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Nutrition and Prevention of Alzheimer's Dementia Arun Swaminathan University of Kentucky, Asw224@Uky.Edu University of Kentucky UKnowledge Neurology Faculty Publications Neurology 10-20-2014 Nutrition and Prevention of Alzheimer's Dementia Arun Swaminathan University of Kentucky, [email protected] Gregory A. Jicha University of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits oy u. Follow this and additional works at: https://uknowledge.uky.edu/neurology_facpub Part of the Neurology Commons Repository Citation Swaminathan, Arun and Jicha, Gregory A., "Nutrition and Prevention of Alzheimer's Dementia" (2014). Neurology Faculty Publications. 8. https://uknowledge.uky.edu/neurology_facpub/8 This Review is brought to you for free and open access by the Neurology at UKnowledge. It has been accepted for inclusion in Neurology Faculty Publications by an authorized administrator of UKnowledge. For more information, please contact [email protected]. Nutrition and Prevention of Alzheimer's Dementia Notes/Citation Information Published in Frontiers in Aging Neuroscience, v. 6, article 282, p. 1-13. © 2014 Swaminathan and Jicha. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Digital Object Identifier (DOI) http://dx.doi.org/10.3389/fnagi.2014.00282 This review is available at UKnowledge: https://uknowledge.uky.edu/neurology_facpub/8 REVIEW ARTICLE published: 20 October 2014 doi: 10.3389/fnagi.2014.00282 Nutrition and prevention of Alzheimer’s dementia Arun Swaminathan and Gregory A. Jicha* Department of Neurology and Sanders-Brown Center on Aging, College of Medicine, University of Kentucky, Lexington, KY, USA Edited by: A nutritional approach to prevent, slow, or halt the progression of disease is a promising Claudia Perez-Cruz, Centro de strategy that has been widely investigated. Much epidemiologic data suggests that Investigación y de Estudios Avanzados del Instituto Politécnico nutritional intake may influence the development and progression of Alzheimer’s dementia Nacional, Mexico (AD). Modifiable, environmental causes of AD include potential metabolic derangements Reviewed by: caused by dietary insufficiency and or excess that may be corrected by nutritional Douglas Watt, Quincy Medical supplementation and or dietary modification. Many nutritional supplements contain a Center/Cambridge Health Alliance, myriad of health promoting constituents (anti-oxidants, vitamins, trace minerals, flavonoids, USA ... Ellen Mitchell, Nestle Institute of lipids, etc.) that may have novel mechanisms of action affecting cellular health and Health Sciences, Switzerland regeneration, the aging process itself, or may specifically disrupt pathogenic pathways *Correspondence: in the development of AD. Nutritional modifications have the advantage of being cost Gregory A. Jicha, Department of effective, easy to implement, socially acceptable and generally safe and devoid of Neurology and Sanders-Brown Center significant adverse events in most cases. Many nutritional interventions have been studied on Aging, College of Medicine, University of Kentucky, Lexington, and continue to be evaluated in hopes of finding a successful agent, combination of agents, KY 40536, USA or dietary modifications that can be used for the prevention and or treatment of AD. The e-mail: [email protected] current review focuses on several key nutritional compounds and dietary modifications that have been studied in humans, and further discusses the rationale underlying their potential utility for the prevention and treatment of AD. Keywords: nutrition, Alzheimer, treatment, clinical trial, prevention OVERVIEW 2011). In response to this consensus statement, there was a broad- Alzheimer’s dementia (AD) is the most commonly recognized based push back by many members of the Alzheimer’s research cause of dementia in the aging population (Brookmeyer et al., community (particularly from the animal model and epidemi- 2007). First described by the German psychiatrist and neu- ological research folks whose data sets were marginalized and ropathologist, Alois Alzheimer, in 1906, the eponymous syndrome patronized as being of “poor scientific quality”). Researchers in is recognized worldwide as a major cause of morbidity and the field of AD were also underrepresented in the consensus group mortality in the aging population contributing to a major bur- leading to further debate as to the validity of the consensus state- den on healthcare systems (Brookmeyer et al., 2007). Amyloid ment. As such it is clear that the field is far from consensus on plaque deposition in the brain, the development of neurofibril- the debate