Body mass index, genetic susceptibility, and Alzheimer's disease: a longitudinal study based on 475,813 participants from the UK Biobank.

Tytuł:: Body mass index, genetic susceptibility, and Alzheimer's disease: a longitudinal study based on 475,813 participants from the UK Biobank.
Autorzy:: Yuan S; Department of Neurology, The First Affiliated Hospital of Jinan University, No. 613, Huangpu Road West, Guangzhou, 510630, Guangdong, China.
Wu W; School of Public Health, Jiaotong University Health Science Center, Shaanxi Province, Xi'an, 710061, China.
Ma W; School of Public Health, Jiaotong University Health Science Center, Shaanxi Province, Xi'an, 710061, China.
Huang X; Department of Neurology, The First Affiliated Hospital of Jinan University, No. 613, Huangpu Road West, Guangzhou, 510630, Guangdong, China.
Huang T; Department of Clinical Research, The First Affiliated Hospital of Jinan University, No. 613, Huangpu Road West, Guangzhou, 510630, Guangdong, China.
Peng M; Department of Neurology, The First Affiliated Hospital of Jinan University, No. 613, Huangpu Road West, Guangzhou, 510630, Guangdong, China.
Xu A; Department of Neurology, The First Affiliated Hospital of Jinan University, No. 613, Huangpu Road West, Guangzhou, 510630, Guangdong, China. .
Lyu J; Department of Clinical Research, The First Affiliated Hospital of Jinan University, No. 613, Huangpu Road West, Guangzhou, 510630, Guangdong, China. .; Guangdong Provincial Key Laboratory of Traditional Chinese Medicine Informatization, Guangzhou, Guangdong, China. .
Źródło:: Journal of translational medicine [J Transl Med] 2022 Sep 09; Vol. 20 (1), pp. 417. Date of Electronic Publication: 2022 Sep 09.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: [London] : BioMed Central, 2003-
MeSH Terms:: Alzheimer Disease*/genetics
Genetic Predisposition to Disease*
Aged ; Biological Specimen Banks ; Body Mass Index ; Humans ; Longitudinal Studies ; Middle Aged ; United Kingdom
References:: Pharmaceuticals (Basel). 2021 Jan 11;14(1):. (PMID: 33440796)
J Evid Based Med. 2020 Feb;13(1):57-69. (PMID: 32086994)
Lancet. 2008 Feb 16;371(9612):569-78. (PMID: 18280327)
Front Cell Neurosci. 2017 Mar 07;11:64. (PMID: 28326017)
Mil Med Res. 2021 Aug 11;8(1):44. (PMID: 34380547)
Arch Neurol. 2010 Apr;67(4):428-33. (PMID: 20385908)
Ann Neurol. 2008 Nov;64(5):492-8. (PMID: 19067364)
Arthritis Res Ther. 2015 Mar 29;17:86. (PMID: 25890172)
Alzheimers Dement. 2015 Dec;11(12):1439-1451. (PMID: 26079416)
Eur Heart J. 2021 Sep 7;42(34):3388-3403. (PMID: 34333589)
Eur Heart J. 2020 Mar 14;41(11):1182-1189. (PMID: 31848595)
Ageing Res Rev. 2016 Jan;25:13-23. (PMID: 26607411)
J Alzheimers Dis. 2020;75(2):385-395. (PMID: 32310176)
J Alzheimers Dis. 2018;65(3):781-791. (PMID: 28697560)
Lancet. 2011 Feb 12;377(9765):557-67. (PMID: 21295846)
Addiction. 2014 Sep;109(9):1462-71. (PMID: 24716453)
Cold Spring Harb Perspect Med. 2011 Sep;1(1):a006189. (PMID: 22229116)
J Alzheimers Dis. 2018;64(3):671-688. (PMID: 29991138)
Eur J Neurol. 2018 Jan;25(1):59-70. (PMID: 28872215)
Lancet Diabetes Endocrinol. 2015 Jun;3(6):431-436. (PMID: 25866264)
Int J Epidemiol. 2003 Feb;32(1):1-22. (PMID: 12689998)
Biomed Pharmacother. 2020 Jun;126:110102. (PMID: 32199223)
Transl Psychiatry. 2018 May 18;8(1):99. (PMID: 29777097)
Sleep Med. 2021 May;81:401-409. (PMID: 33819843)
Lancet Neurol. 2011 Sep;10(9):819-28. (PMID: 21775213)
Neurosci Biobehav Rev. 2019 Aug;103:73-80. (PMID: 31207254)
J Cell Biol. 2018 Feb 5;217(2):459-472. (PMID: 29196460)
Philos Trans R Soc Lond B Biol Sci. 2013 Dec 02;369(1633):20130155. (PMID: 24298156)
Mol Psychiatry. 2021 Oct;26(10):5669-5689. (PMID: 32132650)
Nat Rev Neurosci. 2009 May;10(5):333-44. (PMID: 19339974)
Circulation. 2017 Feb 28;135(9):850-863. (PMID: 28034901)
J Alzheimers Dis. 2010;20(1):313-22. (PMID: 20164583)
Dement Neurocogn Disord. 2022 Jan;21(1):30-41. (PMID: 35154338)
J Neuroinflammation. 2019 May 25;16(1):110. (PMID: 31128596)
Hum Mol Genet. 2014 Sep 15;23(R1):R89-98. (PMID: 25064373)
Lancet. 2020 Aug 8;396(10248):413-446. (PMID: 32738937)
Nature. 2018 Oct;562(7726):203-209. (PMID: 30305743)
Res Synth Methods. 2019 Dec;10(4):486-496. (PMID: 30861319)
Sci Adv. 2021 Jul 28;7(31):. (PMID: 34321204)
Mech Ageing Dev. 1999 Mar 1;107(2):123-36. (PMID: 10220041)
Int J Obes (Lond). 2011 Feb;35(2):300-8. (PMID: 20714329)
Nat Genet. 2019 Mar;51(3):404-413. (PMID: 30617256)
Curr Opin Clin Nutr Metab Care. 2009 Jan;12(1):15-21. (PMID: 19057182)
Lancet Neurol. 2016 Apr;15(5):455-532. (PMID: 26987701)
PLoS Med. 2015 Mar 31;12(3):e1001779. (PMID: 25826379)
Circulation. 2019 Sep 10;140(11):e596-e646. (PMID: 30879355)
Obesity (Silver Spring). 2013 Jan;21(1):E51-5. (PMID: 23401370)
Curr Epidemiol Rep. 2017;4(4):330-345. (PMID: 29226067)
Biol Psychiatry. 2021 Apr 15;89(8):817-824. (PMID: 33766239)
J Am Geriatr Soc. 2008 Dec;56(12):2261-6. (PMID: 19093925)
Arch Neurol. 2009 Mar;66(3):336-42. (PMID: 19273752)
Eur Heart J. 2021 Mar 21;42(12):1136-1143. (PMID: 33313747)
J Clin Endocrinol Metab. 2017 Jul 1;102(7):2310-2320. (PMID: 28609829)
Obes Rev. 2011 May;12(5):e426-37. (PMID: 21348917)
Ann Neurol. 2021 Jan;89(1):177-181. (PMID: 32951248)
Orv Hetil. 2007 Sep 30;148(39):1827-36. (PMID: 17890170)
Neuron. 2017 Dec 6;96(5):1024-1032.e3. (PMID: 29216449)
Grant Information:: MC_PC_17228 United Kingdom MRC_ Medical Research Council; MC_QA137853 United Kingdom MRC_ Medical Research Council
Contributed Indexing:: Keywords: Alzheimer's disease (AD); Bidirectional Mendelian randomization (MR); Body mass index (BMI); Genetic susceptibility; UK Biobank
Entry Date(s):: Date Created: 20220909 Date Completed: 20220913 Latest Revision: 20230308
Update Code:: 20240104
PubMed Central ID:: PMC9463868
DOI:: 10.1186/s12967-022-03621-2
PMID:: 36085169
: Czasopismo naukowe

