Key points are not available for this paper at this time.
Compelling evidence indicates that excess consumption of sugar-sweetened beverages plays an important role in the epidemic of obesity, a major risk factor for type 2 diabetes mellitus. Type 2 diabetes mellitus has been associated with a higher incidence of Alzheimer disease (AD). High fat diets promote AD-like pathology in mice. It is not known whether consumption of excess sugar as in calorically sweetened beverages with an otherwise normal diet affects the development of AD. In the present study, we provided 10% sucrose-sweetened water to a transgenic mouse model of AD with a normal rodent diet. Compared with the control mice with no sucrose added in the water, the sucrose group gained more body weight and developed glucose intolerance, hyperinsulinemia, and hypercholesterolemia. These metabolic changes were associated with the exacerbation of memory impairment and a 2–3-fold increase in insoluble amyloid-β protein levels and deposition in the brain. We further showed that the levels of expression and secretase-cleaved products of amyloid-β precursor protein were not affected by sucrose intake. The steady-state levels of insulin-degrading enzyme did not change significantly, whereas there was a 2.5-fold increase in brain apoE levels. Therefore, we concluded that the up-regulation of apoE accelerated the aggregation of Aβ, resulting in the exacerbation of cerebral amyloidosis in sucrose-treated mice. These data underscore the potential role of dietary sugar in the pathogenesis of AD and suggest that controlling the consumption of sugar-sweetened beverages may be an effective way to curtail the risk of developing AD. Compelling evidence indicates that excess consumption of sugar-sweetened beverages plays an important role in the epidemic of obesity, a major risk factor for type 2 diabetes mellitus. Type 2 diabetes mellitus has been associated with a higher incidence of Alzheimer disease (AD). High fat diets promote AD-like pathology in mice. It is not known whether consumption of excess sugar as in calorically sweetened beverages with an otherwise normal diet affects the development of AD. In the present study, we provided 10% sucrose-sweetened water to a transgenic mouse model of AD with a normal rodent diet. Compared with the control mice with no sucrose added in the water, the sucrose group gained more body weight and developed glucose intolerance, hyperinsulinemia, and hypercholesterolemia. These metabolic changes were associated with the exacerbation of memory impairment and a 2–3-fold increase in insoluble amyloid-β protein levels and deposition in the brain. We further showed that the levels of expression and secretase-cleaved products of amyloid-β precursor protein were not affected by sucrose intake. The steady-state levels of insulin-degrading enzyme did not change significantly, whereas there was a 2.5-fold increase in brain apoE levels. Therefore, we concluded that the up-regulation of apoE accelerated the aggregation of Aβ, resulting in the exacerbation of cerebral amyloidosis in sucrose-treated mice. These data underscore the potential role of dietary sugar in the pathogenesis of AD and suggest that controlling the consumption of sugar-sweetened beverages may be an effective way to curtail the risk of developing AD. Added sugars, mainly sucrose and high fructose corn syrup, are major components of a modern human diet. Compelling evidence indicates that excess consumption of sweet foods, particularly sugar-sweetened beverages, plays an important role in the epidemic of obesity around the world (1Bray G.A. Nielsen S.J. Popkin B.M. Am. J. Clin. Nutr. 2004; 79: 537-543Crossref PubMed Scopus (1489) Google Scholar). In the United States, the percentage of children who are overweight has doubled, and the percentage of teenagers who are overweight has tripled (2Hedley A.A. Ogden C.L. Johnson C.L. Carroll M.D. Curtin L.R. Flegal K.M. J. Am. Med. Assoc. 2004; 291: 2847-2850Crossref PubMed Scopus (3583) Google Scholar, 3Ogden C.L. Flegal K.M. Carroll M.D. Johnson C.L. J. Am. Med. Assoc. 