Please wait a minute...
 Home  About the Journal Editorial Board Aims & Scope Peer Review Policy Subscription Contact us
 
Early Edition  //  Current Issue  //  Open Special Issues  //  Archives  //  Most Read  //  Most Downloaded  //  Most Cited
Aging and disease
Orginal Article |
Physical Activity and Alzheimer’s Disease: A Narrative Review
Piotr Gronek1, Stefan Balko2, Joanna Gronek1, Adam Zajac3, Adam Maszczyk4, Roman Celka1, Agnieszka Doberska1, Wojciech Czarny5, Robert Podstawski6, Cain C. T. Clark7,*, Fang Yu8
1Faculty of Physical Education, Sport and Rehabilitation, Poznan University of Physical Education, Poland.
2Department of Physical Education and Sport, Faculty of Education, Jan Evangelista Purkyne University in Usti nad Labem, Czech Republic.
3Department of Physical Education, University of Physical Education and Sport, Gdansk, Poland.
4Department of Methodology and Statistics, The Jerzy Kukuczka Academy of Physical Education in Katowice, Katowice, Poland.
5Faculty of Physical Education, Department of Human Sciences, University of Rzeszow, ul. Towarnickiego 3, 35-959 Rzeszów, Poland.
6Faculty of Environmental Sciences, University of Warmia and Mazury in Olsztyn, Olsztyn, Poland.
7Faculty of Health and Life Sciences, Coventry University, Coventry, CV1 5FB, United Kingdom.
8School of Nursing, University of Minnesota, Minneapolis, MN 55455, USA
Download: PDF(397 KB)   HTML
Export: BibTeX | EndNote | Reference Manager | ProCite | RefWorks    
Abstract  

Although age is a dominant risk factor for Alzheimer’s disease (AD), epidemiological studies have shown that physical activity may significantly decrease age-related risks for AD, and indeed mitigate the impact in existing diagnosis. The aim of this study was to perform a narrative review on the preventative, and mitigating, effects of physical activity on AD onset, including genetic factors, mechanism of action and physical activity typology. In this article, we conducted a narrative review of the influence physical activity and exercise have on AD, utilising key terms related to AD, physical activity, mechanism and prevention, searching the online databases; Web of Science, PubMed and Google Scholar, and, subsequently, discuss possible mechanisms of this action. On the basis of this review, it is evident that physical activity and exercise may be incorporated in AD, notwithstanding, a greater number of high-quality randomised controlled trials are needed, moreover, physical activity typology must be acutely considered, primarily due to a dearth of research on the efficacy of physical activity types other than aerobic.

Keywords Alzheimer’s disease      prevention      physical activity      exercise      aging     
Corresponding Authors: Cain C. T. Clark   
About author: Copyright: © 2019 Maeso-Díaz R et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Just Accepted Date: 12 March 2019  
Service
E-mail this article
E-mail Alert
RSS
Articles by authors
Piotr Gronek
Stefan Balko
Joanna Gronek
Adam Zajac
Adam Maszczyk
Roman Celka
Agnieszka Doberska
Wojciech Czarny
Robert Podstawski
Cain C. T. Clark
Fang Yu
Cite this article:   
Piotr Gronek,Stefan Balko,Joanna Gronek, et al. Physical Activity and Alzheimer’s Disease: A Narrative Review[J]. Aging and disease, 10.14336/AD.2019.0226
URL:  
http://www.aginganddisease.org/EN/10.14336/AD.2019.0226     OR     http://www.aginganddisease.org/EN/Y0/V/I/0
[1] Yew B, Nation DA. (2017). Cerebrovascular resistance: effects on cognitive decline, cortical atrophy, and progression to dementia. Brain, 140:1987-2001.
[2] Reddy PH, Beal MF. (2008). Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease. Trends Mol Med, 14: 45-53.
[3] Resnick SM, Pham DL, Kraut MA, Zonderman AB, Davatzikos C. (2003). Longitudinal magnetic resonance imaging studies of older adults: a shrinking brain. J Neurosci, 23: 3295-301.
[4] Hoogendam YY, van der Geest JN, Niessen WJ, van der Lugt A, Hofman A, Vernooij MW, et al. (2014). The role of cerebellar volume in cognition in the general elderly population. Alzheimer Dis Assoc Disord, 28:352-7.
[5] Barnes DE, Yaffe K. (2011). The projected effect of risk factor reduction on Alzheimer's disease prevalence. Lancet Neurol, 10: 819-28.
[6] Alzheimer's Disease International. World Alzheimer Report. Prince, M.; Jackson, J. London, UK: UKI; 2009.
