracting DNA from human nucleated cells, Nucleic Acids Res., 16, 1215, 10.1093/nar/16.3.1215 · DOI
  25. Mirra, 1991, The Consortium to Establish a Registry for Alzheimer’s Disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer’s disease, Neurology, 41, 479, 10.1212/WNL.41.4.479 · DOI · Paper page
  26. Moir, 1998, Relative increase in Alzheimer’s disease of soluble forms of cerebral Abeta amyloid protein precursor containing the Kunitz protease inhibitory domain, J. Biol. Chem., 273, 5013, 10.1074/jbc.273.9.5013 · DOI
  27. Preece, 2004, Amyloid precursor protein mRNA levels in Alzheimer’s disease brain, Brain Res. Mol. Brain Res., 122, 1, 10.1016/j.molbrainres.2003.08.022 · DOI
  28. Rebeck, 1993, Apolipoprotein E in sporadic Alzheimer’s disease: allelic variation and receptor interactions, Neuron, 11, 575, 10.1016/0896-6273(93)90070-8 · DOI · Paper page
  29. Rovelet-Lecrux, 2006, APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy, Nat. Genet., 38, 24, 10.1038/ng1718 · DOI
  30. Rumble, 1989, Amyloid A4 protein and its precursor in Down’s syndrome and Alzheimer’s disease, N. Engl. J. Med., 320, 1446, 10.1056/NEJM198906013202203 · DOI
  31. Selkoe, 1999, Translating cell biology into therapeutic advances in Alzheimer’s disease, Nature, 399, A23, 10.1038/399a023 · DOI · Paper page
  32. Selkoe, 2001, Presenilin, Notch, and the genesis and treatment of Alzheimer’s disease, Proc. Natl. Acad. Sci. U. S. A., 98, 11039, 10.1073/pnas.211352598 · DOI
  33. Sinha, 1999, Purification and cloning of amyloid precursor protein beta-secretase from human brain, Nature, 402, 537, 10.1038/990114 · DOI · Paper page
  34. Sola, 1993, Increased levels of the Kunitz protease inhibitor-containing beta APP mRNAs in rat brain following neurotoxic damage, Brain Res. Mol. Brain Res., 17, 41, 10.1016/0169-328X(93)90071-V · DOI
  35. Soriano, 1999, Expression of beta-amyloid precursor protein-CD3gamma chimeras to demonstrate the selective generation of amyloid beta(1–40) and amyloid beta(1–42) peptides within secretory and endocytic compartments, J. Biol. Chem., 274, 32295, 10.1074/jbc.274.45.32295 · DOI
  36. Strittmatter, 1993, Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease, Proc. Natl. Acad. Sci. U. S. A., 90, 1977, 10.1073/pnas.90.5.1977 · DOI · Paper page
  37. Suzuki, 1994, High expression on Kunitz-type protease inhibitor-containing substances in the cerebral vessels of patients with Down syndrome, Tohoku J. Exp. Med., 174, 181, 10.1620/tjem.174.181 · DOI
  38. Theuns, 2006, Promoter mutations that increase amyloid precursor–protein expression are associated with Alzheimer disease, Am. J. Hum. Genet., 78, 936, 10.1086/504044 · DOI
  39. Van Uden, 2000, LDL receptor-related protein (LRP) in Alzheimer’s disease: towards a unified theory of pathogenesis, Microsc. Res. Tech., 50, 268, 10.1002/1097-0029(20000815)50:4<268::AID-JEMT3>3.0.CO;2-1 · DOI
  40. Van Uden, 2000, A protective role of the low density lipoprotein receptor-related protein against amyloid beta-protein toxicity, J. Biol. Chem., 275, 30525, 10.1074/jbc.M001151200 · DOI · Paper page
  41. Wenham, 1991, Apolipoprotein E genotyping by one-stage PCR, Lancet, 337, 1158, 10.1016/0140-6736(91)92823-K · DOI
  42. Zhan, 1995, APP with Kunitz type protease inhibitor domain (KPI) correlates with neuritic plaque density but not with cortical synaptophysin immunoreactivity in Alzheimer’s disease and non-demented aged subjects: a multifactorial analysis, Clin. Neuropathol., 14, 142

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Metadata

Authors
Matsui, T., Ingelsson, M., Fukumoto, H., Ramasamy, K., Kowa, H., Frosch, M. P., Irizarry, M. C., & Hyman, B. T.
Venue
Brain Research
Publisher
Elsevier BV
Published
2007-08
Volume
1161
Pages
116-123
ISSN
0006-8993
Cited by
162
References
4
Language
en

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