2002; 288: 1728-1732Crossref PubMed Scopus (3284) Google Scholar). Overweight children are at an increased risk to become obese adults (4Whitaker R.C. Wright J.A. Pepe M.S. Seidel K.D. Dietz W.H. N. Engl. J. Med. 1997; 337: 869-873Crossref PubMed Scopus (3274) Google Scholar). Even moderate obesity can contribute to chronic metabolic abnormalities leading to type 2 diabetes mellitus (5Grundy S.M. Am. J. Clin. Nutr. 1998; 67: 563S-572SCrossref PubMed Scopus (270) Google Scholar) characterized by glucose intolerance and hyperinsulinemia. Alzheimer disease (AD) 2The abbreviations used are:ADAlzheimer diseaseAPPamyloid-β precursor proteinAβamyloid-β proteinPSpresenilinELISAenzyme-linked immunosorbent assayIDEinsulin-degrading enzymeHDLhigh density lipoproteinTGtriglyceridesCTFC-terminal fragmentsapoapolipoprotein. is a progressive neurodegenerative disease characterized clinically by progressive cognitive impairment. Pathological hallmarks of the AD brain include intracellular neurofibrillary tangles and deposits of aggregated amyloid-β protein (Aβ) in neuritic plaques and cerebral vessels. The pathogenic mechanisms that lead to the development of AD, however, are not fully understood. One of the main hypotheses is that β-amyloidosis (production and deposition of Aβ) plays a crucial role in the pathogenesis of AD (6Selkoe D.J. Neurol. Clin. 2000; 18: 903-922Abstract Full Text Full Text PDF PubMed Scopus (136) Google Scholar). Aβ (39–43 amino acids) is derived from a large transmembrane glycoprotein, amyloid-β precursor protein (APP), via proteolytic processing by secretases (6Selkoe D.J. Neurol. Clin. 2000; 18: 903-922Abstract Full Text Full Text PDF PubMed Scopus (136) Google Scholar). This hypothesis is supported by discoveries of causative mutations in the gene encoding APP and in genes of presenilin (PS)-1 and -2 in early onset familial AD (7Hardy J. Trends Neurosci. 1997; 20: 154-159Abstract Full Text Full Text PDF PubMed Scopus (1277) Google Scholar). Alzheimer disease amyloid-β precursor protein amyloid-β protein presenilin enzyme-linked immunosorbent assay insulin-degrading enzyme high density lipoprotein triglycerides C-terminal fragments apolipoprotein Recently, numerous epidemiological studies suggest that type 2 diabetes mellitus is associated with an increased risk of AD (reviewed in Ref. 8Haan M.N. Nat. Clin. Pract. Neurol. 2006; 2: 159-166Crossref PubMed Scopus (233) Google Scholar), independent of the risk for vascular dementia (9Leibson C.L. Rocca W.A. Hanson V.A. Cha R. Kokmen E. O'Brien P.C. Palumbo P.J. Am. J. Epidemiol. 1997; 145: 301-308Crossref PubMed Scopus (564) Google Scholar, 10Stolk R.P. Breteler M.M. Ott A. Pols H.A. Lamberts S.W. Grobbee D.E. Hofman A. Diabetes Care. 1997; 20: 792-795Crossref PubMed Scopus (182) Google Scholar). The mechanisms by which type 2 diabetes mellitus may impact AD, however, are not well understood. Several lines of evidence indicate that insulin itself and metabolic abnormalities pertinent to diabetes may affect the generation and degradation of Aβ (11Craft S. Watson G.S. Lancet Neurol. 2004; 3: 169-178Abstract Full Text Full Text PDF PubMed Scopus (687) Google Scholar). Higher fat intake and excess body weight increase the risk of AD (12Mattson M.P. Ann. Intern. Med. 2003; 139: 441-444Crossref PubMed Google Scholar). We and others have shown that in transgenic mouse models of AD, high fat diets promote the development of AD-type neuropathology (13Refolo L.M. Malester B. LaFrancois J. Bryant-Thomas T. Wang R. Tint G.S. Sambamurti K. Duff K. Pappolla M.A. Neurobiol. Dis. 2000; 7: 321-331Crossref PubMed Scopus (889) Google Scholar, 14Shie F.S. Jin L.W. Cook D.G. Leverenz J.B. LeBoeuf R.C. Neuroreport. 2002; 13: 455-459Crossref PubMed Scopus (195) Google Scholar, 15Levin-Allerhand J.A. Lominska C.E. Smith J.D. J. Nutr. Health Aging. 2002; 6: 315-319PubMed Google Scholar, 16Li L. Cao D. Garber D.W. Kim H. Fukuchi K. Am. J. Pathol. 2003; 163: 2155-2164Abstract Full Text Full Text PDF PubMed Scopus (116) Google Scholar) and cognitive impairment (16Li L. Cao D. Garber D.W. Kim H. Fukuchi K. Am. J. Pathol. 