[7] World Health Organization. The top 10 causes of death [internet].2017 [cited 2018 Nov 01]. Available from: www.who.int/mediacentre/factsheets/fs310/en/.
[8] O'Keefe JH, Vogel R, Lavie CJ, Cordain L. (2010). Achieving hunter-gatherer fitness in the 21(st) century: back to the future. Am J Med, 123:1082-6.
[9] Booth FW, Lees SJ. (2007). Fundamental questions about genes, inactivity, and chronic diseases. Physiol Genomics, 28:146-157.
[10] Booth FW, Laye MJ, Lees SJ, Rector, RS, Thyfault, JP. (2008). Reduced physical activity and risk of chronic disease: the biology behind the consequences. Eur J Appl Physiol, 102:381-390.
[11] Blair SN, LaMonte MJ, Nichaman MZ. The evolution of physical activity recommendations: how much is enough? Am J Clin Nutr, 79:913S-920S.
[12] Pedersen BK, Saltin B. (2006). Evidence for prescribing exercise as therapy in chronic disease. Scand J Med Sci Sports, 16:S3-63.
[13] Blair SN, Kohl HW 3rd, Paffenbarger RS Jr. Clark DG, Cooper KH, Gibbons LW. (1989). Physical fitness and all-cause mortality. A prospective study of healthy men and women. JAMA, 262:2395-2401.
[14] Kokkinos P, Myers J, Kokkinos JP, Pittaras A, Narayan P, Manolis A, et al. (2008). Exercise capacity and mortality in black and white men. Circulation, 117:614-622.
[15] Lindsay J, Laurin D, Verreault R, Hébert R, Helliwell, B., Hill GB, et al. (2002). Risk factors for Alzheimer’s disease: a prospective analysis from the Canadian Study of Health and Aging. Am. J. Epidemiol, 156:445-453.
[16] Richards M, Hardy R, Wadsworth MEJ. (2003). Does active leisure protect cognition? Evidence from a national birth cohort. Soc. Sci. Med, 56:785-792.
[17] Larson EB, Wang L, Bowen JD, McCormick WC, Teri L, Crane P, et al. (2006). Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older. Ann. Intern. Med, 144:73-81.
[18] Kirkevold M. (1997). Integrative nursing research - an important strategy to further the development of nursing science and practice. J Adv Nurs, 25:977-984
[19] Mays N, Pope C, Popay J. (2005). Systematically reviewing qualitative and quantitative evidence to inform management and policy-making in the health field. J Health Serv Res Policy, 10:6-20.
[20] Greenhalgh TS, Thorne S, Malterud, K. (2018). Time to challenge the spurious hierarchy of systematic over narrative reviews? Eur J Clin Invest, 48: e12931.
[21] Greenhalgh T, Robert G, MacFarlane F, Bate P, Kyriakidou O, Peacock R. (2005). Storylines of research in diffusion of innovation: a meta-narrative approach to systematic review. Soc Sci Med, 61:417-430.
[22] Reitz C, Brayne C, Mayeux R. (2011). Epidemiology of alzheimer disease. Nat Rev Neurol, 7, 137-152.
[23] Alzheimer’s Association (2015). 2015 Alzheimer’s disease facts and figures. Alzheimers Dement, 11:332-384.
[24] Yuyama K, Igarashi Y. (2017). Exosomes as carriers of Alzheimer's amyloid-ß. Front Neurosci, 25:229.
[25] Hardy J, Selkoe, DJ. (2002). The amyloid hypothesis of alzheimer’s disease: progress and problems on the road to therapeutics. Science, 297:353-356.
[26] Karran EH, Allsop D, Christie G, Davis J, Gray C, Mansfield F, Ward RV. (1998). Presenilins--in search of functionality. Biochem Soc Trans, 26:491-6.
[27] Duff K, Eckman C, Zehr C, Yu X, Prada CM, Perez-tur J, et al. (1996). Increased amyloid-beta 42 (43) in brains of mice expressing mutant presenilin 1. Nature, 383:710-713.
[28] Alberici A, Moratto D, Benussi L, Gasparini L, Ghidoni R, Gatta LB, et al. (1999). Presenilin 1 protein directly interacts with Bcl-2. J Biol Chem, 274:30764-30769.
[29] Trushina E, Nemutlu E, Zhang S, Christensen T, Camp J, Mesa J, et al. (2012). Defects in mitochondrial dynamics and metabolomics signatures of evolving energetic stress in mouse models of familial Alzheimer’s disease. PLoS One, 7:e32737.
