Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative condition associated with atrophy and death of nerve cells in affected brain regions. This disease is relatively common, affecting 4 million or more individuals in the United States alone [1]. AD occurs in two relatively distinct forms: an early-onset, familial form and a more common late-onset, sporadic form. Incidence of the latter increases with increasing age, and AD is considered to be the most significant single cause of senile dementia. Indeed, a number of studies have indicated that at least half the total number of cases of dementia in the elderly are attributable to AD [2].
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References
Keefover RW. (1996) The clinical epidemiology of Alzheimer’s disease. Neurol Clin 14: 337–351
Evans DA, Funkenstein HH, Albert MS, et al. (1989) Prevalence of Alzheimer’s disease in a community population of older persons. JAMA 262: 2551–2556
Lee VM-Y, Balin BJ, Otvos L, Trojanowski JQ. (1991) A68-a major subunit of paired helical filaments and derivatized forms of normal tau. Science 251: 675–679
Alonso A, Grundke-Iqbal I, Iqbal K. (1996) Alzheimer’s disease hyperphosphorylated tau sequesters normal tau into tangles of filaments and disassembles microtubules. Nature Med 2: 783–787
Wang J-Z, Grundke-Iqbal I, Iqbal K. (1996) Glycosylation of microtubule-associated protein tau: an abnormal post-translational modification in Alzheimer’s disease. Nature Med 2: 871–875
Goedert M. (1993) Tau protein and the neurofibrillary pathology of Alzheimer’s disease. Trends Neurosci 16: 460–465
Schellenberg GD. (1995) Genetic dissection of Alzheimer’s disease, a heterogeneous disorder. Proc Natl Acad Sci (USA) 92: 8552–8559
Selkoe DJ, Podlisny MD, et al. (1988) β-amyloid precursor protein of AD occurs at 110-to 135-kilodalton membrane-associated proteins in neural and nonneural tissues. Proc Natl Acad Sci (USA) 85: 7341–7345
Yankner BA. (1996) New clues to Alzheimer’s disease: unraveling the roles of amyloid and tau. Nature Med 2: 850–852
Scheuner D, Eckman C, Jensen M, et al. (1996) Secreted amyloid β-protein similar to that in the senile plaques of AD is increased in vivo by the presenilin 1 and 2 mutations linked to familial AD. Nature Med 2: 864–870
Ray WJ, Ashall F, Goate AM. (1998) Molecular pathogenesis of sporadic and familial forms of Alzheimer’s disease. Mol Med Today 4: 151–157
Roses AD. (1996) Apolipoprotein E alleles as risk factor in Alzheimer’s disease. Annu Rev Med 47: 387–400
Itzhaki RJ, Lin WR, Shang D, et al. (1997) Herpes simplex virus type 1 in brain and risk of Alzheimer’s disease. Lancet 349: 241–244
Boyles JK, Pitas RE, Wilson E, et al. (1985) ApoE associated with astrocytic glia of the central nervous system and with nonmyelinating glia of the peripheral nervous system. J Clin Invest 76: 1501–1513
Haan J, Van Broeckhoven C, van Duijn CM, et al. (1994) The apolipoprotein E £4 allele does not influence the clinical expression of the amyloid precursor protein gene codon 693 or 692 mutations. Ann Neurol 36: 434–437
Strittmatter WJ, Weisgraber KH, Huang DY, et al. (1993) Binding of human apolipoprotein E to synthetic amyloid ~ peptide: isoform-specific effects and implications for late-onset Alzheimer’s disease; essentially all Alzheimer’s patients also show a severe deficit in cholinergic nerve function Alzheimer disease. Proc Natl Acad Sci (USA) 90: 8098–8102
Grayston JT. (1992) Chlamydia pneumoniae, strain TWAR pneumonia. Annu Rev Med 43: 317–323
Grayston JT, Campbell LA, Kuo CC, et al. (1990) A new respiratory tract pathogen: Chlamydia pneumoniae strain TWAR. J Infect Dis 161: 618–625