2003; 163: 2155-2164Abstract Full Text Full Text PDF PubMed Scopus (116) Google Scholar). Insulin resistance may be one of the underlying mechanisms for the effects of high fat diets on AD (17Ho L. Qin W. Pompl P.N. Xiang Z. Wang J. Zhao Z. Peng Y. Cambareri G. Rocher A. Mobbs C.V. Hof P.R. Pasinetti G.M. FASEB J. 2004; 18: 902-904Crossref PubMed Scopus (538) Google Scholar). Whether excess consumption of simple sugars as in calorically sweetened beverages with an otherwise normal diet affects the development of AD has not been investigated experimentally. In the present study, we provided sucrose-sweetened water to APP/PS1 double transgenic mice (18Jankowsky J.L. Slunt H.H. Ratovitski T. Jenkins N.A. Copeland N.G. Borchelt D.R. Biomol. Eng. 2001; 17: 157-165Crossref PubMed Scopus (616) Google Scholar, 19Jankowsky J.L. Fadale D.J. Anderson J. Xu G.M. Gonzales V. Jenkins N.A. Copeland N.G. Lee M.K. Younkin L.H. Wagner S.L. Younkin S.G. Borchelt D.R. Hum. Mol. Genet. 2004; 13: 159-170Crossref PubMed Scopus (1143) Google Scholar), an established model of AD, fed a regular low fat diet and assessed the effect of added sucrose in water on AD-like behavior and neuropathology. Our results showed that intake of sucrose-sweetened water induced insulin resistance and exacerbated AD-like memory impairment and cerebral amyloidosis. Animals and Diets—APP/PS1 double transgenic mice used in this study were obtained from Jackson Laboratory (Bar Harbor, ME) (strain name B6C3-Tg(APPswe,PSEN1dE9)85Dbo/J; stock number 004462). These mice express a chimeric mouse/human amyloid-β precursor protein containing the K595N/M596L Swedish mutations and a mutant human presenilin 1 carrying the exon 9-deleted variant under the control of mouse prion promoter elements, directing transgene expression predominantly to central nervous system neurons (18Jankowsky J.L. Slunt H.H. Ratovitski T. Jenkins N.A. Copeland N.G. Borchelt D.R. Biomol. Eng. 2001; 17: 157-165Crossref PubMed Scopus (616) Google Scholar, 19Jankowsky J.L. Fadale D.J. Anderson J. Xu G.M. Gonzales V. Jenkins N.A. Copeland N.G. Lee M.K. Younkin L.H. Wagner S.L. Younkin S.G. Borchelt D.R. Hum. Mol. Genet. 2004; 13: 159-170Crossref PubMed Scopus (1143) Google Scholar). The two transgenes co-segregate in these mice. APP/PS1 mice were maintained as double by with mice on a stock number and were by of from APP/PS1 mice AD-like memory and plaques in the brain by of In this study, APP/PS1 mice were provided with a of 10% sucrose water These mice were on a normal rodent diet mouse diet and of this diet are and corn with of amino and and intake of mice were by the of and of of the the mice were to a of by of metabolic changes and neuropathology as used for this study were and by the and of the of at of and of and were The of the the the for levels and and in the water and were from have been in L. Cao D. Kim H. R. Fukuchi K. Ann. Neurol. 2006; PubMed Scopus Google Scholar, D. Fukuchi K. H. Kim H. L. Neurobiol. Aging. 2006; PubMed Scopus Google Scholar). and memory were in the water of a with water with The of the of the mice to and the in and with the 1 water in the of the In the mouse was to the at which the mouse was to the The mouse was to on the for The and were by the system for for The the a was by the and the mouse to and the The in the was in a the of the was with the 1 water and to the was on of the as a of glucose was as (17Ho L. Qin W. Pompl P.N. Xiang Z. Wang J. Zhao Z. Peng Y. Cambareri G. Rocher A. Mobbs C.V. Hof P.R. Pasinetti G.M. FASEB J. 2004; 18: 902-904Crossref PubMed Scopus (538) Google Scholar) with mice were a of of glucose body and were obtained from the a glucose was by the the insulin levels were by the enzyme-linked immunosorbent assay and high density lipoprotein levels were with levels were with the were with and was via with as an with were and The was in for the and the was in and at for Aβ and and insoluble of Aβ, brain were in containing and 1 of was at for at The was to and at The was to further in the in The was for at at for at the was to and at The levels of and in the and insoluble were with and the The in the brain was with the of was to further with the and as we in L. Cao D. Kim H. R. Fukuchi K. Ann. Neurol. 2006; PubMed Scopus Google Scholar, D. Fukuchi K. H. Kim H. L. Neurobiol. Aging. 