Pełny tekst

Background: The association between body mass index (BMI) and Alzheimer's disease (AD) remains controversial. Genetic and environmental factors are now considered contributors to AD risk. However, little is known about the potential interaction between genetic risk and BMI on AD risk.
Objective: To study the causal relationship between BMI and AD, and the potential interaction between AD genetic risk and BMI on AD risk.
Methods and Results: Using the UK Biobank database, 475,813 participants were selected for an average follow-up time of more than 10 years.
Main Findings: 1) there was a nonlinear relationship between BMI and AD risk in participants aged 60 years or older (p for non-linear < 0.001), but not in participants aged 37-59 years (p for non-linear = 0.717) using restricted cubic splines; 2) for participants aged 60 years and older, compared with the BMI (23-30 kg/m 2 ) group, the BMI (< 23 kg/m 2 ) group was associated with a higher AD risk (HR = 1.585; 95% CI 1.304-1.928, p < 0.001) and the BMI (> 30 kg/m 2 ) group was associated with a lower AD risk (HR = 0.741; 95% CI 0.618-0.888, p < 0.01) analyzed using the Cox proportional risk model; 3) participants with a combination of high AD genetic risk score (AD-GRS) and BMI (< 23 kg/m 2 ) were associated with the highest AD risk (HR = 3.034; 95% CI 2.057-4.477, p < 0.001). In addition, compared with the BMI (< 23 kg/m 2 ), the higher BMI was associated with a lower risk of AD in participants with the same intermediate or high AD-GRS; 4) there was a reverse causality between BMI and AD when analyzed using bidirectional Mendelian randomization (MR).
Conclusion: There was a reverse causality between BMI and AD analyzed using MR. For participants aged 60 years and older, the higher BMI was associated with a lower risk of AD in participants with the same intermediate or high AD genetic risk. BMI (23-30 kg/m 2 ) may be a potential intervention for AD.
(© 2022. The Author(s).)

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