[30] Tomita T, Maruyama K, Saido TC, Kume H, Shinozaki K, Tokuhiro S, et al. (1997).The presenilin 2 mutation (N141I) linked to familial Alzheimer disease (Volga German families) increases the secretion of amyloid beta protein ending at the 42nd (or 43rd) residue. Proc Natl Acad Sci U S A, 4:2025-30.
[31] Levitan D, Greenwald I. Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimer's disease gene. (1995). Nature, 377:351-4
[32] Alzheimer's Association Working Group. (1996). Apolipoprotein E genotyping in Alzheimer's disease. Lancet, 347:1091-1095.
[33] Takashima A, Murayama M, Murayama O, Kohno T, Honda T, Yasutake K, et al. (1998). Presenilin 1 associates with glycogen synthase kinase-3β and its substrate tau. Proc. Natl. Acad. Sci. U. S. A, 95:9637-9641.
[34] Geller LN, Potter H. (1999). Chromosome missegregation and trisomy 21 mosaicism in Alzheimer's disease. Neurobiol Dis, 6:167-79.
[35] Sherrington R, Rogaev EI, Liang Y, Rogaeva EA, Levesque G, Ikeda M, et al. (1995). Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature, 29:754-60.
[36] Kunkle BW, Vardarajan BN, Naj AC, Whitehead PL, Rolati S, Slifer S, et al. (2017). Early-onset Alzheimer disease and candidate risk genes involved in endolysosomal transport. JAMA Neurol, 74:1113-1122.
[37] Huang Y, Mahley RW. (2014). Neurobiology of Disease Apolipoprotein E: structure and function in lipid metabolism, neurobiology, and Alzheimer’s diseases. Neurobiol Dis, 2:3-12.
[38] Van-Giau V, Bagyinszky E, An SSA, Kim SY. (2015). Role of apolipoprotein E in neurodegenerative diseases. Neuropsychiatr Dis Treat, 11:1723-1737.
[39] Ang LS, Cruz RP, Hendel A, Granville DJ. (2008). Apolipoprotein E, an important player in longevity and age-related diseases. Exp Gerontol, 43:615-22.
[40] Moghadasian MH, McManus BM, Nguyen LB, Shefer S, Nadji M, Godin DV, et al. (2001). Pathophysiology of apolipoprotein E deficiency in mice: relevance to apo E-related disorders in humans. FASEB J, 15:2623-30.
[41] Papaioannou I, Simons JP, Owen JS. (2012). Targeted in situ gene correction of dysfunctional APOE alleles to produce atheroprotective plasma ApoE3 protein. Cardiol Res Pract. 2012:148796.
[42] Lusis AJ, Heinzmann C, Sparkes RS, Scott J, Knott TJ, Geller R, et al. (1986). Regional mapping of human chromosome 19: organization ofgenes for plasma lipid transport (APOC1, -C2, and -E and LDLR) and the genes C3, PEPD, and GPI. Proc Natl Acad Sci USA, 83:3929-33.
[43] Corder EH, Saunders AM, Strittmatter WJ, Schmechel DE, Gaskell PC, Small GW, et al. (1993). Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science, 261:921-3.
[44] McKay GJ, Silvestri G, Chakravarthy U, Dasari S, Fritsche LG, Weber BH, et al. (2011). Variations in apolipoprotein e frequency with age in a pooled analysis of a large group of older people. Am J Epidemiol, 173:1357-64.
[45] Kapur S, Sharad S, Kapoor M, Bala K. (2006). ApoE Genotypes: Risk factor for Alzheimer’s Disease. Ind Ac Clin Med, 2:118-122.
[46] Alzheimer's Association Working Group. (1996). Apolipoprotein E genotyping in Alzheimer's disease. Lancet, 347:1091-1095.
[47] Haight T, Bryan RN, Meirelles O, Tracy R, Fornage M, Richard M, et al. (2018). Associations of plasma clusterin and Alzheimer's disease-related MRI markers in adults at mid-life: The CARDIA Brain MRI sub-study. PLoS One, 13:e0190478.
[48] Butcher LR, Thomas A, Backx K, Roberts A, Webb R, Morris K. (2008). Low-intensity exercise exerts beneficial effects on plasma lipids via PPARgamma. Med Sci Sports Exerc, 40:1263-1270.
[49] Yakeu G, Butcher L, Isa S, Webb R., Roberts AW, Thomas AW, et al. (2010). Low-intensity exercise enhances expression of markers of alternative activation in circulating leukocytes: roles of PPARγ and Th2 cytokines. Atherosclerosis, 212:668-673.
[50] Pinto PR, da Silva KS, Iborra RT, Okuda LS, Gomes-Kjerulf D, Ferreira GS, et al. (2018). Exercise Training Favorably Modulates Gene and Protein Expression That Regulate Arterial Cholesterol Content in CETP Transgenic Mice. Front Physiol, 9:502.
