APOE-epsilon 4 polymorphism and cognitive function in Bengkulu obese individuals

Diah Ayu Aguspa Dita, Aribawa Ajid Bhaskara, Altaria Erthafauziah Opaladu, Elvira Yunita

Abstract


Background: While obesity and apolipoprotein E (APOE) are both important risk factors for dementia, the exact role of their interrelationship in influencing dementia risk, particularly across different ethnicities, remains unclear. This study aims to examine the correlations between APOE and the risk of dementia in obese adults from Bengkulu.

Methods: Seventy-two participants from Bengkulu, comprising obese and normal individuals (Mean age = 39.44 years; Mean BMI = 25.64 kg/m²; 33.3% APOE-?4 carriers; 69.4% female), underwent anthropometric assessments, blood sampling for APOE genotyping, and cognitive evaluation using the MoCA-Ina test. The Chi-square analysis was conducted to investigate the association between APOE and the risk of dementia in obese adults from Bengkulu.

Results: Statistical analyses revealed significant differences between obese and non-obese groups regarding age (41.28 ± 6.76 vs 37.61 ± 7.19; p=0.011), sex (80.6% women and 19.4% men vs 58.3% women and 41.7% men; P = .041), BMI (28.64 ± 3.98 vs 22.63 ± 1.86; P < .001), weight (69.01 ± 12.24 vs 57.94 ± 7.97; P < .001), and MoCA-Ina score (19.4% vs 61.1%; P < .001). This study found no significant differences in cognitive decline between APOE-?4 carriers in both obese (OR: 3.67, 95% CI: 0.39 to 34.65, P = .384) and non-obese groups (OR: 0.584, 95% CI: 0.12 to 2.78, P = .706) among individuals from Bengkulu.

Conclusion: We found no evidence of neurodegenerative risk associated with APOE-?4 in obese individuals from Bengkulu. Further research is required to investigate potential characteristics.

Keywords: Apolipoprotein E, Ethnicity, Cognitive Decline, Dementia


Full Text:

PDF

References


Swinburn BA, Kraak VI, Allender S, Atkins VJ, Baker PI, et al. The Global Syndemic of Obesity, Undernutrition, and Climate Change: The Lancet Commission report. Lancet (London, England), (2019); 393(10173): 791-846.

World Health Organization (2025) Obesity and overweight.

Nichols E, Steinmetz JD, Vollset SE, Fukutaki K, Chalek J, et al. Estimation of the global prevalence of dementia in 2019 and forecasted prevalence in 2050: an analysis for the Global Burden of Disease Study 2019. The Lancet Public Health, (2022); 7(2): e105-e125.

Badan Pusat Statistik (2022) Prevalensi Obesitas Pada Penduduk Umur> 18 Tahun Menurut Jenis Kelamin 2013-2018.

Alzheimer’s Association. Alzheimer’s disease facts and figures. Alzheimers Dement, (2022); 18(4): 700-789.

World Health Organization (2025) Dementia.

American Psychiatric Association D, American Psychiatric Association D Diagnostic and statistical manual of mental disorders: DSM-5. (2013); American psychiatric association Washington, DC.

Vemuri P, Knopman DS, Lesnick TG, Przybelski SA, Mielke MM, et al. Evaluation of Amyloid Protective Factors and Alzheimer Disease Neurodegeneration Protective Factors in Elderly Individuals. JAMA Neurology, (2017); 74(6): 718-726.

Ma Y, Ajnakina O, Steptoe A, Cadar D. Higher risk of dementia in English older individuals who are overweight or obese. International Journal of Epidemiology, (2020); 49(4): 1353-1365.

Pedditzi E, Peters R, Beckett N. The risk of overweight/obesity in mid-life and late life for the development of dementia: a systematic review and meta-analysis of longitudinal studies. Age and Ageing, (2016); 45(1): 14-21.

