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Apolipoprotein E ε4 and age effects on florbetapir positron emission tomography in healthy aging and Alzheimer disease.
Neurobiol Aging. 2013 Jan; 34(1):1-12.NA

Abstract

OBJECTIVES

Investigate apolipoprotein E ε4 (APOE4) gene and aging effects on florbetapir F18 positron emission tomography (PET) in normal aging and Alzheimer's disease (AD).

METHODS

Florbetapir F18 PET images were analyzed from 245 participants, 18-92 years of age, from Avid Radiopharmaceutical's multicenter registered trials, including 86 younger healthy control volunteers (yHC), 61 older healthy control volunteers (oHC), 53 mild cognitive impairment (MCI) patients, and 45 AD dementia patients (DAT). Mean florbetapir standard uptake value ratios (SUVRs) were used to evaluate the effects of APOE4 carrier status, older age, and their interaction in each of these groups.

RESULTS

In comparison with non-carriers, the APOE4 carriers in each of the oHC, MCI, and DAT groups had higher mean cortical-to-cerebellar florbetapir SUVRs, patterns of florbetapir PET elevations characteristic of DAT, and a higher proportion meeting florbetapir PET positivity criteria. Only the oHC group had a significant association between mean cortical florbetapir SUVRs and age. In cognitively normal adults, without regards to APOE4 genotype, amyloid began to increase at age 58 (95% confidence interval [CI]: 52.3-63.7), with a predicted typical age of florbetapir positivity occurring around age 71 years. Presence of the APOE4 gene reduced the age of predicted florbetapir positivity in normal aging to around age 56 years, approximately 20 years younger than non-carriers.

INTERPRETATION

Cerebral amyloid deposition is associated with APOE4 carrier status in older healthy control subjects and symptomatic AD patients, and increases with age in older cognitively normal individuals. Amyloid imaging positivity appears to begin near age 56 years in cognitively intact APOE4 carriers and age 76 years in APOE4 non-carriers.

Authors+Show Affiliations

The Banner Alzheimer's Institute, Phoenix, AZ, USA. Adam.fleisher@bannerhealth.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22633529

Citation

Fleisher, Adam S., et al. "Apolipoprotein E Ε4 and Age Effects On Florbetapir Positron Emission Tomography in Healthy Aging and Alzheimer Disease." Neurobiology of Aging, vol. 34, no. 1, 2013, pp. 1-12.
Fleisher AS, Chen K, Liu X, et al. Apolipoprotein E ε4 and age effects on florbetapir positron emission tomography in healthy aging and Alzheimer disease. Neurobiol Aging. 2013;34(1):1-12.
Fleisher, A. S., Chen, K., Liu, X., Ayutyanont, N., Roontiva, A., Thiyyagura, P., Protas, H., Joshi, A. D., Sabbagh, M., Sadowsky, C. H., Sperling, R. A., Clark, C. M., Mintun, M. A., Pontecorvo, M. J., Coleman, R. E., Doraiswamy, P. M., Johnson, K. A., Carpenter, A. P., Skovronsky, D. M., & Reiman, E. M. (2013). Apolipoprotein E ε4 and age effects on florbetapir positron emission tomography in healthy aging and Alzheimer disease. Neurobiology of Aging, 34(1), 1-12. https://doi.org/10.1016/j.neurobiolaging.2012.04.017
Fleisher AS, et al. Apolipoprotein E Ε4 and Age Effects On Florbetapir Positron Emission Tomography in Healthy Aging and Alzheimer Disease. Neurobiol Aging. 2013;34(1):1-12. PubMed PMID: 22633529.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Apolipoprotein E ε4 and age effects on florbetapir positron emission tomography in healthy aging and Alzheimer disease. AU - Fleisher,Adam S, AU - Chen,Kewei, AU - Liu,Xiaofen, AU - Ayutyanont,Napatkamon, AU - Roontiva,Auttawut, AU - Thiyyagura,Pradeep, AU - Protas,Hillary, AU - Joshi,Abhinay D, AU - Sabbagh,Marwan, AU - Sadowsky,Carl H, AU - Sperling,Reisa A, AU - Clark,Christopher M, AU - Mintun,Mark A, AU - Pontecorvo,Michael J, AU - Coleman,R Edward, AU - Doraiswamy,P M, AU - Johnson,Keith A, AU - Carpenter,Alan P, AU - Skovronsky,Daniel M, AU - Reiman,Eric M, Y1 - 2012/05/24/ PY - 2011/12/05/received PY - 2012/04/24/revised PY - 2012/04/28/accepted PY - 2012/5/29/entrez PY - 2012/5/29/pubmed PY - 2013/4/24/medline SP - 1 EP - 12 JF - Neurobiology of aging JO - Neurobiol. Aging VL - 34 IS - 1 N2 - OBJECTIVES: Investigate apolipoprotein E ε4 (APOE4) gene and aging effects on florbetapir F18 positron emission tomography (PET) in normal aging and Alzheimer's disease (AD). METHODS: Florbetapir F18 PET images were analyzed from 245 participants, 18-92 years of age, from Avid Radiopharmaceutical's multicenter registered trials, including 86 younger healthy control volunteers (yHC), 61 older healthy control volunteers (oHC), 53 mild cognitive impairment (MCI) patients, and 45 AD dementia patients (DAT). Mean florbetapir standard uptake value ratios (SUVRs) were used to evaluate the effects of APOE4 carrier status, older age, and their interaction in each of these groups. RESULTS: In comparison with non-carriers, the APOE4 carriers in each of the oHC, MCI, and DAT groups had higher mean cortical-to-cerebellar florbetapir SUVRs, patterns of florbetapir PET elevations characteristic of DAT, and a higher proportion meeting florbetapir PET positivity criteria. Only the oHC group had a significant association between mean cortical florbetapir SUVRs and age. In cognitively normal adults, without regards to APOE4 genotype, amyloid began to increase at age 58 (95% confidence interval [CI]: 52.3-63.7), with a predicted typical age of florbetapir positivity occurring around age 71 years. Presence of the APOE4 gene reduced the age of predicted florbetapir positivity in normal aging to around age 56 years, approximately 20 years younger than non-carriers. INTERPRETATION: Cerebral amyloid deposition is associated with APOE4 carrier status in older healthy control subjects and symptomatic AD patients, and increases with age in older cognitively normal individuals. Amyloid imaging positivity appears to begin near age 56 years in cognitively intact APOE4 carriers and age 76 years in APOE4 non-carriers. SN - 1558-1497 UR - https://www.unboundmedicine.com/medline/citation/22633529/Apolipoprotein_E_ε4_and_age_effects_on_florbetapir_positron_emission_tomography_in_healthy_aging_and_Alzheimer_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-4580(12)00265-5 DB - PRIME DP - Unbound Medicine ER -