Von Hertzen LC. (1998) Chlamydia pneumoniae and its role in chronic obstructive pulmonary disease. Ann Med 30: 27–37
Schumacher HR, Gérard HC, Arayssi T, et al. (1999). Lower prevalence of Chlamydia pneumoniae DNA compared with Chlamydia trachomatis DNA in synovial tissue of arthritis patients. Arthritis Rheum 42: 1889–1893
Kuo CC, Grayston JT, Campbell LA, et al. (1995) Chlamydia pneumoniae (TWAR) in coronary arteries of young adults (15–34 years old). Proc Natl Acad Sci (USA) 92: 6911–6914
Campbell LA, O’Brien ER, Cappuccio AL, et al. (1995) Detection of Chlamydia pneumoniae TWAR in human coronary atherectomy tissues. J Infect Dis 172: 585–588
Kalayoglu MV, Byrne GI. (1998) Induction of macrophage foam cell formation by Chlamydia pneumoniae. J Infect Dis 177: 725–729
Leinonen M. (1993) Pathogenetic mechanisms and epidemiology of Chlamydia pneumoniae. Eur Heart J 14: 57–61
Ward ME. (1995) The immunobiology and immunopathology of chlamydial infections. APMIS 103: 769–796
Chen S, Frederickson RC, Brunden KR. (1996) Neuroglial-mediated immunoinflammatory responses in Alzheimer’s disease: complement activation and therapeutic approaches. Neurobiol Aging 17: 781–787
Balin BJ, Gérard HC, Arking EJ, et al. (1998) Identification and localization of Chlamydia pneumoniae in the Alzheimer’s brain. Med Microbiol Immunol 187: 23–42
Sriram S, Mitchell W, Stratton C. (1998) Multiple sclerosis association with Chlamydia pneumoniae infection of the CNS. Neurology 50: 571–572
Ordovas JM, Litwack-Klein L, Wilson PWF, et al. (1987) ApoE isoform phenotyping methodology and population frequency with identification of apoE1 and apoE5. J Lipid Res 28: 371–380
Gérard HC, Wang GF, Balin BJ, et al. (1999) Frequency of apolipoprotein E (APOE) allele types in patients with Chlamydia-associated arthritis and other arthritides. Microb Pathog 26: 35–42
Bolton CF, Young GB, Zochodne DW. (1993) The neurological consequences of sepsis. Ann Neurol 33: 94–100
Mann DM, Tinkler AM, Yates PO. (1983) Neurological disease and herpes simplex virus. An immunohistochemical study. Acta Neurol 60: 24–28
Pogo BG, Casals J, Elizan TS. (1987) A study of viral genomes and antigens in brains of patients with Alzheimer’s disease. Brain 110: 907–915
Mathews WB. (1986) Unconventional virus infection and neurological disease. Neuropath Appl Neurobiol 12: 111–116
Nicoll JAR, Roberts GW, Graham DI. (1995) Apolipoprotein E £4 allele is associated with deposition of amyloid β-protein following head injury. Nature Med 1: 135–137
Moazed TC, Kuo CC, Patten DL, et al. (1996) Experimental rabbit models of Chlamydia pneumoniae infection. Am J Pathol 148: 667–676
Breitner JC. (1996) The role of anti-inflammatory drugs in the prevention and treatment of Alzheimer’s disease. Annu Rev Med 47: 401–411
Lue L-H, Brachova L, Civin WH, Rogers J. (1996) Inflammation, Aβ deposition, and neurofibrillary tangle formation as correlates of Alzheimer’s disease neurodegeneration. J Neuropathol Exp Neurol 55: 1083–1088
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Hudson, A.P., Gérard, H.C., Whittum-Hudson, J.A., Appelt, D.M., Balin, B.J. (2000). Chlamydia pneumoniae, APOE genotype, and Alzheimer’s disease. In: L’age-Stehr, J. (eds) Chlamydia pneumoniae and Chronic Diseases. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-57195-4_19
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DOI: https://doi.org/10.1007/978-3-642-57195-4_19
Publisher Name: Springer, Berlin, Heidelberg
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