Kivimäki M, Luukkonen R, Batty GD, Ferrie JE, Pentti J, et al. Body mass index and risk of dementia: Analysis of individual-level data from 1.3 million individuals. Alzheimer’s & Dementia, (2018); 14(5): 601-609.

Danat IM, Clifford A, Partridge M, Zhou W, Bakre AT, et al. Impacts of Overweight and Obesity in Older Age on the Risk of Dementia: A Systematic Literature Review and a Meta-Analysis. Journal of Alzheimer’s Disease, (2019); 70(s1): S87-s99.

Zhao T, Zhong T, Zhang M, Xu Y, Zhang M, et al. Alzheimer’s Disease: Causal Effect between Obesity and APOE Gene Polymorphisms. International journal of molecular sciences, (2023); 24(17).

Liu CC, Liu CC, Kanekiyo T, Xu H, Bu G. Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy. Nature reviews Neurology, (2013); 9(2): 106-118.

Farmer BC, Williams HC, Devanney NA, Piron MA, Nation GK, et al. APO?4 lowers energy expenditure in females and impairs glucose oxidation by increasing flux through aerobic glycolysis. Molecular Neurodegeneration, (2021); 16(1): 62.

Rajan KB, Skarupski KA, Rasmussen HE, Evans DA. Gene-environment interaction of body mass index and apolipoprotein E ?4 allele on cognitive decline. Alzheimer disease and associated disorders, (2014); 28(2): 134-140.

Hendrie HC, Murrell J, Baiyewu O, Lane KA, Purnell C, et al. APOE ?4 and the risk for Alzheimer disease and cognitive decline in African Americans and Yoruba. International Psychogeriatrics, (2014); 26(6): 977-985.

Rajabli F, Feliciano BE, Celis K, Hamilton-Nelson KL, Whitehead PL, et al. Ancestral origin of ApoE ?4 Alzheimer disease risk in Puerto Rican and African American populations. PLoS Genetics, (2018); 14(12): e1007791.

Midorikawa K, Soukaloun D, Akkhavong K, Southivong B, Rattanavong O, et al. APOE Genotype in the Ethnic Majority and Minority Groups of Laos and the Implications for Non-Communicable Diseases. PLoS One, (2016); 11(5): e0155072.

Pantelidis P, Lambert-Hammill M, Wierzbicki AS. Simple Sequence-specific-Primer-PCR Method To Identify the Three Main Apolipoprotein E Haplotypes. Clinical Chemistry, (2003); 49(11): 1945-1948.

Al-Jaf SMA. Frequencies of Apolipoprotein E polymorphism in Iraqi Kurdish population. Meta Gene, (2021); (28): 100867.

Foster CM, Kennedy KM, Rodrigue KM. Differential Aging Trajectories of Modulation of Activation to Cognitive Challenge in APOE ?4 Groups: Reduced Modulation Predicts Poorer Cognitive Performance. Journal of Neuroscience, (2017); 37(29): 6894-6901.

Husein N, Lumempouw SF, Ramli Y. Montreal cognitive assessment Versi Indonesia MoCA-INA untuk Skrining Gangguan Fungsi Kognitif. Neurona, (2010); 27(4): 1-13.

Trzepacz PT, Hochstetler H, Wang S, Walker B, Saykin AJ. Relationship between the Montreal Cognitive Assessment and Mini-mental State Examination for assessment of mild cognitive impairment in older adults. BMC Geriatrics, (2015); 15107.

Kapoor N, Arora S, Kalra S. Gender Disparities in People Living with Obesity – An Unchartered Territory. Journal of Mid-life Health, (2021); 12(2): 103-107.

Cooper AJ, Gupta SR, Moustafa AF, Chao AM. Sex/Gender Differences in Obesity Prevalence, Comorbidities, and Treatment. Current Obesity Reports, (2021); 10(4): 458-466.

Shields M, Tremblay MS, Connor Gorber S, Janssen I. Abdominal obesity and cardiovascular disease risk factors within body mass index categories. Health Reports, (2012); 23(2): 7-15.

