RESEARCH PAPER
Cognitive functions, lipid profile, and Apolipoprotein E gene polymorphism in postmenopausal women
 
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1
Department for Health Problems of Ageing, Institute of Rural Health, Lublin, Poland
2
College of Public Health, Zielona Góra, Poland
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Department of Zoonoses, Institute of Rural Health, Lublin, Poland
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Department of Physiopathology, Institute of Rural Health, Lublin, Poland
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Faculty of Health, Catholic University, Ruzomberok, Slovakia
6
Institute of Statistics and Demography, School of Economics, Warsaw, Poland
 
Ann Agric Environ Med. 2015;22(2):313–319
KEYWORDS
ABSTRACT
The objective of the study was investigation of the relationship between cognitive functions and lipid profile, BMI and change of body weight in postmenopausal women carriers of Apolipoprotein E gene polymorphisms (APOE). A group of 170 women was recruited to the study. The inclusion criteria were: minimum of two years after the last menstruation, FSH concentration 30 U/ml and no signs of dementia on the Montreal Cognitive Assessment (MoCA). A computerized battery of Central Nervous System Vital Signs (CNS VS) was used for diagnostic cognitive functions. APOE genotype was performed by multiplex PCR. In blood plasma were determined: triglycerides, total cholesterol and its fractions: HDL cholesterol and LDL cholesterol. Statistical analysis was performed using two-way analysis of variance in STATISTICA software. In the postmenopausal women examined, the carrier state of APOE gene polymorphism was associated with the level of triglycerides, and results concerning three cognitive functions: executive functions, psychomotor speed, and cognitive flexibility. Loss of body weight in postmenopausal women was related with lower results in neurocognitive index and the majority of cognitive functions. The results concerning cognitive functions in postmenopausal women in the study were not significantly related with lipid profile. Significant differences were observed according to APOE gene polymorphism in correlations between LDL/HDL and CHOL/HDL ratios, and results in the processing speed and reaction time, as well as between the BMI and results in processing speed in the postmenopausal women examined.
 
REFERENCES (25)
1.
Bojar I, Gustaw-Rothenberg K, Owoc A. Zaburzenia funkcji poznawczych po menopauzie – problem ciągle aktualny. Prz Menopauz. 2011; 10(1): 68–72 (in Polish).
 
2.
Fillit H, Nash DT, Rundek T, Zuckerman A. Cardiovascular risk factors and dementia. Am J Geriatr Pharmacother. 2008; 6(2): 100–118.
 
3.
Yaffe K. Metabolic syndrome and cognitive disorders: is the sum greater than its parts? Alzheimer Dis Assoc Disord. 2007; 21(2): 167–171.
 
4.
Dickstein DL, Walsh J, Brautigam H, Stockton SD Jr, Gandy S, Hof PR. Role of vascular risk factors and vascular dysfunction in Alzheimer’s disease. Mt Sinai J Med. 2010; 77: 82–102.
 
5.
Wright CB, Festa JR, Paik MC, Schmiedigen A, Brown TR, Yoshita M, DeCarli C, Sacco R, Stern Y. White matter hyperintensities and subclinical infarction: associations with psychomotor speed and cognitive flexibility. Stroke 2008;3 9: 800–805.
 
6.
Tiehuis AM, Vincken KL, van den Berg E, Hendrikse J, Manschot SM, Mali WP, Kappelle LJ, Biessels GJ. Cerebral perfusion in relation to cognitive function and type 2 diabetes. Diabetologia 2008; 51: 1321–1326.
 
7.
van den Berg E, Kloppenborg RP, Kessels RP, Kappelle LJ, Biessels GJ. Type 2 diabetes mellitus, hypertension, dyslipidemia and obesity: a systematic comparison of their impact on cognition. Biochim Biophys Acta. 2009; 1792: 470–481.
 
8.
Norberg J, Graff C, Almkvist O, Ewers M, Frisoni GB, Frölich L, Hampel H, Jones RW, Kehoe PG, Lenoir H, Minthon L, Nobili F, Olde Rikkert M, Rigaud AS, Scheltens P, Soininen H, Spiru L, Tsolaki M, Wahlund LO, Vellas B, Wilcock G, Elias-Sonnenschein LS, Verhey FR, Visser PJ. Regional differences in effects of APOE ε4 on cognitive impairment in non-demented subjects. Dement Geriatr Cogn Disord. 2011; 32(2) 135–142.
 
9.
Caselli RJ. Phenotypic differences between apolipoprotein E genetic subgroups: research and clinical implications. Alzheimers Res Ther. 2012; 4(3): 20.
 