[51] Deeny SP, Poeppel D, Zimmerman JB, Roth SM, Brandauer J, Witkowski S, et al. (2008). Exercise, APOE, and working memory: MEG and behavioral evidence for benefit of exercise in epsilon4 carriers. Biol Psychol, 78:179-187.
[52] Etnier JL, Caselli RJ, Reiman EM, Alexander GE, Sibley BA, Tessier D, et al. (2007). Cognitive performance in older women relative to ApoE-ε4 genotype and aerobic fitness. Med Sci Sports Exerc, 39:199-207.
[53] Niti M, Yap KB, Kua EH, Tan CH, Ng TP. (2008). Physical, social and productive leisure activities, cognitive decline and interaction with APOE-epsilon 4 genotype in Chinese older adults. Int Psychogeriatr, 20:237-251.
[54] Schuit AJ, Feskens EJ, Launer LJ, Kromhout D. (2001). Physical activity and cognitive decline, the role of the apolipoprotein e4 allele. Med Sci Sports Exerc, 33:772-777.
[55] Nichol K, Deeny SP, Seif J, Camaclang K, Cotman CW. (2009). Exercise improves cognition and hippocampal plasticity in APOE epsilon4 mice. Alzheimers Dement, 5:287-294.
[56] Brown BM, Peiffer JJ, Taddei K, Lui JK, Laws SM, Gupta VB, et al. (2013). Physical activity and amyloid-beta plasma and brain levels: results from the Australian Imaging, Biomarkers and Lifestyle Study of Ageing. Mol Psychiatry, 18: 875-81.
[57] Jack CR, Bennett D, Blennow K, Carrillo MC, Dunn B, Elliott C, et al. (2018). NIA-AA Research Framework: Toward a biological definition of Alzheimer's disease. Alzheimers Dement, 14:535-562.
[58] Correia SC, Santos RX, Perry G, Zhu X, Moreira PI, Smith MA. (2011). Insulin-resistant brain state: the culprit in sporadic Alzheimer's disease? Ageing Res Rev, 10:264-273.
[59] Choi DH, Kwon IS, Koo JH, Jang YC, Kang EM, Byun JE, et al. (2014). The effect of treadmill exercise on inflammatory responses in rat model of streptozotocin-induced experimental dementia of Alzheimer's type. Journal Ex Nut Biochem, 18:225-233.
[60] Huang WJ, Zhang X, Chen WW. (2016). Role of oxidative stress in Alzheimer's disease. Biomed Rep, 4:519-522.
[61] Kishimoto Y, Shishido H, Sawanishi M, Toyota Y, Ueno M, Kubota T, et al. (2016). Data on amyloid precursor protein accumulation, spontaneous physical activity, and motor learning after traumatic brain injury in the triple-transgenic mouse model of Alzheimer's disease. Data in brief, 9:62-67.
[62] Nalivaeva NN, Turner AJ. (2013). The amyloid precursor protein: a biochemical enigma in brain development, function and disease. FEBS Lett, 587:2046-2054.
[63] Gu L, Guo Z. (2013). Alzheimer's Abeta42 and Abeta40 peptides form interlaced amyloid fibrils. J Neurochem, 126:305-311.
[64] Iqbal K, Alonso AC, Chen S, Chohan MO, El-Akkad E, Gong CX, et al. (2005). Tau pathology in Alzheimer disease and other tauopathies. Biochim Biophys Acta, 1739:198-210.
[65] Alkadhi KA, Dao AT. (2018). Exercise decreases BACE and APP levels in the hippocampus of a rat model of Alzheimer's disease. Mol Cell Neurosci, 86:25-29.
[66] Neth BJ, Craft S. (2017). Insulin Resistance and Alzheimer's Disease: Bioenergetic Linkages. Front Aging Neurosci, 9:345.
[67] Al-Delaimy WK, von Muhlen D, Barrett-Connor E. (2009). Insulin-like growth factor-1, insulin-like growth factor binding protein-1, and cognitive function in older men and women. J Am Geriatr Soc, 57:1441-1446.
[68] Almeida OP, Hankey GJ, Yeap BB, Chubb SA, Gollege J, Flicker L. (2017). Risk of prevalent and incident dementia associated with insulin-like growth factor and insulin-like growth factor-binding protein 3. Mol Psychiatry, 23:1825-1829.
[69] Evans EM, Racette SB, Peterson LR, Villareal DT, Greiwe JS, Holloszy JO. (2005). Aerobic power and insulin action improve in response to endurance exercise training in healthy 77-87 yr olds. J Appl, 98:40-45.
