Age and apolipoprotein E*4 allele effects on cerebrospinal fluid β-amyloid 42 in adults with normal cognition

Elaine R. Peskind, Ge Li, Jane Shofer, Joseph F. Quinn, Jeffrey A. Kaye, Chris M. Clark, Martin R. Farlow, Charles DeCarli, Murray A. Raskind, Gerard D. Schellenberg, Virginia M Y Lee, Douglas R. Galasko

Research output: Contribution to journalArticle

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Abstract

Background: Decreased cerebrospinal fluid (CSF) β-amyloid 42 (Aβ 42) concentration, but not Aβ 40 concentration, is a biomarker for Alzheimer disease. This Aβ 42 concentration decrease in CSF likely reflects precipitation of Aβ 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 Aβ 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 Aβ 42 and Aβ 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 Aβ 42, but not the Aβ 40, concentration decreased significantly with age. There was a sharp decrease in CSF Aβ 42 concentration beginning in the sixth decade in subjects with the APOE*4 allele. This age-associated decrease in CSF Aβ 42 concentration was significantly and substantially greater in subjects with theAPOE*4 allele compared with those without the APOE*4 allele. Conclusion: These CSF Aβ 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic Aβ 42 brain deposition starting in later middle age in persons with normal cognition.

Original languageEnglish (US)
Pages (from-to)936-939
Number of pages4
JournalArchives of Neurology
Volume63
Issue number7
DOIs
StatePublished - 2006

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Apolipoprotein E4
Amyloid
Cognition
Cerebrospinal Fluid
Alleles
Alzheimer Disease
Allele
Amyloid Plaques
Brain
Needles
Dementia
Healthy Volunteers
Biomarkers
Enzyme-Linked Immunosorbent Assay
Genotype

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Peskind, E. R., Li, G., Shofer, J., Quinn, J. F., Kaye, J. A., Clark, C. M., ... Galasko, D. R. (2006). Age and apolipoprotein E*4 allele effects on cerebrospinal fluid β-amyloid 42 in adults with normal cognition. Archives of Neurology, 63(7), 936-939. https://doi.org/10.1001/archneur.63.7.936

Age and apolipoprotein E*4 allele effects on cerebrospinal fluid β-amyloid 42 in adults with normal cognition. / Peskind, Elaine R.; Li, Ge; Shofer, Jane; Quinn, Joseph F.; Kaye, Jeffrey A.; Clark, Chris M.; Farlow, Martin R.; DeCarli, Charles; Raskind, Murray A.; Schellenberg, Gerard D.; Lee, Virginia M Y; Galasko, Douglas R.

In: Archives of Neurology, Vol. 63, No. 7, 2006, p. 936-939.

Research output: Contribution to journalArticle

Peskind, ER, Li, G, Shofer, J, Quinn, JF, Kaye, JA, Clark, CM, Farlow, MR, DeCarli, C, Raskind, MA, Schellenberg, GD, Lee, VMY & Galasko, DR 2006, 'Age and apolipoprotein E*4 allele effects on cerebrospinal fluid β-amyloid 42 in adults with normal cognition', Archives of Neurology, vol. 63, no. 7, pp. 936-939. https://doi.org/10.1001/archneur.63.7.936
Peskind, Elaine R. ; Li, Ge ; Shofer, Jane ; Quinn, Joseph F. ; Kaye, Jeffrey A. ; Clark, Chris M. ; Farlow, Martin R. ; DeCarli, Charles ; Raskind, Murray A. ; Schellenberg, Gerard D. ; Lee, Virginia M Y ; Galasko, Douglas R. / Age and apolipoprotein E*4 allele effects on cerebrospinal fluid β-amyloid 42 in adults with normal cognition. In: Archives of Neurology. 2006 ; Vol. 63, No. 7. pp. 936-939.
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abstract = "Background: Decreased cerebrospinal fluid (CSF) β-amyloid 42 (Aβ 42) concentration, but not Aβ 40 concentration, is a biomarker for Alzheimer disease. This Aβ 42 concentration decrease in CSF likely reflects precipitation of Aβ 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 Aβ 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 Aβ 42 and Aβ 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 Aβ 42, but not the Aβ 40, concentration decreased significantly with age. There was a sharp decrease in CSF Aβ 42 concentration beginning in the sixth decade in subjects with the APOE*4 allele. This age-associated decrease in CSF Aβ 42 concentration was significantly and substantially greater in subjects with theAPOE*4 allele compared with those without the APOE*4 allele. Conclusion: These CSF Aβ 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic Aβ 42 brain deposition starting in later middle age in persons with normal cognition.",
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T1 - Age and apolipoprotein E*4 allele effects on cerebrospinal fluid β-amyloid 42 in adults with normal cognition

AU - Peskind, Elaine R.

AU - Li, Ge

AU - Shofer, Jane

AU - Quinn, Joseph F.

AU - Kaye, Jeffrey A.

AU - Clark, Chris M.

AU - Farlow, Martin R.

AU - DeCarli, Charles

AU - Raskind, Murray A.

AU - Schellenberg, Gerard D.

AU - Lee, Virginia M Y

AU - Galasko, Douglas R.

PY - 2006

Y1 - 2006

N2 - Background: Decreased cerebrospinal fluid (CSF) β-amyloid 42 (Aβ 42) concentration, but not Aβ 40 concentration, is a biomarker for Alzheimer disease. This Aβ 42 concentration decrease in CSF likely reflects precipitation of Aβ 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 Aβ 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 Aβ 42 and Aβ 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 Aβ 42, but not the Aβ 40, concentration decreased significantly with age. There was a sharp decrease in CSF Aβ 42 concentration beginning in the sixth decade in subjects with the APOE*4 allele. This age-associated decrease in CSF Aβ 42 concentration was significantly and substantially greater in subjects with theAPOE*4 allele compared with those without the APOE*4 allele. Conclusion: These CSF Aβ 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic Aβ 42 brain deposition starting in later middle age in persons with normal cognition.

AB - Background: Decreased cerebrospinal fluid (CSF) β-amyloid 42 (Aβ 42) concentration, but not Aβ 40 concentration, is a biomarker for Alzheimer disease. This Aβ 42 concentration decrease in CSF likely reflects precipitation of Aβ 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 Aβ 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 Aβ 42 and Aβ 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 Aβ 42, but not the Aβ 40, concentration decreased significantly with age. There was a sharp decrease in CSF Aβ 42 concentration beginning in the sixth decade in subjects with the APOE*4 allele. This age-associated decrease in CSF Aβ 42 concentration was significantly and substantially greater in subjects with theAPOE*4 allele compared with those without the APOE*4 allele. Conclusion: These CSF Aβ 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic Aβ 42 brain deposition starting in later middle age in persons with normal cognition.

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