{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:07:01Z","timestamp":1790813221858,"version":"4.1.0"},"reference-count":25,"publisher":"F1000 Research Ltd","license":[{"start":{"date-parts":[[2017,4,3]],"date-time":"2017-04-03T00:00:00Z","timestamp":1491177600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["I01RX002333"],"award-info":[{"award-number":["I01RX002333"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000738","name":"U.S. Department of Veterans Affairs","doi-asserted-by":"publisher","award":["I01RX000684"],"award-info":[{"award-number":["I01RX000684"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["AG05138"],"award-info":[{"award-number":["AG05138"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["U01AG046170"],"award-info":[{"award-number":["U01AG046170"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Louis B. Mayer Foundation"},{"name":"Georgianne and Doctor Reza Khatib Foundation"}],"content-domain":{"domain":["f1000research.com"],"crossmark-restriction":false},"short-container-title":["F1000Res"],"abstract":"<ns4:p>\n                    The basic strategy for focusing exclusively on genetically identified targets for intervening in late life dementias was formulated 30 years ago.\u00a0 Three decades and billions of dollars later, all efforts at disease-modifying interventions have failed.\u00a0 Over that same period, evidence has accrued pointing to dementias as late-life clinical phenotypes that begin as midlife pathologies.\u00a0 Effective prevention therefore may need to begin in midlife, in order to succeed. No current interventions are sufficiently safe to justify their use in midlife dementia prevention trials.\u00a0 Observational studies could be informative in testing the proposal that amyloid imaging and\n                    <ns4:italic>APOE<\/ns4:italic>\n                    \u03b5\n                    <ns4:italic>4<\/ns4:italic>\n                    genotype can predict those who are highly likely to develop Alzheimer\u2019s disease and in whom higher risk interventions might be justifiable. A naturally occurring, diet-responsive cognitive decline syndrome occurs in canines that closely resembles human Alzheimer\u2019s.\u00a0 Canine cognitive dysfunction could be useful in estimating how early intervention must begin in order to succeed.\u00a0 This model may also help identify and assess novel targets and strategies.\u00a0 New approaches to dementia prevention are urgently required, since none of the world\u2019s economies can sustain the costs of caring for this epidemic of brain failure that is devastating half of the over 85-year-olds globally.\n                  <\/ns4:p>","DOI":"10.12688\/f1000research.11140.1","type":"journal-article","created":{"date-parts":[[2017,4,3]],"date-time":"2017-04-03T10:35:50Z","timestamp":1491215750000},"page":"413","update-policy":"https:\/\/doi.org\/10.12688\/f1000research.crossmark-policy","source":"Crossref","is-referenced-by-count":17,"title":["Midlife interventions are critical in prevention, delay, or improvement of Alzheimer\u2019s disease and vascular cognitive impairment and dementia"],"prefix":"10.12688","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6455-4721","authenticated-orcid":false,"given":"Sam","family":"Gandy","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tamas","family":"Bartfai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Graham V.","family":"Lees","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary","family":"Sano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"2560","published-online":{"date-parts":[[2017,4,3]]},"reference":[{"key":"ref-1","doi-asserted-by":"publisher","first-page":"97","DOI":"10.1016\/S1474-4422(16)30395-7","article-title":"Solanezumab: too late in mild Alzheimer's disease?","volume":"16","year":"2017","journal-title":"Lancet 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Genet."},{"key":"ref-12","article-title":"After Solanezumab: Where Should Alzheimer\u2019s Research Go?","author":"B De Strooper","year":"2017","journal-title":"Alzforum."},{"key":"ref-13","doi-asserted-by":"publisher","first-page":"422-8","DOI":"10.1016\/j.biopsych.2012.08.015","article-title":"Effect of complement CR1 on brain amyloid burden during aging and its modification by APOE genotype.","volume":"73","author":"M Thambisetty","year":"2013","journal-title":"Biol Psychiatry."},{"key":"ref-14","doi-asserted-by":"publisher","first-page":"393-5","DOI":"10.1016\/j.biopsych.2013.01.013","article-title":"CR1 and the \"vanishing amyloid\" hypothesis of Alzheimer's disease.","volume":"73","author":"S Gandy","year":"2013","journal-title":"Biol Psychiatry."},{"key":"ref-15","doi-asserted-by":"publisher","first-page":"9831-9","DOI":"10.1523\/JNEUROSCI.6194-09.2010","article-title":"Synergistic effects of long-term antioxidant diet and behavioral enrichment on beta-amyloid load and non-amyloidogenic processing in aged canines.","volume":"30","author":"V Pop","year":"2010","journal-title":"J Neurosci."