Late life vascular risk factors and their association with dementia and Alzheimer’s disease

Updata:01-01-1970

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By:Abeer Abdelzaher Ibrahim, Hussain Younes Haji, Azza Mohamed Hassan

DOI: https://doi.org/10.30564/jgm.v4i1.4548

Abstract:

Background : Epidemiological studies have demonstrated associations between higher levels of vascular risk factors  in midlife  and  later development of  dementia, particularly Alzheimer's disease (AD). However, in elderly subjects with dementia, some studies have shown that these associations may decrease or even reverse. Therefore , our study aimed to find the association between late life cardiovascular risk factors and neurodegenerative dementia in general and AD in particular. Methods :It is a retrospective case control study using electronic medical records  that included   elderly patients  that were reviewed in  Ahmadi hospital  geriatric  clinic , Kuwait , from the period of 1/7/2019 to 1/2/2020. Two hundred and three (203) elderly  patients  with neurodegenerative  dementia  (study group) were recruited for this retrospective study and compared to two hundred and one (201) controls with normal cognition for the presence of vascular risk factors.Results :The study included 404 subjects .Age ranged from 60 to 107 years (mean age 78.79, ±  8.13 SD). AD was found to be the most prevalent  type  of  dementia in the study group  , as 49.3 % (100/203) of the demented patients were diagnosed with AD. No significant  statistical association was found between vascular risk factors  and  dementia (P>0.05) , except for obesity which showed negative association (P<0.001). Regarding AD , no statistical significance was found between AD and diabetes, hyperlipidemia, smoking nor atrial fibrillation. On the other hand, we  found obesity  and hypertension  more prevalent in the normal cognition group (negative association with P value <0.001,0.05 respectively).    Conclusion : The results of our study support an emerging concept  that, while elevated levels of vascular risk factors in midlife increase the risk of development of dementia and AD later in life, once dementia begins , these associations may be diminished or reversed in the elderly

 

References:

