Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2014 Nov;10(6):630-6.
doi: 10.1016/j.jalz.2014.03.004. Epub 2014 Jun 28.

APOE ε4 influences β-amyloid deposition in primary progressive aphasia and speech apraxia

Affiliations

APOE ε4 influences β-amyloid deposition in primary progressive aphasia and speech apraxia

Keith A Josephs et al. Alzheimers Dement. 2014 Nov.

Abstract

Background: Apolipoprotein E ε4 (APOE ε4) is a risk factor for β-amyloid deposition in Alzheimer's disease dementia. Its influence on β-amyloid deposition in speech and language disorders, including primary progressive aphasia (PPA), is unclear.

Methods: One hundred thirty subjects with PPA or progressive speech apraxia underwent APOE genotyping and Pittsburgh compound B (PiB) PET scanning. The relationship between APOE ε4 and PiB status, as well as severity and regional distribution of PiB, was assessed.

Results: Forty-five subjects had an APOE ε4 allele and 60 subjects were PiB-positive. The odds ratio for a subject with APOE ε4 being PiB-positive compared with a subject without APOE ε4 being PiB-positive was 10.2 (95% confidence interval, 4.4-25.5; P < .0001). The APOE ε4 allele did not influence regional PiB distribution or severity.

Conclusion: APOE ε4 increases the risk of β-amyloid deposition in PPA and progressive speech apraxia but does not influence regional β-amyloid distribution or severity.

Keywords: Apolipoprotein; Logopenic aphasia; Pittsburgh compound B; Primary progressive aphasia; Speech apraxia.

PubMed Disclaimer

Conflict of interest statement

Conflicts of interest: none

Figures

Figure 1
Figure 1. Voxel-level maps of PiB-PET uptake in PiB-positive APOE4 negative and PiB-positive APOE4 positive subjects compared to controls
Results are shown after correction for multiple comparisons at p<0.05. Renders were generated using the BrainNet Viewer (http://www.nitrc.org/projects/bnv/).

References

    1. Corder EH, Saunders AM, Strittmatter WJ, Schmechel DE, Gaskell PC, Small GW, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science. 1993;261:921–923. - PubMed
    1. Gomez-Isla T, West HL, Rebeck GW, Harr SD, Growdon JH, Locascio JJ, et al. Clinical and pathological correlates of apolipoprotein E epsilon 4 in Alzheimer’s disease. Ann Neurol. 1996;39:62–70. - PubMed
    1. Farrer LA, Cupples LA, Haines JL, Hyman B, Kukull WA, Mayeux R, et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium. JAMA : the journal of the American Medical Association. 1997;278:1349–1356. - PubMed
    1. McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology. 1984;34:939–944. - PubMed
    1. Gorno-Tempini ML, Hillis AE, Weintraub S, Kertesz A, Mendez M, Cappa SF, et al. Classification of primary progressive aphasia and its variants. Neurology. 2011;76:1006–1014. - PMC - PubMed

Publication types

LinkOut - more resources