10.
Mendel T, Gromadzka G. Polimorfizm genu apolipoproteiny E (APOE) a ryzyko i rokowanie w krwotokach mózgowych spowodowanych przez mózgową angiopatię amyloidową. Neurol Neurochir Pol. 2010; 44(6): 591–597.
 
11.
Nyholt DR, Yu CE, Visscher PM. On Jim Watson’s APOE status: genetic information is hard to hide. Eur J Hum Genet. 2009; 17: 147–149.
 
12.
Scarmeas N, Luchsinger JA, Stern Y, Gu Y, He J, Decarli C, Brown T, Brickman AM. Mediterranean diet and magnetic resonance imaging-assessed cerebrovascular disease. Ann Neurol. 2011; 69(2): 257–268.
 
13.
Jiang Q, Lee CY, Mandreka, S, Wilkinson B, Cramer P, Zelcer N, Mann K, Lamb B, Willson TM, Collins JL, Richardson JC, Smith JD, Comery TA, Riddell D, Holtzman DM, Tontonoz P, Landreth GE. ApoE promotes the proteolytic degradation of Abeta. Neuron. 2008; 58: 681–693.
 
14.
Arbones-Mainar JM, Johnson LA, Altenburg MK, Maeda N. Differential modulation of diet-induced obesity and adipocyte functionality by human apolipoprotein E3 and E4 in mice. Int J Obes (Lond). 2008; 32(10): 1595–1605.
 
15.
Magierska J, Magierski R, Sobow T, Kloszewska I. The Polish adaptation of the Montreal Cognitive Assessment (MoCA) and preliminary results of its clinical utility in the screening for cognitive impairment. ICAD Conference Poster; 2008; Chicago.
 
16.
Gualtieri CT, Johnson LG. Reliability and validity of a computerized neurocognitive test battery, CNS Vital-Signs. Arch Clin Neuropsychol. 2006; 21(7): 623–643.
 
17.
Young GY, Jong YK, Su JP, Suhng WK, Ok-Hee J, Doo-Sik K. Apolipoprotein E genotyping by multiplex tetra-primer amplification refractory mutation system PCR in single reaction tube. J Biotech. 2007; 131: 106–110.
 
18.
Small GW. Use of neuroimaging to detect early brain changes in people at genetic risk for Alzheimer’s disease. Adv Drug Deliv Rev. 2002; 54: 1561–1566.
 
19.
Lin SK, Kao JT, Tsai SM,Tsai LY, Lin MN, Lai ChJ, Zhong WL. Association of Apolipoprotein E Genotypes with Serum Lipid Profiles in a Healthy Population of Taiwan. Ann Clin Lab Sci. 2004; 34(4): 443–448.
 
20.
Bennet AM, Di Angelantonio E, Ye Z, Wensley F, Dahlin A, Ahlbom A, Keavney B, Collins R, Wiman B, de Faire U, Danesh J. Association of apolipoprotein E genotypes with lipid levels and coronary risk. JAMA. 2007; 298(11): 1300–1311.
 
21.
Moon K, Sung SH, Chang YK, Park IK, Paek YM, Kim SG, Choi TI, Jin YW. The association between Apolipoprotein E genotype and lipid profiles in healthy woman workers. J Prev Med Public Health. 2010; 43(3): 213–221.
 
22.
Sertic J, Juricic L, Ljubic H, Bozina T, Lovric J, Markeljevic J, Jelakovic B, Merkler M, Reiner Z. Variants of ESR1, APOE, LPL and IL-6 loci in young healthy subjects: association with lipid status and obesity. BMC Research Notes 2009; 2: 203.
 
23.
Katerina H, Michaela S, Michal V, Helena S, Jana Z, Jaroslav H, Richard C. Interaction of common sequence variants and selected risk factors in determination of HDL cholesterol levels. Clin Biochem. 2010; 43(9): 754–758.
 
24.
Benito-León J, Mitchell AJ, Hernández-Gallego J, Bermejo-Pareja F. Obesity and impaired cognitive functioning in the elderly: a population-based cross-sectional study (NEDICES). Eur J Neurol. 2013; 20(6): 899-e77.
 
25.
Kerwin DR, Gaussoin SA, Chlebowski RT, Kuller LH, Vitolins M, Coker LH, Kotchen JM, Nicklas BJ, Wassertheil-Smoller S, Hoffmann RG, Espeland MA. Women’s Health Initiative Memory Study, Interaction between body mass index and central adiposity and risk of incident cognitive impairment and dementia: results from the Women’s Health Initiative Memory Study. J Am Geriatr Soc. 2011; 59(1): 107–112.
 
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