Evidence map›Paper›PMID 38507884›Full record

ArticleThe journal of nutrition, health & aging2024

Dietary fats and the APOE-e4 risk allele in relation to cognitive decline: a longitudinal investigation in a biracial population sample.

Xiaoran Liu, Todd Beck, Klodian Dhana, Christy C Tangney, Pankaja Desai, Kristin Krueger, Denis A Evans, Kumar B Rajan

Abstract read
In one paragraph

Article in The journal of nutrition, health & aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Xiaoran LiuRush Institute for Healthy Aging, Rush University Medical Center, Chicago, IL, USA; Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA. Electronic address: Xiaoran_Liu@rush.edu.
Todd BeckRush Institute for Healthy Aging, Rush University Medical Center, Chicago, IL, USA; Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA.
Klodian DhanaRush Institute for Healthy Aging, Rush University Medical Center, Chicago, IL, USA; Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA.
Christy C TangneyDepartment of Clinical Nutrition & Preventive Medicine, Rush University Medical Center, Chicago, IL, USA.
Pankaja DesaiRush Institute for Healthy Aging, Rush University Medical Center, Chicago, IL, USA; Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA.
Kristin KruegerRush Institute for Healthy Aging, Rush University Medical Center, Chicago, IL, USA; Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA.
Denis A EvansRush Institute for Healthy Aging, Rush University Medical Center, Chicago, IL, USA; Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA.
Kumar B RajanRush Institute for Healthy Aging, Rush University Medical Center, Chicago, IL, USA; Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA.

Funding

Impact of Neuroinflammation on AD Occurrence: A Bi-Generational Population StudyR01AG073627 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI NEELUM T. AGGARWAL, DENIS A EVANS · 2021 to 2026
$14.0M
Preserving Cognitive Resilience: A Biracial Parent-Offspring Study (18-4674) - Feasibility StudyR01AG058679 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI EVANS, DENIS A, RAJAN, KUMAR B. · 2019 to 2024
$13.8M
A Population-Based Latinx Community Study of Alzheimer’s DiseaseUH2AG083289 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI KRUEGER, KRISTIN R, RAJAN, KUMAR B. · 2023 to 2024
$1.1M
NIA NIH HHS R01 AG058679NIA NIH HHS R01 AG073627NIA NIH HHS UH2 AG083289
6 · The paper itself

Abstract

backgroundAPOE-e4 is the strongest genetic risk factor for Alzheimer's disease. However, the influence of APOE-e4 on dietary fat intake and cognition has not been investigated.

objectiveWe aim to examine the association of types of dietary fat and their association to cognitive decline among those with and without the APOE-e4 allele.

methodsThe study included 3,360 Chicago Health and Aging Project (CHAP) participants from four Southside Chicago communities. Global cognition was assessed using a composite score of episodic memory, perceptual speed, MMSE, and diet using a 144-item food frequency questionnaire. APOE genotype was assessed by the hME Sequenom mass-array platform. Longitudinal mixed-effect regression models were used to examine the association of dietary fat and the APOE-e4 allele with cognitive decline, adjusted for age, sex, education, smoking status, and calorie intake.

resultsThe present study involved 3,360 participants with a mean age of 74 at baseline, 62% African Americans, 63% females, and a mean follow-up of 7.8 years. Among participants with the APOE-e4 risk allele, higher intakes of total and saturated fat (SFA) were associated with a faster decline in global cognition. Among individuals with the APOE-e4 risk allele, a 5% increase in calories from SFA was associated with a 21% faster decline (β = -0.0197, P = 0.0038). In contrast, a higher intake of long-chain n-3 polyunsaturated fatty acids (LC-n3 PUFA) was associated with a slower rate of decline in global cognition among APOE-e4 carriers. Specifically, for every 1% energy increment from LC-n3 PUFA, the annual rate of global cognitive decline was slower by 0.024 standardized unit (SD 0.010, P = 0.023), about 30.4% slower annual cognitive decline. Higher SFA or other types of dietary fat were not associated with cognitive decline among APOE-e4 non-carriers.

conclusionsOur study found a significant association between SFA and faster cognitive decline, LC-n3 PUFA and slower cognitive decline among those with the APOE-e4 allele. Our findings suggested that higher intake of SFA might contribute faster cognitive decline in combination with APOE-e4 whereas LC-n3 PUFA might compensate the adverse effects of APOE-e4. The interaction between intakes of different types of dietary fat and APOE-e4 on cognitive function warrants further research.

Indexed as

AllelesApolipoprotein E4Cognitive DysfunctionDietary FatsAgedAged, 80 and overBlack or African AmericanChicagoCognitionFemaleGenotypeHumansLongitudinal StudiesMaleRisk FactorsApolipoprotein E4Dietary FatsAPOECognitionCohortDietary fatLong-chain fatty acidNutritionSaturated fat

Identifiers

PMID38507884
PMCPMC11623058

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.