[1]Kalaria, R.N., Maestre, G.E., Arizaga, R., et al., 2008. Alzheimer’s disease and vascular dementia in developing countries: prevalence, management, and risk factors. The Lancet Neurology. 7(9), 812-826. [2]Horton, R., 2012. GBD 2010: understanding disease, injury, and risk. The Lancet. 380(9859), 2053-2054. [3]Simpson, J.R., 2014. DSM-5 and neurocognitive disorders. Journal of the American Academy of Psychiatry and the Law Online. 42(2), 159-164. [4]Ferri, C.P., Prince, M., Brayne, C., et al., 2005. Global prevalence of dementia: a Delphi consensus study. Alzheimer’s Disease International. Lancet. 366(9503), 2112-2117. [5]Fratiglioni, L., Launer, L.J., Andersen, K., et al., 2000. Incidence of dementia and major subtypes in Europe: a collaborative study of population-based cohorts. Neurologic diseases in the elderly research group. Neurology. 54(11 suppl 5), S10-S15. [6]Vijayan, M., Reddy, P.H., 2016. Stroke, Vascular Dementia, and Alzheimer’s Disease: Molecular Links. Journal of Alzheimers Disease. 54(2), 427-443. [7]Elibol, B., Kilic, U., 2018. High Levels of SIRT1 Expression as a Protective Mechanism Against Disease-Related Conditions. Frontiers in Endocrinology. DOI: https://doi.org/10.3389/fendo.2018.00614 [8]White, H., Pieper, C., Schmader, K., 1998. The association of weight change in Alzheimer’s disease with severity of disease and mortality: a longitudinal analysis. Journal of the American Geriatrics Society. 46, 1223-1227. [9]Posner, H., Tang, M., Luchsinger, J., et al., 2002. The relationship of hypertension in the elderly to AD, vascular dementia, and cognitive function. Neurology. 58, 1175-1181. [10]Mielke, M., Zandi, P., Sjogren, M., et al., 2005. High total cholesterol levels in late life associated with a reduced risk of dementia. Neurology. 64, 1689-1695. [11]Stewart, R., Masaki, K., Xue, Q., et al., 2005. A 32- year prospective study of change in body weight and incident dementia: the Honolulu-Asia Aging Study. JAMA Neurology. 62, 55-60. [12]Rosano, C., Newman, A., 2006. Cardiovascular disease and risk of Alzheimer’s disease. Neurological Research. 28, 612-620. [13]Emmerzaal, T.L., Kiliaan, A.J., Gustafson, D.R., 2015. 2003-2013: a decade of body mass index, Alzheimer’s disease, and dementia. Journal of Alzheimers Disease. 43, 739-755. [14]Gu, Y., Scarmeas, N., Cosentino, S., et al., 2014. Change in body mass index before and after Alzheimer’s disease onset. Current Alzheimer Research. 11, 349-356. [15]Buchman, A.S., Schneider, J.A., Wilson, R.S., et al., 2006. Body mass index in older persons is associated with Alzheimer disease pathology. Neurology. 67, 1949-1954. [16]Beach, T.G., Maarouf, C.L., Brooks, R.G., et al., 2011. Reduced clinical and postmortem measures of cardiac pathology in subjects with advanced Alzheimer’s Disease. BMC Geriatrics. 11, 3. [17]Singh, S., Mulley, G.P., Losowsky, M.S., 1988. Why are Alzheimer patients thin? Age Ageing. 17, 21-28. [18]Sanderson, M., Wang, J., Davis, D.R., et al., 2002. Co-morbidity associated with dementia. American Journal of Alzheimers Disease & Other Dementias. 17, 73-78. [19]Wolf-Klein, G.P., Siverstone, F.A., Brod, M.S., et al., 1988. Are Alzheimer patients healthier? Journal of the American Geriatrics Society. 36, 219-224. [20]Kiliaan, A.J., Gustafson, D.R., 2015. A decade of body mass index, Alzheimer’s disease, and dementia. Emmerzaal TL. Journal of Alzheimers Disease. 43(3), 739-755. [21]Beach, T.G., 1987. The history of Alzheimer’s disease: three debates. Journal of the History of Medicine and Allied Sciences. 42, 327-349. DOI: https://doi.org/10.1093/jhmas/42.3.327 [22]Corder, E.H., Saunders, A.M., Strittmatter, W.J., et al., 1993. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science. 261, 921-923. DOI:https://doi.org/10.1126/science.8346443 [23]Nash, D.T., Fillit, H., 2006. Cardiovascular disease risk factors and cognitive impairment. American Journal of Cardiology. 97, 1262-1265. DOI: https://doi.org/10.1016/j.amjcard.2005.12.031 [24]Wolozin, B., Bednar, M.M., 2006. Interventions for heart disease and their effects on Alzheimer’s disease. Neurological Research. 28, 630-636. DOI: https://doi.org/10.1179/016164106X130515 [25]Luchsinger, J.A., Reitz, C., Honig, L.S., et al., 2005. Aggregation of vascular risk factors and risk of incident Alzheimer disease. Neurology. 