Apolipoprotein E in neurology

Current Opinion in Neurology

Volumn 9, Issue 4, 1996, Pages 265-270

  Roses, Allen D ^a  

^a DUKE UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

APOLIPOPROTEIN E;

ALZHEIMER DISEASE; BRAIN METABOLISM; CENTRAL NERVOUS SYSTEM FUNCTION; DEGENERATIVE DISEASE; FAMILIAL DISEASE; HUMAN; ONSET AGE; REVIEW;

EID: 0029743646     PISSN: 13507540     EISSN: None     Source Type: Journal    
DOI: 10.1097/00019052-199608000-00004     Document Type: Review

References (63)

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7. Roses AD: Apolipoprotein E affects the rate of Alzheimer disease expression: beta-amyloid burden is a secondary consequence dependent on APOE genotype and duration of disease. J Neuropathol Exptl Neurol 1994, 53:429-437.
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23. Farrer LA, Cupples LA, van Duijn CM, Kurz A, Zimmer R, Muller U, Green RC, Clarke V, Shoffner J, Wallace DC et al.: APOE genotyping in patients with Alzheimer disease: implications for the risk of dementia among relatives. Ann Neurol 1995, 38:797-808. The authors combined a large number of patients and examined risks for relatives of patients with clinical Alzheimer's disease. It should be appreciated that under the best circumstances, the real prevalence of Alzheimer's disease is 80-90%. As the ascertainment was through clinical Alzheimer's disease patients, with more women than men, the risks to relatives of men who die from competing risks before the age of onset of Alzheimer's disease is not included.
24. Polvikoski T, Sulkava R, Haltia M, Kainulainen K, Vuorio A, Verkkoniemi A, Niinisto L, Halonen P, Kontula K: Apolipoprotein E. dementia, and cortical deposition of beta-amyloid protein. N Engl J Med 1995, 333:1242-1247. This is an epidemiological study of the elderly in Vantaa, Finland and, unlike most epidemiological studies, the diagnoses are autopsy-confirmed rather than clinical diagnoses. The ε4 allele was confirmed as a risk factor, even in this > 85-years-old age group. In addition, amyloid deposition was related to the ε4 allele, whether or not the patients were demented. Several cognitively normal individuals had pathology consistent with Alzheimer's disease, so that the specificity of the pathological criteria alone (without dementia) are again questioned.
25. Corder EH, Saunders AM, Strittmatter WJ, Schmechel DE, Gaskell PC, Rimmler JB, Locke PA, Conneally PM, Schmader KE, Tanzi RE et al.: Apolipoprotein E, survival in Alzheimer's disease patients, and the competing risks of death and Alzheimer's disease. Neurology 1995, 45:1323-1328. The authors demonstrated that survival after onset is related to age of onset, not apoE genotype. Thus Alzheimer's disease patients with the ε3/ε3 genotype who develop Alzheimer's disease at the same age as patients with the ε4/ε4 genotype can be expected to have the same duration of disease, despite the marked differences in amyloid deposition documented in other studies.
26. Schmechel DE, Saunders AM, Strittmatter WJ, Crain BJ, Hulette CM, Joo SH, Pericak-Vance MA, Goldgaber D, Roses AD: Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease. Proc Natl Acad Sci U S A 1993, 90:9649-9653.
27. Rebeck GW, Reiter JS, Strickland DK, Hyman BT: Apolipoprotein E in sporadic Alzheimer's disease: allelic variation and receptor interactions. Neuron 1993, 11:575-580.
28. Oyama F, Shimada H, Oyama R, Ihara Y: Apolipoprotein E genotype, Alzheimer's pathologies and related gene expression in the aged population. Brain Res Mol Brain Res 1995, 29:92-98.
29. Lippa CF, Smith TW, Saunders AM, Crook R, Pulaski-Salo D, Davies P, Hardy J, Roses AD, Dickson D: Apolipoprotein E genotype and Lewy body disease. Neurology 1995, 45:97-103.
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31. Hyman BT, West HL, Rebeck GW, Buldyrev SV, Mantegna RN, Ukleja M, Havlin S, Stanley HE: Quantitative analysis of senile plaques in Alzheimer disease: observation of log-normal size distribution and molecular epidemiology of differences associated with apolipoprotein E genotype and trisomy 21 (Down syndrome). Proc Natl Acad Sci U S A 1995, 92:3586-3590. These authors report on the size distribution of senile plaques in Alzheimer's disease and Down syndrome, with larger plaques in trisomy-21 and increased numbers of plaques with ε4 compared with non-ε4 Alzheimer's disease.
32. Strittmatter WJ, Roses AD: Apolipoprotein E and Alzheimer disease. Proc Natl Acad Sci U S A 1995, 92:4725-4727.