},{"key":"ref-16","doi-asserted-by":"publisher","first-page":"2255-63","DOI":"10.1016\/S0140-6736(15)60461-5","article-title":"A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial.","volume":"385","author":"T Ngandu","year":"2015","journal-title":"Lancet."},{"key":"ref-17","doi-asserted-by":"publisher","first-page":"299-307","DOI":"10.1111\/j.1600-0447.2007.01006.x","article-title":"Prevalence of dementia in a southern European population in two different time periods: the ZARADEMP Project.","volume":"116","author":"A Lobo","year":"2007","journal-title":"Acta Psychiatr Scand."},{"key":"ref-18","doi-asserted-by":"publisher","first-page":"319-25","DOI":"10.1111\/j.1600-0447.2010.01587.x","article-title":"Trends 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Hong Kong and taiwan: a systematic review and meta-analysis.","volume":"8","author":"Y Wu","year":"2013","journal-title":"PLoS One."},{"key":"ref-22","doi-asserted-by":"publisher","first-page":"1888-94","DOI":"10.1212\/WNL.0b013e318292a2f9","article-title":"Twenty-year changes in dementia  occurrence suggest decreasing incidence in central Stockholm, Sweden.","volume":"80","author":"C Qiu","year":"2013","journal-title":"Neurology."},{"key":"ref-23","doi-asserted-by":"publisher","first-page":"387-96","DOI":"10.3233\/JAD-150708","article-title":"Cohort Effects in the Prevalence and Survival of People with Dementia in a Rural Area in Northern Sweden.","volume":"50","author":"A Wimo","year":"2016","journal-title":"J Alzheimers Dis."},{"key":"ref-24","doi-asserted-by":"publisher","first-page":"32-37","DOI":"10.1038\/scientificamerican0417-32","article-title":"A Rare Success against Alzheimer\u2019s.","volume":"316","author":"M Kivipelto","year":"2017","journal-title":"Sci 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Jack","year":"2015","journal-title":"Brain."}],"container-title":["F1000Research"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/f1000research.com\/articles\/6-413\/v1\/xml","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/f1000research.com\/articles\/6-413\/v1\/pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/f1000research.com\/articles\/6-413\/v1\/iparadigms","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2018,12,6]],"date-time":"2018-12-06T10:18:16Z","timestamp":1544091496000},"score":1,"resource":{"primary":{"URL":"https:\/\/f1000research.com\/articles\/6-413\/v1"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2017,4,3]]},"references-count":25,"URL":"https:\/\/doi.org\/10.12688\/f1000research.11140.1","relation":{"has-review":[{"id-type":"doi","id":"10.5256\/f1000research.12018.r21939","asserted-by":"subject"},{"id-type":"doi","id":"10.5256\/f1000research.12018.r21956","asserted-by":"subject"},{"id-type":"doi","id":"10.5256\/f1000research.12018.r21939","asserted-by":"object"},{"id-type":"doi","id":"10.5256\/f1000research.12018.r21956","asserted-by":"object"}]},"ISSN":["2046-1402"],"issn-type":[{"value":"2046-1402","type":"electronic"}],"subject":[],"published":{"date-parts":[[2017,4,3]]},"assertion":[{"value":"Indexed","URL":"https:\/\/f1000research.com\/articles\/6-413\/v1#article-reports","order":0,"name":"referee-status","label":"Referee status","group":{"name":"current-referee-status","label":"Current Referee Status"}},{"value":"10.5256\/f1000research.12018.r21939, W.Sue T Griffin, Orwa Aboud, Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA, 18 Apr 2017, version 1, indexed","URL":"https:\/\/f1000research.com\/articles\/6-413\/v1#referee-response-21939","order":0,"name":"referee-response-21939","label":"Referee Report","group":{"name":"article-reports","label":"Article Reports"}},{"value":"<b>William Grant<\/b>; \n<i>Posted: 15 May 2017<\/i>; The opinion article by Gandy et al. discusses some important issues regarding preventing, delaying, and \/or preventing Alzheimer's disease (AD).\n<sup>1<\/sup> Near the end, they discuss the role of diet and lifestyle in affecting risk of AD, a topic I have studied for 20 years. In this commentary I add a few observations regarding that point.From the study of AD prevalence rates with respect to national diets, it is found that diet appears to be the most important risk-modifying factor. For example, AD prevalence rates for elderly in Japan increased from 1% in 1985 to 7% in 2008, lagging the nutrition transition from the traditional Japanese diet to the Western diet by 15-25 years.\n<sup>2<\/sup> The major changes were a 5-fold increase in meat consumption and a 50% reduction in rice consumption. In a recent 10-country study, it was found that meat, eggs, fish, and cheese were highly correlated with AD prevalence.