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Apolipoprotein C-I expression in the brain in Alzheimer's disease.

Petit-Turcotte, Caroline, Stohl, Sheldon M., Beffert, Uwe, Cohn, Jeffrey S., Aumont, Nicole, Tremblay, Michel, Dea, Doris, Yang, Lin, Poirier, Judes, Shachter, Neil S.·2001·Neurobiology of Disease
DOI 10.1006/nbdi.2001.0441
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Abstract

The H2 allele of apolipoprotein (apo) C-I is associated with Alzheimer's disease (AD). However, this association is potentially confounded by the linkage disequilibrium of H2 with the epsilon2 and epsilon4 alleles of apoE and of H1 with the epsilon3 allele. To establish plausibility for a direct role for apoC-I in AD, we compared apoC-I and apoE protein and mRNA levels in postmortem specimens of frontal cortex and hippocampus from AD patients with levels in nondemented controls. In H2-allelic individuals (usually also epsilon4 carriers), apoC-I mRNA levels were strikingly lower with AD (by 65%, P < 0.05), but apoC-I protein levels in AD were significantly higher (by 34%, P < 0.05). The opposite direction of the apoC-I mRNA and apoC-I protein level changes in AD in the epsilon4/H2 genotype may reflect decreased clearance of CNS lipoproteins associated with apoE4. In H1/H1 (usually epsilon3/epsilon3) individuals, both apoC-I protein and mRNA were lower in AD. ApoC-I protein levels in hippocampus were nearly twice those in frontal cortex. Immunohistochemistry of hippocampus revealed colocalization of apoC-I protein with the astrocytic marker GFAP. In addition, cultured human astrocytes expressed the mRNA for apoC-I. This study confirms apoC-I expression in the CNS and identifies astrocytes as the source of apoC-I. In addition, it has revealed differences in apoC-I expression based on site, genotype, and disease status that may reflect a role for apoC-I in the pathogenesis of AD.

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  • APOC1 is involved in amyloid-β accumulation and contributes to cognitive decline and memory impairment, similar to the effects observed with APOE ε4.

    “Multiple studies have confirmed that APOC1 is involved in amyloid-β (Aβ) accumulation and contributes to cognitive decline and memory impairment, similar to the effects observed with APOE ε4 [13, 14].”

    From Association of APOC1 with cortical atrophy during conversion to Alzheimer’s disease (2025) · cites this paper as [14]

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Research works printed but not linked: 34

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Metadata

Authors
Petit-Turcotte, C., Stohl, S. M., Beffert, U., Cohn, J. S., Aumont, N., Tremblay, M., Dea, D., Yang, L., Poirier, J., & Shachter, N. S.
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2001-12
Volume
8
Issue
6
Pages
953-963
ISSN
0969-9961
DOI
10.1006/nbdi.2001.0441
Cited by
50
References
2
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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