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Age and Apolipoprotein E*4 Allele Effects on Cerebrospinal Fluid β-Amyloid 42 in Adults With Normal Cognition
Abstract
BACKGROUND: Decreased cerebrospinal fluid (CSF) beta-amyloid 42 (A beta 42) concentration, but not A beta 40 concentration, is a biomarker for Alzheimer disease. This A beta 42 concentration decrease in CSF likely reflects precipitation of A beta 42 in amyloid plaques in brain parenchyma. This pathogenic plaque deposition begins years before the clinical expression of dementia in Alzheimer disease. Normal aging and the presence of the apolipoprotein E (APOE*4) allele are the most important known risk factors for Alzheimer disease. OBJECTIVE: To estimate the interactive effects of normal aging and presence of the APOE*4 allele on CSF A beta 42 concentration in adults with normal cognition across the life span. DESIGN: The CSF was collected in the morning after an overnight fast using Sprotte 24-g atraumatic spinal needles. The CSF A beta 42 and A beta 40 concentrations were measured in the 10th milliliter of CSF collected by sandwich enzyme-linked immunosorbent assay. The APOE genotype was determined by a restriction digest method. Subjects One hundred eighty-four community volunteers with normal cognition aged 21 to 88 years. RESULTS: The CSF A beta 42, but not the A beta 40, concentration decreased significantly with age. There was a sharp decrease in CSF A beta 42 concentration beginning in the sixth decade in subjects with the APOE*4 allele. This age-associated decrease in CSF A beta 42 concentration was significantly and substantially greater in subjects with the APOE*4 allele compared with those without the APOE*4 allele. CONCLUSION: These CSF A beta 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic A beta 42 brain deposition starting in later middle age in persons with normal cognition.
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“Studies of non-demented individuals report that while CSF Aβ levels seem to decline during young adulthood, during late mid-life CSF Aβ levels may actually slightly increase [219, 220].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [220]
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“The A peptide is generated by proteolytic processing of the amyloid precursor protein into a series of fragments 38 to 42 amino acids long; A 42 represents about 10% of synthesized A but is by far the earliest and predominant A species deposited in plaques in AD.(5) Decreased concentration of A 42 in CSF is a consiste…”
BackgroundInfluentialCSF Aβ 42 levels correlate with amyloid-neuropathology in a population-based autopsy study
Strozyk, D., Blennow, K., White, L. R., & Launer, L. J. (2003) · Neurology · doi:10.1212/01.wnl.0000046581.81650.d0 · Cited by 621
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Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade
Jack, C. R., Knopman, D. S., Jagust, W. J., Shaw, L. M., Aisen, P. S., Weiner, M. W., Petersen, R. C., & Trojanowski, J. Q. (2010) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70299-6 · Cited by 4,806
Fagan, A. M., Roe, C. M., Xiong, C., Mintun, M. A., Morris, J. C., & Holtzman, D. M. (2007) · Archives of Neurology · doi:10.1001/archneur.64.3.noc60123 · Cited by 897
The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives
Swerdlow, R. H., Burns, J. M., & Khan, S. M. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2013.09.010 · Cited by 786
Jack, C. R., Knopman, D. S., Weigand, S. D., Wiste, H. J., Vemuri, P., Lowe, V., Kantarci, K., Gunter, J. L., Senjem, M. L., Ivnik, R. J., et al. (2012) · Annals of Neurology · doi:10.1002/ana.22628 · Cited by 602
BrainAGE in Mild Cognitive Impaired Patients: Predicting the Conversion to Alzheimer’s Disease
Gaser, C., Franke, K., Klöppel, S., Koutsouleris, N., Sauer, H., & Initiative, A. D. N. (2013) · PLoS ONE · doi:10.1371/journal.pone.0067346 · Cited by 555
Metadata
- Authors
- Peskind, E. R., Li, G., Shofer, J., Quinn, J. F., Kaye, J. A., Clark, C. M., Farlow, M. R., DeCarli, C., Raskind, M. A., Schellenberg, G. D., Lee, V. M.-Y., & Galasko, D. R.
- Affiliations
- University of Washington (US)
- Oregon Health & Science University (US)
- University of Pennsylvania (US)
- Indiana University – Purdue University Indianapolis (US)
- University of California, Davis (US)
- University of California San Diego (US)
- ORCID
- Venue
- Archives of Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2006-07-01
- Volume
- 63
- Issue
- 7
- Pages
- 936
- ISSN
- 0003-9942 (ISSN-L)
- OpenAlex
- W2104954974
- Cited by
- 131
- References
- 20
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 5 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 7 · 2019: 4 · 2018: 2 · 2017: 7 · 2016: 3 · 2015: 5 · 2014: 4 · 2013: 14 · 2012: 17
- FWCI
- 6.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Archives of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ag008419-15)
- National Institute on Aging (AG 10133, P30AG010133, AG08419, AG 08017, AG23185, AG 05136, P30AG010124, P30AG008017, AG-10124, R01AG023185, P50AG005136)
- National Center for Research Resources (M01RR000034)
- 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
- Health Sciences › Medicine › Clinical Neurology › Cerebrospinal fluid and hydrocephalus
- Keywords
- Aβ40, normal aging, Alzheimer's disease risk, cerebrospinal fluid biomarkers, normal cognition
- MeSH terms
- Adult, Aged, Aged, 80 and over, Aging, Alleles, Apolipoproteins E, Brain, Cognition, Female, Genotype, Humans, Male, Middle Aged, Peptide Fragments, Biomarkers, Amyloid beta-Peptides, Apolipoprotein E4
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