\n<sup>3<\/sup>The Mediterranean diet, which is touted as reducing risk of AD by about 50%, was found to lie in the middle of the regression fit to AD prevalence vs. meat consumption. The mechanisms whereby eating animal products increases risk of AD include the effects of cholesterol and increasing the intake of heavy metals while reducing intake of beneficial trace minerals (calcium, magnesium, potassium), thereby leading to increased destruction of neurons by free radicals. Cooking meat at high, dry temperatures also increases production of advanced glycation end products (AGEs), which also increase risk of AD.\n<sup>4<\/sup>&nbsp;The dietary links to AD are somewhat similar to those for coronary heart disease (CHD).\n<sup>5<\/sup> Thus, the experience in reducing risk of CHD through diet and lifestyle changes should provide some guidance for preventing AD. A good example comes from Finland. A young physician, Pekka Puska, observed that the highest cardiovascular disease mortality rates in the world were in North Karelia and were associated with high intake of saturated fats and high serum cholesterol levels.\n<sup>6<\/sup> He organized a community-based program that reduced intake of saturated fats from 20% to 12% in 2007. This project led to large reductions in CHD mortality rates, from 647\/100,000\/yr for men and 114\/100,000\/yr for women in 1969-72 to from 289\/100,000\/yr for men and 36\/100,000\/yr for women in 1992.\n<sup>7<\/sup>&nbsp;Higher sun exposure and vitamin D status are also associated with reduced risk of AD.\n<sup>8<\/sup> Interestingly, a study in New York state found that those who had non-melanoma skin cancer had a greatly reduced incidence of AD.\n<sup>9<\/sup>&nbsp;It is unlikely that public health policies in the U.S. and many other countries will lead to reduced consumption of animal products among those middle aged or older anytime soon. However, individuals can learn the advantages of whole-plant based diets and reduce their personal risk of AD, CHD, and, as an added bonus, many types of cancer.\n<sup>10,11<\/sup>References1. Gandy S, Bartfai T, Lees GV, Sano M. Midlife interventions are critical in prevention, delay, or improvement of&nbsp;Alzheimer's&nbsp;disease&nbsp;and vascular cognitive impairment and dementia. F1000Res. 2017 Apr 3;6:4132. Grant WB. Trends in diet and Alzheimer\u2019s disease during the nutrition transition in Japan and developing countries. J Alz Dis. 2014;38(3):611-20.3. Grant WB. Using Multicountry Ecological and Observational Studies to Determine Dietary Risk Factors for Alzheimer\u2019s Disease. J Am Coll Nutr, 2016;35(5):476\u2013489.&nbsp; http:\/\/www.tandfonline.com\/doi\/full\/10.1080\/07315724.2016.11615664. Perrone L, Grant WB. Observational and ecological studies&nbsp; of dietary advanced glycation end products &nbsp;in national diets and Alzheimer\u2019s disease incidence and prevalence. J Alz Dis. 2015;45: 965\u201379.5. Rafique R, Amjad N. Dietary predictors of early-onset ischaemic&nbsp;heart&nbsp;disease&nbsp;in a sample drawn from a Pakistani population. Heart&nbsp;Asia. 2012;4(1):129-34.6. Vartiainen E, Laatikainen T, Tapanainen H, Puska P. Changes in Serum Cholesterol and Diet in North Karelia and All Finland. Glob&nbsp;Heart. 2016;11(2):179-84.&nbsp;7. Vartiainen E,&nbsp;Puska P,&nbsp;Pekkanen J,&nbsp;et al. Changes in risk factors explain changes in mortality from ischaemic heart disease in Finland. BMJ. 1994;309(6946):23-7.8. Afzal S, Bojesen SE, Nordestgaard BG. Reduced 25-hydroxyvitamin D and risk of Alzheimer's disease and vascular dementia. Alzheimers Dement. 2014;10(3):296-302.9. White RS, Lipton RB, Hall CB, Steinerman JR. Nonmelanoma skin cancer is associated with reduced Alzheimer disease risk. Neurology. 2013;80(21):1966-72.10. Aune&nbsp;D, De Stefani E, Ronco A, Boffetta P, Deneo-Pellegrini H, Acosta G, Mendilaharsu M. Meat&nbsp;consumption and&nbsp;cancer&nbsp;risk: a case-control study in&nbsp;Uruguay. Asian Pac J&nbsp;Cancer&nbsp;Prev.&nbsp;2009;10(3):429-36.11. Grant WB. A multicountry ecological study of cancer incidence rates in 2008 with respect to various risk-modifying factors, Nutrients. 2013;\n<i>6<\/i>(1):163-189.","URL":"https:\/\/f1000research.com\/articles\/6-413\/v1#referee-comment-2706","order":1,"name":"referee-comment-2706","label":"Referee Comment","group":{"name":"article-reports","label":"Article Reports"}},{"value":"10.5256\/f1000research.12018.r21956, Domenico Pratico, Department of Pharmacology, Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA, 19 Apr 2017, version 1, indexed","URL":"https:\/\/f1000research.com\/articles\/6-413\/v1#referee-response-21956","order":2,"name":"referee-response-21956","label":"Referee Report","group":{"name":"article-reports","label":"Article Reports"}},{"value":"<b>Feng-Yen Li<\/b>; \n<i>Posted: 17 Aug 2017<\/i>; The authors pinpointed a number of important caveats with the current therapeutic development pipeline for Alzheimer\u2019s disease and related dementia. They astutely recognized that \u201cwe must be open-minded about the trap laid by the early success of identifying genes and molecular mechanisms of the familial Alzheimer\u2019s patients.