APOLIPOPROTEIN-E GENOTYPE IN DIVERSE NEURODEGENERATIVE DISORDERS

被引：71

作者：

SCHNEIDER, JA

GEARING, M

ROBBINS, RS

DELAUNE, W

MIRRA, SS

机构：

[1] VET AFFAIRS MED CTR,DEPT PATHOL & LAB MED,DECATUR,GA 30033

[2] EMORY UNIV,SCH MED,ATLANTA,GA

来源：

ANNALS OF NEUROLOGY | 1995年 / 38卷 / 01期

关键词：

D O I：

10.1002/ana.410380122

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

While the apolipoprotein E (ApoE) epsilon 4 allele is a recognized risk factor for Alzheimer's disease (AD), an association of epsilon 4 with other neurodegenerative diseases (NDs) has not been extensively explored. We examined 51 cases of neuropathologically confirmed ND. After eliminating 18 cases exhibiting pathology sufficient to warrant an additional diagnosis of AD, three disorders characterized by tau-related cytoskeletal pathology, i.e., Pick's disease, corticobasal degeneration, and progressive supranuclear palsy, showed increased epsilon 4 frequencies. Since the number of cases within each category was small, these increased epsilon 4 frequencies were not statistically significant. beta-Amyloid (beta A4) immunoreactive diffuse plaques were observed in many of these cases. While we cannot eliminate the possibility that these patients were destined to develop AD, these changes may merely reflect an independent association of epsilon 4 with amyloid deposition. These preliminary data affirm the need for further study of well-characterized cases to explore the relationship of ApoE to cytoskeletal pathology and ND.

引用

页码：131 / 135

页数：5

共 21 条

[1]

Saunders AM, Strittmatter WJ, Schmechel D, Et al., Association of apolipoprotein E allele ϵ4 with late‐onset familial and sporadic Alzheimer's disease, Neurology, 43, pp. 1467-1472, (1993)

[2]

Strittmatter WJ, Saunders AM, Schmechel D, Et al., Apolipoprotein E: High avidity binding to beta‐amyloid and increased frequency of type 4 allele in late onset familial Alzheimer's disease, Proc Natl Acad Sci USA, 90, pp. 1977-1981, (1993)

[3]

Schmechel DE, Saunders AM, Strittmatter WJ, Et al., Increased amyloid β‐peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late‐onset Alzheimer disease, Proc Natl Acad Sci USA, 90, pp. 9649-9653, (1993)

[4]

Rebeck GW, Reiter JS, Strickland DK, Hyman BT, Apolipoprotein E in sporadic Alzheimer's disease: allelic variation and receptor interactions, Neuron, 11, pp. 575-580, (1993)

[5]

Strittmatter WJ, Weisgraber KH, Goedert M, Et al., Hypothesis: microtubule instability and paired helical filament formation in the Alzheimer disease brain are related to apolipoprotein E genotype, Exp Neurol, 125, pp. 163-171, (1994)

[6]

Khachaturian ZS, Diagnosis of Alzheimer's disease, Arch Neurol, 42, pp. 1097-1105, (1985)

[7]

Mirra SS, Heyman A, McKeel D, Et al., The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part II. Standardization of the neuropathological assessment of Alzheimer's disease, Neurology, 41, pp. 479-486, (1991)

[8]

Gearing M, Schneider JA, Rebeck GW, Et al.

[9]

Mayeux R, Stern Y, Ottman R, Et al., The apolipoprotein ϵ4 allele in patients with Alzheimer's disease, Ann Neurol, 34, pp. 752-754, (1993)

[10]

Hixson JE, Vernier DT, Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with Hba I, J Lipid Res, 31, pp. 545-548, (1990)

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