65, 545-551. DOI: https://doi.org/10.1212/01.wnl.00001729 14.08967.dc [26]Starr, J.M., Whalley, L.J., Inch, S., et al., 1993. Blood pressure and cognitive function in healthy old people. Journal of the American Geriatrics Society. 41, 753- 756. [27]Seux, M.L., Thijs, L., Forette, F., et al., 1998. Correlates of cognitive status of old patients with isolated systolic hypertension: the Syst-Eur Vascular Dementia Project. Journal of Hypertension. 16, 963- 969. [28]Farmer, M.E., White, L.R., Abbott, R.D., et al., 1987. Blood pressure and cognitive performance. The Framingham Study. American Journal of Epidemiology. 126, 1103-1114. [29]Scherr, P.A., Hebert, L.E., Smith, L.A., et al., 1991. Relation of blood pressure to cognitive function in the elderly. American Journal of Epidemiology. 134, 1303-1315. [30]Tzourio, C., Dufouil, C., Ducimetiere, P., et al., 1999. Cognitive decline in individuals with high blood pressure: a longitudinal study in the elderly. EVA Study Group. Epidemiology of Vascular Aging. Neurology. 53, 1948-1952. [31]Elias, M.F., Wolf, P.A., D’Agostino, R.B., et al., 1993. Untreated blood pressure level is inversely related to cognitive functioning: the Framingham Study. American Journal of Epidemiology. 138, 353- 364. [32]Hanon, O., Latour, F., Seux, M.L., et al., 2005. REAL.FR Group. Evolution of blood pressure in patients with Alzheimer’s disease: a one year survey of a French Cohort (REAL.FR) Journal of Nutrition Health & Aging. 9, 106-111. [33]Verghese, J., Lipton, R.B., Hall, C.B., et al., 2003. Low blood pressure and the risk of dementia in very old individuals. Neurology. 61, 1667-1672. [34]Wang, P.N., Yang, C.L., Lin, K.N., et al., 2004. Weight loss, nutritional status and physical activity in patients with Alzheimer’s disease. A controlled study. Journal of Neurology. 251, 314-320. DOI:https://doi.org/10.1007/s00415-004-0316-4 [35]Stegmayer, B., Asplund, K., 1995. Diabetes as a risk factor for stroke. A population perspective. Diabetologia. 38, 1061-1068. [36]Xue, M., Xu, W., Ou, Y.N., et al., 2019. Diabetes mellitus and risks of cognitive impairment and dementia: A systematic review and meta-analysis of 144 prospective studies. Ageing Research Reviews. 55, 100944. [37]Zhang, J., Chen, C., Hua, S., et al., 2017. An updated meta-analysis of cohort studies: Diabetes and risk of Alzheimer’s disease. Diabetes Research & Clinical Practice. 124, 41-47. [38]Yaffe, K., Vittinghoff, E., Hoang, T., et al., 2021. Cardiovascular Risk Factors Across the Life Course and Cognitive Decline: A Pooled Cohort Study. Neurology. 96(17), e2212-e2219. [39]Ganguli, M., Jia, Y., Hughes, T.F., et al., 2019. Mild cognitive impairment that does not progress to dementia: a population-based study. Journal of theAmerican Geriatrics Society. 67, 232-238. DOI:https://doi.org/10.1111/jgs.15642 [40]Viticchi, G., Falsetti, L., Vernieri, F., et al., 2012. Vascular predictors of cognitive decline in patients with mild cognitive impairment. Neurobiology of Aging. 33, 1127.e11127.e9. DOI:https://doi.org/10.1016/j.neurobiolaging.2011. 11.027 [41]Curb, J.D., Rodriguez, B.L., Abbott, R.D., et al., 1999. Longitudinal association of vascular and Alzheimer’s dementias, diabetes, and glucose tolerance. Neurology. 52, 971-975. [42]Wang, H.L., Wang, Y.Y., Liu, X.G., et al., 2016. Cholesterol, 24-Hydroxy cholesterol, and 27-Hydroxycholesterol as Surrogate Biomarkers in Cerebrospinal Fluid in Mild Cognitive Impairment and Alzheimer’s Disease: A Meta-Analysis. Journal of Alzheimer’s Disease. 51, 45-55. [43]Shibata, N., Ohnuma, T., Higashi, S., et al., 2005. No genetic association between PCSK9 polymorphisms and Alzheimer’s disease and plasma cholesterol level in Japanese patients. Psychiatric Genetics. 15, 239. [44]WHO, 2019. Risk reduction of cognitive decline and dementia: WHO guidelines. World Health Organization, Geneva. [45]Prince, M., Albanese, E., Guerchet, M., et al., 2014. World Alzheimer Report 2014. Dementia and risk reduction: an analysis of protective and modifiable factors. Alzheimer’s Disease International, London 2014 View in ArticleGoogle Scholar. [46]Anstey, K.J., Lipnicki, D.M., Low, L.F., 2008. Cholesterol as a risk factor for dementia and cognitive decline: a systematic review of prospective studies with meta-analysis. The American Journal of Geriatric Psychiatry. 