[70] Robinson MM, Lowe VJ, Nair KS. (2018). Increased brain glucose uptake after 12 weeks of aerobic high-intensity interval training in young and older adults. J Clin Endocrinol Metab, 103:221-227.
[71] Nascimento CM, Pereira JR, de Andrade LP, Garuffi M, Talib LL, Forlenza OV, et al. (2014). Physical exercise in MCI elderly promotes reduction of pro-inflammatory cytokines and improvements on cognition and BDNF peripheral levels. Curr Alzheimer Res, 11:799-805.
[72] Marques-Aleixo I, Santos-Alves E, Balca MM, Rizo-Roca D, Moreira PI, Oliveira PJ, et al. (2015). Physical exercise improves brain cortex and cerebellum mitochondrial bioenergetics and alters apoptotic, dynamic and auto(mito)phagy markers. Neuroscience, 301:480-495.
[73] Bernardo TC, Marques-Aleixo I, Beleza J, Oliveira PJ, Ascensao A, Magalhaes J. (2016). Physical exercise and brain mitochondrial fitness: The possible role against Alzheimer's disease. Brain Pathol, 26:648-663.
[74] Marques-Aleixo I, Oliveira PJ, Moreira PI, Magalhaes J, Ascensao A. (2012). Physical exercise as a possible strategy for brain protection: evidence from mitochondrial-mediated mechanisms. Prog Neurobiol, 99:149-162.
[75] Fox MD Snyder AZ.; Vincent JL, Corbetta M, Van Essen DC, Raichle ME. (2005). The human brain is intrinsically organized into dynamic, anticorrelated functional networks. PNAS, 102: 9673-678.
[76] Voss MW, Prakash RS, Erickson KI, Basak C, Chaddock L, Kim JS, et al. (2010). Plasticity of brain networks in a randomized intervention trial of exercise training in older adults. Front Ag Neurosci 2:32.
[77] Buckner RL, Andrews-Hanna JR, Schacter DL. (2008). The brain’s default network: anatomy, function, and relevance to disease. Ann NY Acad Sci, 1124:1-38.
[78] Schilbach L, Eickhoff SB, Rotarska-Jagiela A, Fink GR, Vogeley K. (2008). Minds at rest? Social cognition as the default mode of cognizing and its putative relationship to the “default system” of the brain. Conscious Cogn, 17:457-467.
[79] Andrews-Hanna JR, Snyder AZ, Vincent JL, Lustig C, Head D, Raichle ME, et al. (2007). Disruption of large-scale brain systems in advanced aging. Neuron, 56:924-935.
[80] Damoiseaux JS, Beckmann CF, Arigita EJS, Barkhof F, Scheltens P, Stam CJ, et al. (2008). Reduced resting-state brain activity in the “default network” in normal aging. Cereb Cortex, 18:1856-1864.
[81] Hampson M, Driesen NR, Skudlarski P, Gore JC, Constable RT. (2006). Brain connectivity related to working memory performance. J Neurosci, 26:13338-13343.
[82] Ozbeyli D, Sari G, Ozkan N, Karademir B, Yuksel M, Kaya OT, et al. (2017). Protective effects of different exercise modalities in an Alzheimer's disease-like model. Behav Brain Res, 328:159-177.
[83] Cotman CW, Berchtold NC, Christie LA. (2007). Exercise builds brain health: key roles of growth factor cascades and inflammation. Trends Neurosci, 30:464-72.
[84] Vivar C, Potter MC, van Praag H. (2013). All about running: synaptic plasticity, growth factors and adult hippocampal neurogenesis. Curr Top Behav Neurosci, 15:189-210.
[85] Sleiman SF, Chao MV. (2015). Downstream consequences of exercise through the action of BDNF. Brain Plasticity, 1:143-8.
[86] Pereira AC, Huddleston DE, Brickman AM, Sosunov AA, Hen R, McKhann GM, et al. (2007). An in vivo correlate of exercise-induced neurogenesis in the adult dentate gyrus. Proc Natl Acad Sci USA, 104:5638-43.
[87] Eadie BD, Redila VA, Christie BR. (2005). Voluntary exercise alters the cytoarchitecture of the adult dentate gyrus by increasing cellular proliferation, dendritic complexity, and spine density. J Comp Neurol, 486:39-47.
[88] Stranahan AM, Khalil D, Gould E. (2007). Running induces widespread structural alterations in the hippocampus and entorhinal cortex. Hippocampus, 17:1017-22.
[89] Siette J, Westbrook RF, Cotman C, Sidhu K, Zhu W, Sachdev P, et al. (2013). Age-specific effects of voluntary exercise on memory and the older brain. Biol Psychiatry, 73:435-42.