Gierach M, Gierach J, Ewertowska M, Arndt A, Junik R. Correlation between Body Mass Index and Waist Circumference in Patients with Metabolic Syndrome. International Scholarly Research Notices, (2014); 2014514589.

Lentoor AG, Myburgh L. Correlation between Body Mass Index (BMI) and Performance on the Montreal Cognitive Assessment (MoCA) in a Cohort of Adult Women in South Africa. Behavioural Neurology, (2022); 2022(1):8994793.

Uranga RM, Keller JN. The Complex Interactions Between Obesity, Metabolism and the Brain. Frontiers in Neuroscience, (2019); 13513.

Wang C, Chan JS, Ren L, Yan JH. Obesity Reduces Cognitive and Motor Functions across the Lifespan. Neural Plasticity, (2016); 2016(1):2473081.

Umayal C, Sasirekha G, Suganthapriya S, Viji D, Niveditha P. Assessment of cognition in obese young adults. National Journal of Physiology, (2021); 9(1).

Forny-Germano L, De Felice FG, Vieira M. The Role of Leptin and Adiponectin in Obesity-Associated Cognitive Decline and Alzheimer’s Disease. Frontiers in Neuroscience, (2018); 121027.

Valladolid-Acebes I. Hippocampal Leptin Resistance and Cognitive Decline: Mechanisms, Therapeutic Strategies and Clinical Implications. Biomedicines, (2024); 12(11): 2422.

Josefsson M, Larsson M, Nordin S, Adolfsson R, Olofsson J. APOE-?4 effects on longitudinal decline in olfactory and non-olfactory cognitive abilities in middle-aged and old adults. Scientific Reports, (2017); 7(1): 1286.

Qiu C, Winblad B, Fratiglioni L. Cerebrovascular disease, APOE epsilon4 allele and cognitive decline in a cognitively normal population. Neurological Research, (2006); 28(6): 650-656.

Sun S, Fu J, Chen J, Pang W, Hu R, et al. ApoE type 4 allele affects cognitive function of aged population in Tianjin City, China. American Journal of Alzheimer’s Disease and Other Dementias, (2015); 30(5): 503-507.

Gui W, Qiu C, Shao Q, Li J. Associations of Vascular Risk Factors, APOE and TOMM40 Polymorphisms With Cognitive Function in Dementia-Free Chinese Older Adults: A Community-Based Study. Frontiers in Psychiatry, (2021); (12): 617773.

Suchy-Dicey A, Howard B, Longstreth WT, Jr., Reiman EM, Buchwald D. APOE genotype, hippocampus, and cognitive markers of Alzheimer’s disease in American Indians: Data from the Strong Heart Study. Alzheimer’s & Dementia: The Journal of The Alzheimer’s Association, (2022); 18(12): 2518-2526.

Farrer LA, Cupples LA, Haines JL, Hyman B, Kukull WA, 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 Networks, (1997); 278(16): 1349-1356.

Lim YY, Williamson R, Laws SM, Villemagne VL, Bourgeat P, et al. Effect of APOE Genotype on Amyloid Deposition, Brain Volume, and Memory in Cognitively Normal Older Individuals. Journal of Alzheimer’s Disease, (2017); 58(4): 1293-1302.

Marioni RE, Campbell A, Scotland G, Hayward C, Porteous DJ, et al. Differential effects of the APOE e4 allele on different domains of cognitive ability across the life-course. European Journal of Human Genetics, (2016); 24(6): 919-923.

Luck T, Then FS, Luppa M, Schroeter ML, Arélin K, et al. Association of the apolipoprotein E genotype with memory performance and executive functioning in cognitively intact elderly. Neuropsychology, (2015); 29(3): 382-387.




DOI: https://doi.org/10.62940/als.v13i2.2336

Refbacks

  • There are currently no refbacks.