RESEARCH PAPER
Homocysteine, antioxidant vitamins and lipids as biomarkers of neurodegeneration in Alzheimer’s disease versus non-Alzheimer’s dementia
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1
Department of Physiopathology, Institute of Rural Health, Lublin, Poland
2
Department of Neurodegenerative Diseases, Institute of Rural Health, Lublin, Poland
3
Department of Psychiatry Yale University School of Medicine, New Haven, USA
Corresponding author
Grzegorz Raszewski
Department of Physiopathology, Institute of Rural Health, Lublin, Poland
Ann Agric Environ Med. 2016;23(1):193-196
KEYWORDS
ABSTRACT
Introduction and objective:
Evidence for the benefit of antioxidants’ based therapeutic intervention in dementia are inconsistent. Parallel studies in disease forms of dementia different than Alzheimer’s are even less conclusive. In this study, the role of serum levels of homocysteine (tHcy), lipids and antioxidants in predicting the risk of cognitive decline in Alzheimer’s disease (AD) versus non-Alzheimer’s dementias (n-AD). The objective was to add to the ongoing cumulative research to establish the biochemical baseline for potential nutri-therapeutic intervention in different forms of dementia.
Material and Methods:
65 participants with dementia (DP-s) were divided into two groups: ADP – patients with Alzheimer’s disease and n-ADP – patients with dementia of a different etiology than primary neurodegenerative dementia in the course of Alzheimer’s disease. Cognitive function was assessed by Mini-Mental State Examination (MMSE) and related to plasma levels of tHcy, folate, vitamins B-6, B-12, lipids and vitamins A and E for both groups. Also examined were associations between cognitive impairment and several variables (age, education, duration of dementia) that might confound nutrition-cognition associations.
Results:
A significant reduction in serum vitamin A levels and elevation of total cholesterol levels were shown for the DP-s group compared to those in the control group. Moreover, significant differences were found in MMSE data and serum vitamin E and tHcy levels between patients with ADP and n-ADP. The scores for MMSE showed a correlation with the vitamin E levels and duration of dementia in the ADP group and/or correlation with tHcy, levels of vitamins A and/or E, and duration of dementia in the n-ADP group.
Conclusions:
The results obtained suggest that elevated serum tHcy and decreased levels of vitamins A and E are associated with an increased risk of non-Alzheimer’s dementias, although further studies involving a larger cohort are now needed to verify these results.
REFERENCES (23)
1.
Ferri CP, Prince M, Brayne C, BrodatyH, Fratiglioni L, Ganguli M, et al. Global prevalence of dementia: a Delphi consensus study. Lancet 2005; 366: 2112–2117.
2.
Pratico D. Oxidative stress hypothesis in Alzheimer’s disease: a reappraisal. Trends Pharmacol Sci. 2008; 12: 609–615.
3.
Savitha S, Tamilselvan J, Anusuyadevi M, Panneerselvam Ch. Oxidative stress on mitochondrial antioxidant defense system in the aging process: Role of dl-α-lipoic acid and l-carnitine. Clin Chim Acta. 2005; 355: 173–180.
4.
Evidence of oxidative stress in Alzheimer’s disease brain and antioxidant therapy: lights and shadows. Ann N Y Acad Sci. 2008; 1147: 70–78.
5.
Villa P, Bosco P, Ferri R, Perri C, Suriano R, Costantini B, et al. Fasting and post-methionine homocysteine levels in Alzheimers disease and vascular dementia Int J Vitam Nutr Res. 2009; 79(3): 166–172.
6.
Panza F, D’Introno A, Colacicco AM. Lipid metabolism in cognitive decline and dementia. Brain Res Rev. 2006; 51: 275–292.
7.
American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC, USA: American Psychiatric Association, 2000.
8.
McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer’s disease: Report of the NINCDS-ADRDA work group under the auspices of department of health and human services task force on Alzheimer’s disease. Neurology 1984; 34: 939–944.
9.
Folstein MF, Folstein SE. “Mini-Mental State:” a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975; 2: 189–198.
10.
Chwatko G, Bald E. Determination of different species of homocysteine in human plasma by high-performance liquid chromatography with ultraviolet detection. J Chromatogr A. 2002; 949: 141–151.
11.
Dunn JE, Weintraub S, Stoddard AN, Banks S. Serum a-tocopherol, concurrent and past vitamin E intake, and mild cognitive impairment. Neurology 2007; 68: 670–676.
12.
Cherubini A, Martin A, Andres-Lacueva C, DiIorio A, Lamponi M, Mecocci P. Vitamin E levels, cognitive impairment and dementia in older persons: the In CHIANTI study. Neurobiol Aging. 2005; 26: 987–994.
13.
Grodstein F, Chen J, Willet WC. High-dose antioxidant supplements and cognitive function in community-dwelling elderly women. Am J Clin Nutr. 2003; 77: 975–984.
14.
Engelhart MJ, Ruitenberg A, Meijer J, Kiliaan A, van Swieten JC, Hofman A, et al. Plasma levels of antioxidants are not associated with Alzheimer’s disease or cognitive decline. Dement Geriatr Cogn Disord. 2005; 19: 134–139.
15.
Lepara O, Alajbegovic A, Zaciragic A, Nakas-Icindic E, Valjevac A, Lepara D, et al. Elevated serum homocysteine level is not associated with serum C-reactive protein in patients with probable Alzheimer’s disease. J Neural Transm. 2009; 116(12): 1651–1656.
16.
Li L, Cao D, Desmond R, Rahman A, Lah J, Levey A, et al. Cognitive Performance and Plasma Levels of Homocysteine, Vitamin B 12, Folate and Lipids in Patients with Alzheimer Disease. Dement Geriatr Cogn Disord. 2008; 26: 384–390.
17.
Clarke R. B-vitamins and prevention of dementia. Proc Nutr Soc. 2008; 67: 75–81.
18.
Annerbo S, Kivipelto M, Lökk J. A prospective study on the development of Alzheimer’s disease with regard to thyroid-stimulating hormone and homocysteine. Dement Geriatr Cogn Disord. 2009; 28: 275–280.
19.
Kalmijn S, Launer L, Lindemans J, Bots ML, Hofman A, Breteler MM. Total homocysteine and cognitive decline in a community-based sample of elderly subjects: the Rotterdam Study. Am J Epidemiol. 1999; 150: 283–289.
20.
Tucker KL, Qiao N, Scott T, Rosenberg I, Spiro A. High homocysteine and low B vitamins predict cognitive decline in aging men: the Veterans Affairs Normative Aging Study. Am J Clin Nutr. 2005; 82: 627–635.
21.
Levine GN, Keaney JF, Vita JA. Cholesterol reduction in cardiovascular disease. Clinical benefits and possible mechanisms. N Engl J Med. 1995; 332: 512–521.
22.
van Exel E, de Craen AJ, Gussekloo J, Houx P, Bootsma-van der Wiel A, Macfarlane PW. et al. Association between high-density lipoprotein and cognitive impairment in the oldest old. Ann Neurol. 2002; 51: 716–721.
23.
Merched A, Xia Y, Visvikis S, Serot JM, Siest G. Decreased high-density lipoprotein cholesterol and serum apolipoprotein AI concentrations are highly correlated with the severity of Alzheimer’s disease. Neurobiol Aging. 2000; 21: 27–3.