[90] Duzel E, van Praag H, Sendtner M. (2016). Can physical exercise in old age improve memory and hippocampal function? Brain, 139:662-673.
[91] Creer DJ, Romberg C, Saksida LM, van Praag H, Bussey TJ. (2010). Running enhances spatial pattern separation in mice. Proc Natl Acad Sci USA, 107:2367-72.
[92] van Praag H. (2008). Neurogenesis and exercise: past and future directions. Neuromolecular Med, 10:128-40.
[93] Marlatt MW, Lucassen PJ, van Praag H. (2010). Comparison of neurogenic effects of fluoxetine, duloxetine and running in mice. Brain Res, 1341:93-9.
[94] Opendak M, Gould E. (2015). Adult neurogenesis: a substrate for experience dependent change. Trends Cogn Sci, 19:151-61.
[95] Bolz L, Heigele S, Bischofberger J. (2015). Running improves pattern separation during novel object recognition. Brain Plasticity, 1:129-141.
[96] Whiteman AS, Young DE, Budson AE, Stern CE, Schon K. (2015). Entorhinal volume, aerobic fitness, and recognition memory in healthy young adults: A voxel-based morphometry study. NeuroImage, 126:229-238.
[97] Spirduso WW, Clifford P. (1978). Replication of age and physical activity effects on re action time movement time. J Gerontol, 33:23-30.
[98] Jedrziewski MK, Ewbank DC, Wang H, Trojanowski JQ. (2014). The impact of exercise, cognitive activities, and socialization on cognitive function: results from the national long-term care survey. Am J Alzheimers Dis Other Demen, 29:372-378.
[99] Sung YH. (2015). Effects of treadmill exercise on hippocampal neurogenesis in an MPTP/probenecid-induced Parkinson's disease mouse model. J Phys Ther Sci, 27:3203-6.
[100] Nokia MS, Lensu S, Ahtiainen JP, Johansson PP, Koch LG, Britton SL, Kainulainen H. (2016). Physical exercise increases adult hippocampal neurogenesis in male rats provided it is aerobic and sustained. J Physiol, 594:1855-73.
[101] Speisman RB, Kumar A, Rani A, Foster TC, Ormerod BK. (2013). Daily exercise improves memory, stimulates hippocampal neurogenesis and modulates immune and neuroimmune cytokines in aging rats. Brain Behav Immun, 28:25-43.
[102] Verghese J, Lipton RB, Katz MJ, Hall CB, Derby CA, Kuslansky G, et al. (2003). Leisure Activities and the Risk of Dementia in the Elderly. N Engl J Med, 348:2508-2516.
[103] Beckett MW, Ardern CI, Rotondi MA. (2015). A meta-analysis of prospective studies on the role of physical activity and the prevention of Alzheimer’s disease in older adults. BMC Geriatr, 15:9.
[104] Stephen R, Hongisto K, Solomon A, Lonnroos E. (2017). Physical activity and Alzheimer’s disease: a systematic review. J Gerontol A Biol Sci Med Sci, 72:733-739.
[105] Colcombe SJ, Erickson KI, Raz N, Webb AG, Cohen NJ, McAuley E, et al. (2003). Aerobic fitness reduces brain tissue loss in aging humans. J Gerontol A Biol Sci Med Sci, 58:176-180.
[106] Swain RA, Harris AB, Wiener EC, Dutka MV, Morris HD, Theien BE, et al. (2003). Prolonged exercise induces angiogenesis and increases cerebral blood volume in primary motor cortex of the rat. Neuroscience, 117:1037-1046.
[107] McCloskey DP, Adamo DS, Anderson BJ. (2001). Exercise increases metabolic capacity in the motor cortex and striatum, but not in the hippocampus. Brain Res, 891:168-175.
[108] Larsen JO, Skalicky M, Viidik A. (2000). Does long-term physical exercise counteract age-related Purkinje cell loss? A stereological study of rat cerebellum. J Comp Neurol, 428:213-222.
[109] Andrieu S, Coley N, Lovestone S, Aisen PS, Vellas B. (2015). Prevention of sporadic Alzheimer’s disease: lessons learned from clinical trials and future directions. Lancet Neurol, 14:926-944.
[110] Paillard T, Rolland Y, de Barreto PS. (2015). Protective effects of physical exercise in Alzheimer’s disease and Parkinson’s disease: a narrative review. J Clin Neurol, 11:212-219.
[111] Ji LL. (2015). Redox signaling in skeletal muscle: role of aging and exercise. Adv Physiol Educ, 39:352-9.