33. Namba Y, Tomonaga M, Kawasaki H, Otomo E, Ikeda K: Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease. Brain Res 1991, 541:163-166.
34. Han SH, Hulette C, Saunders AM, Einstein G, Pericak-Vance MA, Strittmatter WJ, Roses AD, Schmechel DE: Apolipoprotein E is present in hippocampal neurons without neurofibrillary tangles in Alzheimer's disease and in age-matched controls. Exp Neurol 1994, 128:13-26.
35. Han SH, Einstein G, Weisgraber KH, Strittmatter WJ, Saunders AM, Pericak-Vance MA, Roses AD, Schmechel DE: Apolipoprotein E is localized to the cytoplasm of human cortical neurons: a light and electron microscopic Study. J Neuropathol Exptl Neurol 1994, 53:535-544.
36. Benzing WC, Mufson EJ: Apolipoprotein E immunoreactivity within neurofibrillary tangles: relationship to tau and PHF in Alzheimer's disease. Exp Neurol 1995, 132:162-171. The authors of this immunohistochemical report studied the relationship between apoE and cytoskeletal protein tau and paired helical filaments. They confirmed intraneural apoE in neurons undergoing cytoskeletal pathology, but made temporal sequence speculations based of the appearance of immunoreactivity to different antibodies.
37. Rebeck GW, Harr SD, Strickland DK, Hyman BT: Multiple, diverse senile plaque-associated proteins are ligands of an apolipoprotein E receptor, the alpha-2-macroglobulin receptor/low-density-lipoprotein receptor-related protein. Ann Neurol 1995, 37:211-217. The authors demonstrate that seven known ligands of the lipoprotein receptor-related protein receptor, including apoE, accumulate in senile palques of Alzheimer's disease. As the binding site of apoE for Aβ amyloid peptide is different from the lipoprotein receptor-related protein binding site, they provide additional evidence for the secondary accumulation of Aβ in senile plaques through apoE binding.
38. Nathan BP, Chang KC, Bellosta S, Brisch E, Ge N, Mahley RW, Pitas RE: The inhibitory effect of apolipoprotein E4 on neurite outgrowth is associated with microtubule depolymerization. Biol Chem 1995, 270:19791-19799. The authors provide evidence for the differential effects of ε3 and ε4 on neurite outgrowth and the cytoskeleton of neuronal cells in culture. The effect of ε4 on depolymerization of microtubules supported involvement of apoE with the microtubule system in the pathogenesis of Alzheimer's disease.
39. Nathan BP, Bellosta S, Sanan DA, Weisgraber KH, Mahley RW, Pitas RE: Differential effects of apolipoproteins E3 and E4 on neuronal growth in vitro. Science 1994, 264:850-852.
40. Holtzman DM, Pitas RE, Kilbridge J, Nathan B, Mahley RW, Bu GJ, Schwartz AL: Low density lipoprotein receptor-related protein mediates apolipoprotein E-dependent neurite outgrowth in a central nervous system-derived neuronal cell line. Proc Natl Acad Sci U S A 1995, 92:9480-9484. In a central nervous system-derived neuronal cell line, ε3 increased neurite extension and could be blocked by anti-low density lipoprotein-related receptor antibody and a 39-kDa protein that regulates ligand binding to low density lipoprotein-related receptor. These data are consistent with apoE entry into neurons via this route, and an apoE isoform-specific interaction of ε3 in promoting neurite outgrowth.
41. Strittmatter WJ, Saunders AM, Goedert M, Weisgraber KH, Dong L-M, Jakes R, Huang DY, Pericak-Vance MA, Schmechel D, Roses AD: Isoform-specific interactions of apolipoprotein E with microtubule-associated protein tau: implications for Alzheimer disease. Proc Natl Acad Sci U S A 1994, 91:11183-11186.
42. Huang DY, Goedert M, Jakes R, Weisgraber K, Garner C, Saunders AM, Pericak-Vance MA, Schmechel D, Roses AD, Strittmater WJ: Isoform-specific interactions of apolipoprotein E with the microtubule associated protein MAP2c: implications for Alzheimer's disease. Neurosci Lett 1994, 182:55-58.
43. Huang DY, Weisgraber KH, Goedert M, Saunders AM, Roses AD, Strittmatter WJ: ApoE3 binding to tau tandem repeat I is abolished by tau serine 262 phosphorylation. Neurosd Lett 1995, 192:209-212. In domain 1 of tau there is a phosphorylation site at Ser 262, the only phosphorylation site in the microtubule binding domain. Phosphorylation of Ser 262 abolishes tau binding by ε3 and decreases tau binding to microtubules, consistent with proposed hypotheses (see [8, 10*, 44]).
44. Strittmatter WJ, Weisgraber KH, Goedert M, Saunders A M, Huang D, Corder EH, Dong LM, Jakes R, Alberts MJ, Gilbert JR, Roses AD: Hypothesis: microtubule instability and paired helical filament formation in the Alzheimer disease brain are related to apolipoprotein E genotype. Exp Neurol 1994, 125:163-171.
