Molecular Basis of Alzheimer Desease

The prevalence of Alzheimer's disease ranges from 3 -11% in persons over ages 65 years. It is a significant problem about aging. It is reported that most of 70 to50% of demantias is Alzheimer`s disease in Western Europe and the United States according to Japan moreover Russia researchers have been reported that there is more multi infarct demantias. In addition, the incidence of the disease and epidemiological studies have not still determine yet in Turkey.A great deal of research has been conducted recently; and the knowledge of the clinical characteristics, neuropathology, genetics, and possible treatments has accumulated. In this review, these improvements will be summarised. Key Words: Alzheimer disease, clinical carecteristics, neuropathology, genetics, treatments

Keywords:

Alzheimer disease, clinical carecteristics, neuropathology genetics, treatments,

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[1] . Curtis B. Dobson, Ruth F. Itzhak “Neurobiology of Aging”, 20(4):457-465 July-August (1999).
[2]. Gauthier S (ed). “Clinical diagnosis and management of Alzheimer's disease”, 2nd ed.London: Martin Dunitz. (1999)
[3] Lovestone S, Gauthier S (eds).”Management of dementia”, 1st edn. London: Martin Dunitz, (2001).
[4] Growdon JH, Rossor MN (eds). “The dementias”,. Boston: Butterworth Heinemann, (2000).
[5] Maj & Sartorius (eds). “Dementia. Chicester”, John Wiley & Sons Ltd, (2000).
[6] “Research and practice in Alzheimer's disease”, Serdi Publisher & Springer Publishing Company, 3 (2000).
[7] Wilson C, Wardell MR, Weisgraber KH, Mahley RW, Agard DA. “Three-dimensional structure of the LDL receptor-binding domain of human apolipoprotein E.”, Science; 252:1817–1822 (1991).
[8] Mark T. Wagner, Joy H. Wymer, Noelle E. Carlozzi, David Bachman, Aljoeson Walker, “Jacobo Mintzer and Alzheimer Study Group” Archives of Clinical Neuropsychology, 22 (3):405- 414 March (2007)
[9] Brown WR, Moody DM, Thore CR ve ark. “Cerebrovascular pathology in Alzheimer’s disease and leukoaiosis”, Ann N Y Acad Sci, 903:39- 45(2000).
[10] “Ann Intern Med”. 139:450 (2003).
[11] Terry RD, Katzman R, Bick KL, Sisodia SS. “Alzheimer Hastalığı”, Çeviri editörü: İ. Hakan Gürvit. İstanbul: Yelkovan yayıncılık; (2001).
[12] Souder E, Beck C. “Overview of Alzheimer’s disease”, Nurs Clin North Am, 39: 545-59 (2004).
[13] Reitz C, Tang MX, “Luchsinger J, et al. Relation of plasma lipids to Alzheimer disease and vascular dementia”, Arch Neurol 61:705-14 (2004).
[14] Karaman Y. “Alzheimer Hastalığı ve diğer demanslar”. 1. baskı. Ankara: Lebib Yalkın Matbaası (2002).
[15] Luchsinger JA, Tang MX, Stern Y, et al. “Diabetes mellitus and risk of Alzheimer’s disease and dementia with stroke in a multiethnic cohort.”, Am J Epidemiol; 154: 635-41 (2001).
[16] Munoz DG. “Is exposure to aluminum a risk factor for the development of Alzheimer disease?- -No. Arch Neurol; 55: 737-739 (1998).
[17] Bulut S. Alzheimer hastalığında oksidatif stres. Türkiye Klinikleri Nöroloji Dergisi 2003; 1: 54- 62.
[18] .Engelhart MJ, Geerlings MI, Ruitenberg A, et al. “Dietary intake of antioxidants and risk of Alzheimer disease”, JAMA 287:3223- 3229(2002).
[19] Ewins DL, Rossor MN, Butler J, et al. “Association between autoimmune thyroid disease and familial Alzheimer’s disease”, Clin Endocrinol (Oxf); 35 :93-96 (1991).
[20] Kurt GS. “Alzheimer Hastalığında genetik dışı etyolojik faktörler”, Türkiye Klinikleri Nöroloji Dergisi; 1: 38-44 (2003).
[21] Klapper PE, Cleator GM, Longson M., “Mild forms of herpes encephalitis”. J Neurol Neurosurg Psychiatry; 47:1247–1250(1984).
[22] Fodor PA, Levin MJ, Weinberg A, Sandberg E, Sylman J, Tyler KL. “A typical herpes simplex virus encephalitis diagnosed by PCR amplification of viral DNA from CSF”. Neurology 51:554–559 (1998).
[23] Itzhaki RF, Lin WR, Shang D, Wilcock GK, Faragher B, Jamieson GA. “Herpes simplex virus type1 in brain and risk of Alzheimer’s disease”,Lancet;349:241–244 (1997).
[24] Poirier J., “Apolipoprotein E, cholesterol transport and synthesis in sporadic Alzheimer’s disease”, Neurobiol Aging 26:355–361(2005).
[25] .Manelli AM, Stine WB, Van Eldik LJ, LaDu MJ. “ApoE and Abeta1-42 interactions: effects of isoform and conformation on structure and function”, J Mol Neurosci 23:235–246 (2004).
