The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
APOE ε4 allele is associated with reduced cerebrospinal fluid levels of Aβ42
Abstract
The epsilon4 allele of APOE is a risk factor for Alzheimer disease (AD). By analysis of a large cohort of AD patients (n = 563) and control subjects (n = 118), it is shown that the epsilon4 allele is strongly associated with reduced CSF levels of beta-amyloid (1-42) (Abeta42) in both AD (p < 10(-9)) and control (p = 0.0012) populations. As no associations of APOE variants with other indexes of AD severity were observed, this effect may reflect a fundamental involvement of ApoE in Abeta metabolism.
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“In addition, APOE4 carriers display decreased Aβ42 levels in CSF compared to non-carriers [460, 461].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [460]
Citations
Cites
CSF markers for incipient Alzheimer's disease
Blennow, K., & Hampel, H. (2003) · The Lancet Neurology · doi:10.1016/s1474-4422(03)00530-1 · Cited by 1,291
Self-citationApolipoprotein E: a pathological chaperone protein in patients with cerebral and systemic amyloid
Wisniewski, T., & Frangione, B. (1992) · Neuroscience Letters · doi:10.1016/0304-3940(92)90444-c · Cited by 802
Improved discrimination of AD patients using β-amyloid (1-42) and tau levels in CSF
Hulstaert, F., Blennow, K., Ivanoiu, A., Schoonderwaldt, H. C., Riemenschneider, M., Deyn, P. P. D., Bancher, C., Cras, P., Wiltfang, J., Mehta, P. D., et al. (1999) · Neurology · doi:10.1212/wnl.52.8.1555 · Cited by 724
Self-citationReduction of β‐amyloid peptide42 in the cerebrospinal fluid of patients with Alzheimer's disease
Motter, R., Vigo‐Pelfrey, C., Kholodenko, D., Barbour, R., Johnson‐Wood, K., Galasko, D., Chang, L., Miller, B., Clark, C., Green, R., et al. (1995) · Annals of Neurology · doi:10.1002/ana.410380413 · Cited by 701
Plasma and Cerebrospinal Fluid Levels of Amyloid β Proteins 1-40 and 1-42 in Alzheimer Disease
Mehta, P. D., Pirttilä, T., Mehta, S. P., Sersen, E. A., Aisen, P. S., & Wisniewski, H. M. (2000) · Archives of Neurology · doi:10.1001/archneur.57.1.100 · Cited by 582
Galasko, D., Chang, L., Motter, R., Clark, C. M., Kaye, J., Knopman, D., Thomas, R., Kholodenko, D., Schenk, D., Lieberburg, I., et al. (1998) · Archives of Neurology · doi:10.1001/archneur.55.7.937 · Cited by 442
Fagan, A. M., Watson, M., Parsadanian, M., Bales, K. R., Paul, S. M., & Holtzman, D. M. (2002) · Neurobiology of Disease · doi:10.1006/nbdi.2002.0483 · Cited by 290
Prince, J. A., Feuk, L., Howell, W. M., Jobs, M., Emahazion, T., Blennow, K., & Brookes, A. J. (2001) · Genome Research · doi:10.1101/gr.150201 · Cited by 188
Self-citationBlennow, K., Ricksten, A., Prince, J. A., et al. (2000) · Journal of Neural Transmission · doi:10.1007/s007020070052 · Cited by 105
Self-citationJi, Y., Permanne, B., Sigurdsson, E. M., Holtzman, D. M., & Wısnıewskı, T. (2001) · Journal of Alzheimer s Disease · doi:10.3233/jad-2001-3105 · Cited by 86
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Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy
Liu, C.-C., Kanekiyo, T., Xu, H., & Bu, G. (2013) · Nature Reviews Neurology · doi:10.1038/nrneurol.2012.263 · Cited by 3,459
Blennow, K., de Leon, M. J., & Zetterberg, H. (2006) · The Lancet · doi:10.1016/s0140-6736(06)69113-7 · Cited by 3,134
Self-citationMolecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease
Guo, T., Zhang, D., Zeng, Y., Huang, T. Y., Xu, H., & Zhao, Y. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00391-7 · Cited by 994
Mosconi, L., De Santi, S., Brys, M., Tsui, W. H., Pirraglia, E., Glodzik-Sobanska, L., Rich, K. E., Switalski, R., Mehta, P. D., Pratico, D., et al. (2008) · Biological Psychiatry · doi:10.1016/j.biopsych.2007.05.030 · Cited by 238
Self-citationHigher Rates of Decline for Women and Apolipoprotein E ε4 Carriers
Holland, D., Desikan, R. S., Dale, A. M., & McEvoy, L. K. (2013) · American Journal of Neuroradiology · doi:10.3174/ajnr.a3601 · Cited by 219
Metadata
- Authors
- Prince, J. A., Zetterberg, H., Andreasen, N., Marcusson, J., & Blennow, K.
- Affiliations
- Sahlgrenska University Hospital (SE)
- Venue
- Neurology
- Published
- 2004-06-08
- Volume
- 62
- Issue
- 11
- Pages
- 2116-2118
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2041378923
- Cited by
- 128
- References
- 10
- Citations by year
- 2024: 1 · 2023: 1 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 6 · 2017: 6 · 2016: 6 · 2015: 4 · 2014: 6 · 2013: 9 · 2012: 2
- FWCI
- 6.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- APOE ε4, amyloid-beta 42, cerebrospinal fluid, Alzheimer's disease, amyloid metabolism, genetic risk factors
- MeSH terms
- Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Apolipoproteins E, Female, Gene Frequency, Genotype, Humans, Male, Peptide Fragments, Cohort Studies, Amyloid beta-Peptides, Genetic Predisposition to Disease, Apolipoprotein E4
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