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48. Masliah E, Mallory M, Ge N, Alford M, Veinbergs I, Roses AD: Neurodegeneration in the central nervous system of apoE-deficient mice. Exp Neurol 1995, 136:107-122. Using MAP2 and synaptophysin as markers, these authors demonstrated decreased density of synapses over time in a strain of apoE-deficient 'knock-out' mice. Electron microscopy by the authors also demonstrated fragmentation of the microtubular system in synapses.
49. Xu P-T, Schmechel D, Rothrock T, Qiu HL, Popko B, Maeda N, Saunders AM, Roses AD, Gilbert JR: Expression of human isoform specific apolipoprotein E2 and E4 in transgenic mice [Abstract]. Am J Hum Genet 1995, 57:A254. This abstract documents ε4 and ε2 transgenic mice on the apoE-deficient 'knock-out' background. These transgenic animals were created using human genomic apoE with normal human promoters.
50. Horsburgh K, Nicoll JAR: Selective alterations in the cellular distribution of apolipoprotein E immunoreactivity following transient cerebral ischaemia [Abstract]. Alzheimer's Res 1995, 1(suppl 1):22. The authors demonstrate that apoE is synthesized in astrocytes and gets transferred to specifically vulnerable neurons in a standardized stroke model.
51. Einstein G, Bautista P, Patel V, Kenna M, Melone L, Fader R, Karson K, Saunders A, Hulette C, Roses A, Schmechel D: Does apoE-immunoreactivity mark vulnerable neurons in Alzheimer's disease? [Abstract]. Alzheimer's Res 1995, 1(suppl 1):22.
52. Tardiff B, Newman M, Saunders A, Strittmatter W, Smith LR, Roses A, Reves JG: Apolipoprotein E allele frequency in patients with cognitive defects following cardiopulmonary bypass. Circulation 1994, 90:1-201.
53. Newman MF, Croughwell ND, Blumenthal JA, Lowry E, White WD, Spillane W, Davis RD Jr, Glower DD, Smith LR, Mahanna EP, Reves JG: Predictors of cognitive decline after cardiac operation. Ann Thorac Surg 1995, 59:1326-1330.
54. Mayeau R, Ottman R, Maestre G, Ngai C, Tang M-X, Ginsberg H, Chun M, Tycko B, Shelanski M: Synergistic effects of traumatic head injury and apolipoprotein-ε4 in patients with Alzheimer's disease. Neurology 1995, 45:555-557.
55. Nicoll JAR, Roberts GW, Graham DI: Apolipoprotein E E4 allele is associated with deposition of amyloid β-protein following head injury. Nature Med 1995, 1:135-137.
56. Roses AD, Saunders AM: Head injury, amyloid p and Alzheimer's disease. Nature Med 1995, 1:603-604.
57. Alberts MJ, Graffagnino C, McClenny C, DeLong D, Strittmatter W, Saunders AM, Roses AD: ApoE genotype and survival from intracerebral hemorrhage. Lancet 1995, 346:575. These authors demonstrate that patients with the ε3/ε4 genotype have higher mortality and less neurologic functional recovery following intracerebral hemorrhages compared to ε3/ε3 and ε2/ε3 patients.
58. Roses AD: Apolipoprotein E genotyping in differential diagnosis, not prediction, of Alzheimer's disease [Point of View]. Ann Neurol 1995, 38:6-14. An invited commentary of the current non-role of apoE genotyping for prediction in asymptomatic individuals and as a promising adjunct for the diagnosis of demented patients.
59. Bird TD: Apolipoprotein E genotyping in the diagnosis of Alzheimer's disease: a cautionary view [Editorial]. Ann Neurol, 1995, 36:2-3.
60. Farrer LA, Brin MF, Elsas L, Goate A, Kennedy J, Mayeux R, Myers RH, Reilly P, Risch NJ: Statement on use of apolipoprotein E testing for Alzheimer disease. JAMA 1995, 274:1627-1629.
61. Relkin N: Apolipoprotein E genotyping in Alzheimer's disease: consensus statement of the National Institute of Aging/Alzheimer's Association Working Group. Lancet 1996, 347:1091-1095.
62. Saunders AM, Hulette C, Welsh KA, Schmechel DE, Crain B, Burke JR, Alberts MJ, Strittmatter WJ, Breitner, JCS, Rosenberg C et al.: Specificity, sensitivity and predictive value of apolipoprotein E genotyping in a consecutive autopsy series of sporadic Alzheimer disease patients. Lancet 1996 (In press).
63. Small GW, Mazziotta JC, Collins MT, Baxter LR, Phelps ME, Mandelkern MA, Kaplan A, La Rue A, Adamson CF, Chang L et al.: Apolipoprotein E type 4 allele and cerebral glucose metabolism in relatives at risk for familial Alzheimer disease. JAMA 1995, 273:942-947. Using positron emission tomography, the authors demonstrate that a group of ε3/ε4 carriers approximately 20 y younger than their expected age of onset distribution have decreased parietal glucose metabolism, supporting the view that Alzheimer's disease develops over a long period of metabolic abnormalities.