[26] Sonia Franco, Maria A. Blasco, Sandra L. Siedlak, Peggy L.R. Harris, Paula I. Moreira, George Perry, Mark A. Smith “Alzheimer's and Dementia”, 2(3):164-168 July (2006).
[27] “Alzheimer’s Disease International”, March in (1999).
[28] Goate AM, Haynes AR, Owen MJ, et al. “Predisposing locus for Alzheimer’s disease on chromosome” 21. Lancet (1989).
[29] Theuns J, Marjaux E, Vandenbulcke M, et al. “Alzheimer dementia caused by a novel mutation located in the APP C-terminal intracytosolic fragment”, Hum Mutat (2006).
[30] Schellenberg GD, Bird TD, Wijsman EM, Orr HT, Anderson L, Nemens E, White JA, Bonnycastle L, Weber JL, Alonso ME, et al. (Nov 1992). "Genetic linkage evidence for a familial Alzheimer's disease locus on chromosome 14". Science 258: 668–71(5082).
[31] "Entrez Gene: PSEN1 presenilin 1 (Alzheimer disease 3)"
[32] Cruts M, Van Broeckhoven C. “Presenilin mutations in Alzheimer’s disease”, Hum Mutat 1998
[33] Hutton M, Busfield F, Wragg M, et al. “Complete analysis of the presenilin 1 gene in early onset Alzheimer’s disease”, Neuroreport (1996).
[34] Selkoe DJ. “Alzheimer's disease: genes, proteins, and therapy”, Physiol Rev. Apr; 81(2):741- 66(2001).
[35] Thinakaran G, Parent AT. “Identification of the role of presenilins beyond Alzheimer's disease”, Pharmacol Res. Oct;50(4):411-8 (2004)
[36] Levy-Lahad E, WijsmanEM, Nemens E, et al. “Afamilial Alzheimer’s disease locus on chromosome1”, Science (1995).
[37] Rogaev EI, Sherrington R, Rogaeva EA, 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).
[38] R.F. Itzhaki, M.A. “Wozniak / Progress in Lipid” Research 45:73–90 (2006).
[39] Neels JG, Horn IR, van der Berg BMM, “Pannekoek H, van Zonneveld A-J. Ligand– receptor interactions of the low density lipoprotein receptor-related protein, a multi-ligand endocytic receptor”, Fibrinolysis Proteolysis;12:219–40(1998) .
[40] Mahley RW, Rall Jr SC. “Apolipoprotein E: far more than a lipid transport protein”, Annu Rev Genom Hum Genet;1:507–537 (2000).
[41] Eden R. Martin, John R. Gilbert, Eric H. Lai, John Riley, Allison R. Rogala, Brandon D. Slotterbeck, Catherine A. Sipe, Janet M. Grubber, Liling L. Warren, P. Michael Conneally, Ann M. Saunders, Donald E. Schmechel, Ian Purvis, Margaret A. Pericak-Vance, Allen D. Roses, Jeffery M. Vance Genomics, 63(1): 7-12 1 January (2000)
[42] Mark T. Wagner, Joy H. Wymer, Noelle E. Carlozzi, David Bachman, Aljoeson Walker, “Jacobo Mintzer and Alzheimer Study Group” Archives of Clinical Neuropsychology, 22(3): 405-414 (2007).
[43] J. D. Yang, G. Y. Feng, J. Zhang, J. Cheung, D. St. Clair, L. He, Neuroscience Letters, 350(1): 25-28, 16 October 2003
[44] ., Ryo Kimura, Mitsuko Yamamoto, Takashi Morihara, Hiroyasu Akatsu, Takashi Kudo, Kouzin Kamino, Masatoshi Takeda Neuroscience Letters 461(2): 177-180, 11 September (2009)
[45] NTV Science Magazine-num 1-March 2009(page 106-109)
[46] Behl, C., “Nature Rev”,. Neuroscience, , 3: 433 (2002).
[47]. C. Behl et al, Mol. Pharmacol., , 51, 535 (1997).
[48] P I Moreira, X Zhu and M A Smith, G Perry “Alzheimer’s Disease: An Overview”, 259- 263(2009).
[49] Strittmatter, W. J., Saunders, A. M., Schmechel, D., Pericak-Vance, M.,Enghild, J., Salvesen, G. S., and Roses, A. D. (1993). “Apolipoprotein E: High-avidity binding to ß-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease”, Proc Natl Acad Sci USA 90, 1977–1981.
[50] Saunders, A. M., Strittmatter, W. J., Schmechel, D., George-Hyslop, P. H.,Pericak-Vance, M. A., Joo, S. H. et al. “Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer’s disease”. Neurology 43, 1467–1472(1993).
[51] Corder, E. H., Saunders, A. M., Risch, N. J., Strittmatter, W. J., Schmechel,D. E., Gaskell, P. C. et al. “Protective effect of polipoprotein E type 2 allele for late onset Alzheimer disease”, Nat Genet 7, 180–184(1994).
[52] Myers, A. J., Kaleem, M., Marlowe, L., Pittman, A. M., Lees, A. J., Fung,H. C. et al. “The H1c haplotype at the MAPT locus is associated with Alzheimer’s disease”, Hum Mol Genet 14, 2399– 2404(2005).
[53] Bertram, L., McQueen, M. B., Mullin, K., Blacker, D., and Tanzi, R. E. “Systematic metaanalyses of Alzheimer disease genetic association studies: The AlzGene database”. Nat Genet 39, 17–23(2007)

Gazi University Journal of Science-Cover

Yayın Aralığı: Yılda 4 Sayı
Başlangıç: 1988
Yayıncı: Gazi Üniversitesi, Fen Bilimleri Enstitüsü

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