\u201d As indicated by the continuing failures of pharmacological developments, researchers are focusing on the wrong targets. Their advice to shift the research focus from anti-proteinopathy treatments to modifying midlife risk factors with lifestyle interventions is very sound, insightful, and well-supported: \u201cIn the meantime, the importance and potential benefit of safe and easy diet and lifestyle changes for humans should be a topic of much stronger advocacy.\u201d However, their suggestion to use canine models to further such studies may not be a wise recommendation as there will always be physiological differences between animals and humans that can limit translation. After all, despite the potential of the dietary and behavioral intervention to modulate amyloid-beta in the canine model, the cited study in the paper for this model stated that \u201camyloid-beta measures did not correlate with cognitive performance on any of the 6 tasks assessed, suggesting that modulation of amyloid-beta alone may be a relatively minor mechanism mediating cognitive benefits of the interventions.\u201d Plus, any findings in such animal models will need to be confirmed in humans. Given that dietary and lifestyle interventions can be directly tested in humans without safety concerns, it would best to complete such studies in humans rather than animal models to avoid the extra cost, time, and potential misleading conclusions.The commentary posted by William Grant above pointed to strong epidemiological evidence for the association of AD prevalence and animal product consumption. He also makes the astute observation that the risk factors of AD are similar to those of CHD and provides lessons to be learned from studies demonstrating the feasibility of using dietary and lifestyle interventions to reduce CHD mortality. He further suggests a whole-plant based diet together with supplementation of important nutrients like vitamin D as an effective strategy to reduce the prevalence of many chronic diseases, including AD, CHD, and many cancers. Indeed, the effectiveness of such dietary interventions has already been shown to be highly effective even for reversing CHD, diabetes, and even cancers\n<sup>1-5<\/sup>. A randomized controlled trial testing the efficacy of the whole food plant-based diet supplemented with key anti-inflammatory, neuroprotective nutrients (e.g. vitamin D, B12, algae-based omega-3, turmeric, etc) for the prevention or reversal AD and related dementia promises to help reverse the current epidemiological trends for this burdensome disease.  Esselstyn CB Jr, Gendy G, Doyle J, Golubic M, Roizen MF. A way to reverse CAD? J Fam Pract. 2014 Jul;63(7):356-364b. Lee YM, Kim SA, Lee IK, Kim JG, Park KG, Jeong JY, Jeon JH, Shin JY, Lee DH. Effect of a Brown Rice Based Vegan Diet and Conventional Diabetic Diet on Glycemic Control of Patients with Type 2 Diabetes: A 12-Week Randomized Clinical Trial. PLoS One. 2016 Jun 2;11(6):e0155918. Barnard ND, Cohen J, Jenkins DJ, Turner-McGrievy G, Gloede L, Green A, Ferdowsian H. A low-fat vegan diet and a conventional diabetes diet in the treatment of type 2 diabetes: a randomized, controlled, 74-wk clinical trial. Am J Clin Nutr. 2009 May;89(5):1588S-1596S. Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO, Crutchfield L, Yglecias L, Carroll PR, Ornish D. Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology. 2008 Dec;72(6):1319-23 Saxe GA, Major JM, Nguyen JY, Freeman KM, Downs TM, Salem CE. Potential attenuation of disease progression in recurrent prostate cancer with plant-based diet and stress reduction. Integr Cancer Ther. 2006 Sep;5(3):206-13.","URL":"https:\/\/f1000research.com\/articles\/6-413\/v1#article-response-2961","order":3,"name":"article-response-2961","label":"Article Comment","group":{"name":"article-comments","label":"Article Comments"}},{"value":"MS and SG would like to acknowledge the support of National Institute on Aging P50 Alzheimer\u2019s Disease Research Center (AG05138) to MS. SG would also like to acknowledge the support of the Louis B. Mayer Foundation, the Georgianne and Doctor Reza Khatib Foundation, VA MERIT (I01RX002333 and I01RX000684), and NIH Accelerating Medicines Partnership (U01AG046170) to Eric Schadt, Icahn School of Medicine. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.","order":4,"name":"grant-information","label":"Grant Information"},{"value":"This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Data associated with the article are available under the terms of the Creative Commons Zero \"No rights reserved\" data waiver (CC0 1.0 Public domain dedication).","order":0,"name":"copyright-info","label":"Copyright"}]}}