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A broader horizon of Alzheimer pathogenesis: ALZAS — an early serum biomarker?

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Ageing and Dementia Current and Future Concepts

Part of the book series: Journal of Neural Transmission. Supplementa ((NEURAL SUPPL,volume 62))

Abstract

Recently, a novel risk gene protein expressed in elderly patientswith the diagnosis of Alzheimer disease (AD) was discovered on chromosome 21 within the APP (amyloid precursor protein) region. This 79 amino acidprotein, ALZAS (Alzheimer Associated Protein) contains the β-amyloid peptide 1–42 fragment, the APP transmembrane signal, and a unique 12 aminoacid c-terminal which is not present in any known allele of the APP gene.Reverse transcription-peR revealed that the transcript of ALZAS was ex-pressed in cortical and hippocampal regions of human Alzheimer diseasebrain as well as in leukocytes derived from AD patients. Most specifically, anendogenous antibody was found in patients with confirmed AD, in patientswith depression, and in subjects suggested to have presymptomatic AD,where it was directed against epitopes within the intron encoded amino acidc-terminal sequence.

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References

  • Bullido M, Munoz-Fernandez MA, Recuero M, Fresno M, Valdivieso F (1996)Alzheimer’s amyloid precursor pprotein is expressed on the surface of hematopoieticcells upon activation. Biochim Biophys Acta 1313: 54–62

    Google Scholar 

  • Butterfield DA, Drake J, Pocernich C, Castegna A (2001) Evidence of oxidative damagein Alzheimer’s disease brain: central role for amyloid ~-peptide. TIMM 7: 548–554

    CAS  Google Scholar 

  • Evenhuis HM (1997) The natural history of dementia in ageing people with intellectualdisability. J Intellect Disabil Res 41: 92–96

    Article  PubMed  Google Scholar 

  • Geerlings MI, Schoevers RA, Beekman AT, Jonker C, Deeg DJ, Schmand B, Ader HJ,Bouter LM, Van Tilburg W (2000) Depression and risk of cognitive decline andAlzheimer’s disease. Results of two prospective community-based studies in TheNetherlands. Br J Psychiatry 176: 568–75

    CAS  Google Scholar 

  • Ikin A.F., Annaert W.G., Takei K, De Camilli P, Jahn R, Greengard P, Buxbaum J.D (1996)Alzheimer amyloid protein precursor is localizsed in nerve terminal preparations toRab5-containing vesicular organelles distinct from those implicated in the synapticvesicle pathway. J Bioi Chem 271: 31783–31786

    Google Scholar 

  • Jellinger KA, Rosier N (2000) Neuropathology and biological markers of degenerativedementias. Internist 41: 524–537

    Article  CAS  PubMed  Google Scholar 

  • Kokmen E, Beard C.M., Chandra V., Offord K.P., Schoenberg B.S., Ballard D.J. (1991)Clinical risk factors for Alzheimer’s diseasee: a population-based case-control study.Neurology 41: 1393–1397

    Article  CAS  PubMed  Google Scholar 

  • Koudinov A, Matsubara E, Frangione B, Ghiso J (1994) The soluble form ofAlzheimer’samyloid beta protein is complexed to high density lipoprotein 3 and very high densitylipoprotein in normal human plasma. Biochem Biophys Res Commun 205: 1164–1171

    Article  CAS  PubMed  Google Scholar 

  • Li QX, Fuller StJ. Beyreuther K, Masters CL (1999) The amyloid precursor protein ofAlzheimer disease in human brain and blood. J Leuk Bio 66: 567–574

    Google Scholar 

  • Lin H, Bhatia R, Lal R (2001) Amyloid beta protein forms ion channels: implications forAlzheimer’s disease pathology. FASEB J 15: 2433–2444

    Article  CAS  PubMed  Google Scholar 

  • McGeer PI, McGeer EG, Yasojima K (2000) Alzheimer disease and neuroinflammation.J Neural Transm [Suppl] 59: 53–57

    CAS  Google Scholar 

  • Mirra SS, Hart MN, Terry RD (1993) Making the diagnosis of Alzheimer’s disease. Aprimer for practicing pathologists.Arch Pathol Lab Med 117: 132–144

    CAS  PubMed  Google Scholar 

  • Parvathy S., Davies P., Haroutunian V., Purohit DP, Davis K.L., Mohs R.C., Park H,Moran TM,Chan J.Y., Buxbaum J.D. (2001) Correlation between Ax-40-, Ah-42 andA~x,43-containing amyloid plaques and cognitive decline. Arch Neurol58: 2025–3230

    Google Scholar 

  • Pimplikar S.W.(2002) A~PP, apoptosis and Alzheimer’s disease. J Alzheimer Dis 4: 39–40

    Google Scholar 

  • Qiu W.Q., Ferreira A, Miller C, Koo EH, Selkoe DJ (1995) Cell-surface~-amyloid precur-sor protein stimulates neurite outgrowth of hippocampal neurons in an isoform-dependent manner. J Neurosci 15: 2157–2167

    Google Scholar 

  • Rhee SK, Quist AP, Lal R (1998) Amyloid beta protein-(1–42) forms calcium-permeable,Zn2+-sensitive channel. J Bioi Chern 273: 13379–13382

    Article  CAS  Google Scholar 

  • Saunders AM (2000) Apolipoprotein E and Alzheimer disease: an update on genetic andfunctional analyses. J Neuropathol Exp Neurol59: 751–758

    Google Scholar 

  • Selkoe DJ (2000) The genetics and molecular pathology of Alzheimer’s disease: roles ofamyloid and the presenilins. Neurol Clin 18: 903–922

    Article  CAS  PubMed  Google Scholar 

  • Selkoe DJ (2001) Clearing the brain’s amyloid cobwebs. Neuron 32(2): 177–180

    Article  CAS  PubMed  Google Scholar 

  • Strohmeyer R, Rogers J (2001) Molecular and cellular mediators of Alzheimer’s diseaseinflammation. J Alzheimer Dis 3: 131–157

    CAS  Google Scholar 

  • The Ronald and Nancy Reagan Research Institute of the Alzheimer’s Association andthe National Institute on Aging Working Group (1998) Consensus report of theWorking Group on “Molecular and biochemical markers of Alzheimer disease”.Neurobiol Aging 19: 109–116

    Google Scholar 

  • Wilson CA, Doms RW, Lee VM (1999) Intracellular APP processing and A beta produc-tion in Alzheimer disease. J Neuropathol Exp Neurol58: 787–794

    Article  Google Scholar 

  • Wisniewski H.M. andWegiel J. (1994) amyloid formation by myocytes ofleptomeningealvessels. Acta Neuropathol 87: 233–241

    Article  CAS  PubMed  Google Scholar 

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© 2002 Springer-Verlag Wien

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Kienzl, E., Jellinger, K., Janetzky, B., Steindl, H., Bergmann, J. (2002). A broader horizon of Alzheimer pathogenesis: ALZAS — an early serum biomarker?. In: Jellinger, K.A., Schmidt, R., Windisch, M. (eds) Ageing and Dementia Current and Future Concepts. Journal of Neural Transmission. Supplementa, vol 62. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6139-5_9

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  • DOI: https://doi.org/10.1007/978-3-7091-6139-5_9

  • Publisher Name: Springer, Vienna

  • Print ISBN: 978-3-211-83796-2

  • Online ISBN: 978-3-7091-6139-5

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