[112] Do K, Laing BT, Landry T, Bunner W, Mersaud N, Matsubara T, et al. (2018). The effects of exercise on hypothalamic neurodegeneration of Alzheimer's disease mouse model. PLoS One, 13:e0190205.
[113] Marosi K, Mattson MP. (2014). BDNF mediates adaptive brain and body responses to energetic challenges. Trends Endocrinol Metab, 25(2):89-98.
[114] Emmerzaal TL, Kiliaan AJ, Gustafson DR. (2015). 2003-2013: a decade of bodymass index, Alzheimer’s disease, and dementia. J Alzheimer’s Dis, 43:739-755.
[115] Parise G, Brose AN, Tarnopolsky MA. (2005). Resistance exercise training decreases oxidative damage to DNA and increases cytochrome oxidase activity in older adults. Exp Gerontol, 40:173-80.
[116] Cassilhas RC, Viana VA, Grassmann V, Santos RT, Santos RF, Tufik S, et al. (2007). The impact of resistance exercise on the cognitive function of the elderly. Med Sci Sports, 39:1401-7.
[117] Coelho FM, Pereira DS, Lustosa LP, Silva JP, Dias JM, Dias RC, et al. (2012). Physical therapy intervention (PTI) increases plasma brain-derived neurotrophic factor (BDNF) levels in non-frail and pre-frail elderly women. Arch Gerontol Geriatr, 54:415-20.
[118] Liu-Ambrose T, Nagamatsu MA, Graf P, Beattie BL, Ashe M, Handy TC. (2010). Resistance Training and executive functions. Arch Intern Med,170:170-8.
[119] Hauer K, Schwenk M, Zieschang T, Essig M, Becker C, Oster P. (2012). Physical training improves motor performance in people with dementia: a randomized controlled trial. J Am Geriatr Soc, 60:8-15.
[120] Portugal EM., Vasconcelos PGT, Souza R, Lattari E, Monteiro-Junior RS, Machado S, et al. (2015). Aging process, cognitive decline and Alzheimer`s disease: can strength training modulate these responses? CNS & Neurol Disord Drug Targets, 14:1-6
[121] Hurley BF, Hanson ED, Sheaff AK. (2011). Strength training as a countermeasure to aging muscle and chronic disease. Sports Med. 41:289-306.
[122] Porat S, Goukasian N, Hwang KS, Zanto T, Do T, Pierce J, et al. (2016). Dance experience and associations with cortical gray matter thickness in the aging population. Dement Geriatr Cogn Disord Extra, 6:508-517.
[123] Schellenberg EG, Hallam S. (2005). Music listening and cognitive abilities in 10- and 11-year-olds: the blur effect. Ann NY Acad Sci, 1060: 202-209.
[124] Nair BR, Browne W, Marley J, Heim C. (2013). Music and dementia. Degener Neurol Neuromuscul Dis, 3:47-51.
[125] Schlaug G. (2015). Musicians and music making as a model for the study of brain plasticity. Prog Brain Res, 217:37-55.
[126] Burunat I, Brattico E, Puoliväli T, Ristaniemi T, Sams M, Toiviainen P. (2015). Action in perception: prominent visuo-motor functional symmetry in musicians during music listening. PLoS One, 10:e0138238.
[1] Jong Bin Bae,Ji Won Han,Kyung Phil Kwak,Bong Jo Kim,Shin Gyeom Kim,Jeong Lan Kim,Tae Hui Kim,Seung-Ho Ryu,Seok Woo Moon,Joon Hyuk Park,Jong Chul Youn,Dong Young Lee,Dong Woo Lee,Seok Bum Lee,Jung Jae Lee,Jin Hyeong Jhoo,Ki Woong Kim. Is Dementia More Fatal Than Previously Estimated? A Population-based Prospective Cohort Study[J]. Aging and disease, 2019, 10(1): 1-11.
[2] Tingting Sui,Di Liu,Tingjun Liu,Jichao Deng,Mao Chen,Yuanyuan Xu,Yuning Song,Hongsheng Ouyang,Liangxue Lai,Zhanjun Li. LMNA-mutated Rabbits: A Model of Premature Aging Syndrome with Muscular Dystrophy and Dilated Cardiomyopathy[J]. Aging and disease, 2019, 10(1): 102-115.
[3] Michael G. Flynn,Melissa M. Markofski,Andres E. Carrillo. Elevated Inflammatory Status and Increased Risk of Chronic Disease in Chronological Aging: Inflamm-aging or Inflamm-inactivity?[J]. Aging and disease, 2019, 10(1): 147-156.