16, 343-354. [47]Shepardson, N.E., Shankar, G.M., Selkoe, D.J., 2011. Cholesterol level and statin use in Alzheimer disease: I. Review of epidemiological and preclinical studies. Archives of Neurology. 68, 1239-1244. [48]Anstey, K.J., Ashby-Mitchell, K., Peters, R., 2017. Updating the evidence on the association between serum cholesterol and risk of late-life dementia: review and meta-analysis. Journal of Alzheimers Disease. 56, 215-228. [49]Hersi, M., Irvine, B., Gupta, P., et al., 2017. Risk factors associated with the onset and progression of Alzheimer’s disease: a systematic review of the evidence. Neurotoxicology. 61, 143-187. [50]Ott, A., Slooter, A.J., Hofman, A., et al., 1998. Smoking and risk of dementia and Alzheimer’s disease in a population-based cohort study: the Rotterdam Study. Lancet. 351, 1840-1843. [51]Merchant, C., Tang, M.X., Albert, S., et al., 1999. The influence of smoking on the risk of Alzheimer’s disease. Neurology. 52, 1408-1412. [52]Calle, E.E., Thun, M.J., Petrelli, J.M., et al., 1999. Body-mass index and mortality in a prospective cohort of U.S. adults. New England Journal of Medicine. 341, 1097-1105. DOI:https://doi.org/10.1056/NEJM1999100734-11501 [53]Calle, E.E., Rodriguez, C., Walker-Thurmond, K., et al., 2003. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. New England Journal of Medicine. 348, 1625- 1638. DOI:https://doi.org/10.1056/NEJMoa021423 [54]Fitzpatrick, A.L., Kuller, L.H., Lopez, O.L., et al., 2009. Midlife and late-life obesity and the risk of dementia: cardiovascular health study. Archives of Neurology. 66, 336-342. DOI:https://doi.org/10.1001/archneurol.2008.582 [55]Cournot, M., Marquié, J.C., Ansiau, D., et al., 2006. Relation between body mass index and cognitive function in healthy middle-aged men and women. Neurology. 67, 1208. [56]Albanese, E., Davis, B., Jonsson, P.V., et al., 2015. Overweight and Obesity in Midlife and Brain Structure and Dementia 26 Years Later: The AGES -Reykjavik Study. American Journal of Epidemiology. 181, 672. [57]Burns, J.M., Johnson, D.K., Watts, A., et al., 2010. Reduced lean mass in early Alzheimer disease and its association with brain atrophy. Archives of Neurology. 67, 428. [58]Alhurani, R.E., Vassilaki, M., Aakre, J.A., et al., 2016. Decline in Weight and Incident Mild Cognitive Impairment: Mayo Clinic Study of Aging. JAMA Neurol. 73, 439-446. DOI:https://doi.org/10.1001/jamaneurol.2015.4756 [59]Gao, S., Nguyen, J.T., Hendrie, H.C., et al., 2011. Accelerated weight loss and incident dementia in an elderly African-American cohort. Journal of the American Geriatrics Society. 59, 18-25. DOI:https://doi.org/10.1111/j.1532-5415.2010. 03169.x [60]Müller, S., Preische, O., Sohrabi, H.R., et al., 2017. Decreased body mass index in the preclinical stage of autosomal dominant Alzheimer’s disease. Scientific Reports. 7, 1225. DOI:https://doi.org/10.1038/s41598-017-01327-w [61]Landin, K., Blennow, K., Wallin, A., et al., 1993. Low blood pressure and blood glucose levels in Alzheimer’s disease: evidence for a hypometabolicdisorder? Journal of Internal Medicine. 233(4), 357- 363. [62]Singh, S., Mulley, G.P., Losowsky, M.S., 1988. Why are Alzheimer patients thin? Age Ageing. 17, 21-28. [63]Markus, H.S., Tomkins, A.M., Stern, G.M., 1993. Increased prevalence of undernutrition in Parkinson’s disease and its relationship to clinical disease parameters. Journal of Neural Transmission Parkinsons Disease. 5, 117-125. [64]Jaafar, A.F., Gray, W.K., Porter, B., et al., 2010. A cross-sectional study of the nutritional status of community-dwelling people with idiopathic Parkinson’s disease. Bmc Neurology. 10, 124. [65]Yu, W., Qin, J.J., Chen, Ch.J., et al., 2018. Moderate calorie restriction attenuates ageassociated alterations and improves cardiac function by increasing SIRT1 and SIRT3 expression.Molecular Medicine Reports. pp. 4087-4094. DOI:https://doi.org/10.3892/mmr.2018.9390 [66]Irina, A., Seppo, H., Arto, M., et al., 1999. Beta-amyloid load is not influenced by the severity of cardiovascular disease in aged and demented patients. Stroke. 30, 613-618. [67] Sanderson, M., Wang, J., Davis, D.R., et al., 2002. Co-morbidity associated with dementia. American Journal of Alzheimers Disease & Other Dementias. 17, 73-78. DOI:https://doi.org/10.1177/153331750201700210

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