of whether viable interventions for the prevention of lary pathology, neuronal loss and dysfunction of neuroanatomic AD exist. While the search for a cure remains elusive, there is systems, including those affecting cholinergic transmission, are much hope that preventative strategies, such as dietary modifi- among the commonly described findings in persons with AD cation and nutritional supplementation, may reduce the global (Jicha and Carr, 2010). In addition to these core pathological burden of AD. features of AD, much evidence has accumulated that increased A nutritional approach to prevent, slow, or halt the progression oxidative stress, defects in mitochondrial dysfunction and cellu- of disease is a promising strategy that has been widely investi- lar energy production, and chronic inflammatory mechanisms gated. Much epidemiologic data suggests that nutritional intake contribute to the degenerative cascade in this complex disease may influence the development and progression of AD (Gillette- (Rao and Balachandran, 2002; Cunnane et al., 2011; Rubio- Guyonnet et al., 2013). Modifiable, environmental causes of AD Perez and Morillas-Ruiz, 2012). A cure for the condition is not include potential metabolic derangements caused by dietary insuf- known and current treatment approaches include maximizing ficiency (Knopman et al., 2001; Kamphuis and Scheltens, 2010; transmission of acetylcholine and other neurotransmitters while Cunnane et al., 2011; Cardoso et al., 2013; Hu et al., 2013; Lopes da also using other medications and multidisciplinary strategies Silva et al., 2014). In addition, many nutritional supplements and to treat associated comorbidities focused on improving qual- dietary modifications may directly influence the pathological con- ity of life and alleviating symptom burden (Jicha and Carr, tributions of increased oxidative stress, defects in mitochondrial 2010). dysfunction and cellular energy production, chronic inflammatory A recent NIH scientific roundtable concluded that there is mechanisms, and even direct pathways to amyloid accumulation no definitive evidence for benefit of any preventive strategy for and neurofibrillary degeneration that contribute to the degen- AD, however, this working group also concluded that preventa- erative cascade in AD (Figure 1; Rao and Balachandran, 2002; tive strategies focused on modifying environmental risk factors Lau et al., 2007; Weih et al., 2007; Pasinetti and Eberstein, 2008; deserves further scientific exploration and study (Daviglus et al., Kamphuis and Scheltens, 2010; Cunnane et al., 2011; Pocernich Frontiers in Aging Neuroscience www.frontiersin.org October 2014 | Volume 6 | Article 282 | 1 Swaminathan and Jicha Nutrition and prevention of Alzheimer’s dementia FIGURE 1 | Diagram of multiple influences of dietary constituents on vascular integrity, and neuronal injury and loss. Note: specific dietary cellular pathways and process linked to neurodegeneration in AD. factors may have more than one potential mechanism of action on the Antioxidants, trace minerals, flavonoids, metabolic substrates and pathogenic processes contributing to neurodegeneration in AD. Links modulators, vitamins, and omega-3 fatty acids, among others, have all between pathological processes implicated in the development of AD may been shown to downregulate the many pathological processes linked to not be linear, but rather additive and are shown in a circular fashion the development of AD, including aging, amyloid deposition, neurofibrillary without implication for specific linkages or temporal associations between degeneration, synapse loss, inflammation, metabolic compromise, loss of such processes. et al., 2011; Solfrizzi et al., 2011; Rubio-Perez and Morillas-Ruiz, prevention of AD; (2) Considerations of dietary excess and the 2012; Thaipisuttikul and Galvin, 2012; Gillette-Guyonnet et al., negative consequences of some dietary constituents (especially 2013; Hu et al., 2013; Shah, 2013). Nutritional modifications those characterizing the current “Western” diet, may interfere have the advantage of being cost effective, easy to implement, with the potentially positive effects of specific nutritional inter- socially acceptable and generally safe and devoid of significant ventions). This has been clearly shown in regards to benefits of adverse events in most cases. Many nutritional interventions have omega-3 fatty acids that are neutralized by high dietary intake been studied and continue to be evaluated in hopes of finding of omega-6 and saturated fats; (3) Our current understanding of a successful compound that can be used
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