[4] Dong Liu,Liqun Xu,Xiaoyan Zhang,Changhong Shi,Shubin Qiao,Zhiqiang Ma,Jiansong Yuan. Snapshot: Implications for mTOR in Aging-related Ischemia/Reperfusion Injury[J]. Aging and disease, 2019, 10(1): 116-133.
[5] Wanying Duan, Yuehua Pu, Haiyan Liu, Jing Jing, Yuesong Pan, Xinying Zou, Yilong Wang, Xingquan Zhao, Chunxue Wang, Yongjun Wang, Ka Sing Lawrence Wong, Ling Wei, Liping Liu, . Association between Leukoaraiosis and Symptomatic Intracranial Large Artery Stenoses and Occlusions: the Chinese Intracranial Atherosclerosis (CICAS) Study[J]. Aging and disease, 2018, 9(6): 1074-1083.
[6] Antonina Luca, Carmela Calandra, Maria Luca. Molecular Bases of Alzheimer’s Disease and Neurodegeneration: The Role of Neuroglia[J]. Aging and disease, 2018, 9(6): 1134-1152.
[7] Calvin Pak-Wing Cheng, Sheung-Tak Cheng, Cindy Woon-Chi Tam, Wai-Chi Chan, Winnie Chiu-Wing Chu, Linda Chiu-Wa Lam. Relationship between Cortical Thickness and Neuropsychological Performance in Normal Older Adults and Those with Mild Cognitive Impairment[J]. Aging and disease, 2018, 9(6): 1020-1030.
[8] Yu-Wen Huang, Ming-Fu Chiang, Che-Sheng Ho, Pi-Lien Hung, Mei-Hsin Hsu, Tsung-Han Lee, Lichieh Julie Chu, Hsuan Liu, Petrus Tang, Wailap Victor Ng, Dar-Shong Lin. A Transcriptome Study of Progeroid Neurocutaneous Syndrome Reveals POSTN As a New Element in Proline Metabolic Disorder[J]. Aging and disease, 2018, 9(6): 1043-1057.
[9] Manuel Scimeca, Federica Centofanti, Monica Celi, Elena Gasbarra, Giuseppe Novelli, Annalisa Botta, Umberto Tarantino. Vitamin D Receptor in Muscle Atrophy of Elderly Patients: A Key Element of Osteoporosis-Sarcopenia Connection[J]. Aging and disease, 2018, 9(6): 952-964.
[10] Charlene Greenwood, John Clement, Anthony Dicken, Paul Evans, Iain Lyburn, Richard M. Martin, Nick Stone, Peter Zioupos, Keith Rogers. Age-Related Changes in Femoral Head Trabecular Microarchitecture[J]. Aging and disease, 2018, 9(6): 976-987.
[11] Ashok K. Shetty, Maheedhar Kodali, Raghavendra Upadhya, Leelavathi N. Madhu. Emerging Anti-Aging Strategies - Scientific Basis and Efficacy[J]. Aging and disease, 2018, 9(6): 1165-1184.
[12] Ze Teng, Aibo Wang, Peng Wang, Rui Wang, Wei Wang, Hongbin Han. The Effect of Aquaporin-4 Knockout on Interstitial Fluid Flow and the Structure of the Extracellular Space in the Deep Brain[J]. Aging and disease, 2018, 9(5): 808-816.
[13] Stefano Rizza, Marina Cardellini, Alessio Farcomeni, Pasquale Morabito, Daniele Romanello, Giovanni Di Cola, Maria Paola Canale, Massimo Federici. Low Molecular Weight Adiponectin Increases the Mortality Risk in Very Old Patients[J]. Aging and disease, 2018, 9(5): 946-951.
[14] Stefanie Hardt, Lucie Valek, Jinyang Zeng-Brouwers, Annett Wilken-Schmitz, Liliana Schaefer, Irmgard Tegeder. Progranulin Deficient Mice Develop Nephrogenic Diabetes Insipidus[J]. Aging and disease, 2018, 9(5): 817-830.
[15] Yong-Fei Zhao, Qiong Zhang, Jian-Feng Zhang, Zhi-Yin Lou, Hen-Bing Zu, Zi-Gao Wang, Wei-Cheng Zeng, Kai Yao, Bao-Guo Xiao. The Synergy of Aging and LPS Exposure in a Mouse Model of Parkinson’s Disease[J]. Aging and disease, 2018, 9(5): 785-797.
Viewed
Full text


Abstract

Cited

  Shared   
Copyright © 2014 Aging and Disease, All Rights Reserved.
Address: Aging and Disease Editorial Office 3400 Camp Bowie Boulevard Fort Worth, TX76106 USA
Fax: (817) 735-0408 E-mail: editorial@aginganddisease.org
Powered by Beijing Magtech Co. Ltd