2006; PubMed Scopus Google Scholar). used for amino of mouse apoE the of APP and insulin-degrading enzyme a the were and with a mouse and of Aβ for have been L. Cao D. Kim H. R. Fukuchi K. Ann. Neurol. 2006; PubMed Scopus Google Scholar). and were to the The used for of Aβ deposition was The in the and of mouse brain were a were and from of mouse brain. of the Aβ was to the as a percentage of by Aβ were as of was by and of was used for was of APP/PS1 APP/PS1 mice used in this study a chimeric mouse/human APP containing the K595N/M596L Swedish mutations and a mutant human with the exon under the control of mouse prion promoter (18Jankowsky J.L. Slunt H.H. Ratovitski T. Jenkins N.A. Copeland N.G. Borchelt D.R. Biomol. Eng. 2001; 17: 157-165Crossref PubMed Scopus (616) Google Scholar, 19Jankowsky J.L. Fadale D.J. Anderson J. Xu G.M. Gonzales V. Jenkins N.A. Copeland N.G. Lee M.K. Younkin L.H. Wagner S.L. Younkin S.G. Borchelt D.R. Hum. Mol. Genet. 2004; 13: 159-170Crossref PubMed Scopus (1143) Google Scholar). The two transgenes co-segregate in these mice. APP/PS1 mice were maintained as double AD-like memory and plaques in the brain by of In this study, APP/PS1 mice were fed a normal rodent diet and provided with a of 10% sucrose water of at an of the mice were to a of by of metabolic changes and neuropathology. of to and in APP/PS1 and water intake of the mice were the the sucrose-sweetened water, the mice the sucrose group intake was higher in the sucrose group of which was by in the water control group body weight showed that the mice with to sucrose-sweetened water to more body weight the mice the sucrose at and this was for the of the the of the the body weight of the sucrose group was higher that of the control group glucose in these an glucose was in which glucose was an of glucose body in mice. The sucrose group an glucose of for for In with these insulin levels were by in the sucrose group showed that sucrose intake a increase in levels no effect on levels of high density lipoprotein and These data that intake of sucrose-sweetened water to increased body weight and induced insulin resistance in APP/PS1 mice fed a normal diet. of and in APP/PS1 whether sucrose intake affects in APP/PS1 a of was The water was to the and memory of the mice. as a normal a group of mice of APP/PS1 were in the shown in mice to the of Compared with APP/PS1 control mice showed the of The sucrose-treated APP/PS1 however, to the at the of The by the sucrose group indicates a as to a not there was no in In a the mice of in a the by APP/PS1 mice and was not the and the APP/PS1 mice the the sucrose-treated APP/PS1 mice showed no memory of the In the of the water that there were no changes of and associated with sucrose In sucrose intake no effects on in an on in a on in an These data further indicate that impairment of and memory by sucrose intake was not by and levels of APP/PS1 of in the central to of in in a of in APP/PS1 the effect of sucrose-sweetened water intake on cerebral in APP/PS1 Aβ in the and insoluble in the were by no in and was the two insoluble were increased in the of mice sucrose-sweetened water showed that Aβ was increased by in the sucrose group and with these and showed that there was a increase in Aβ deposition in the brain of mice in the sucrose group of cerebral amyloidosis in APP/PS1 mice sucrose-sweetened of Aβ levels in the cerebral of by the of with the levels in control group as The Aβ was increased in the sucrose and of brain from a control and sucrose-treated cerebral Aβ by and The was increased by in the sucrose on of the APP and C-terminal of APP by and whether the increase of Aβ levels in the brain of mice in the sucrose group was by an increase in the generation of Aβ from we the levels of APP and of APP by and by The results showed that there were no in the of and that the expression of the APP transgene and the processing of APP by and were not affected by excess intake of sucrose-sweetened water in APP/PS1 mice. of on the of and in the of APP/PS1 no changes in the of Aβ from we the that are in Aβ degradation and for to has been as one of the to Aβ D.J. 2001; Full Text Full Text PDF PubMed Scopus Google Scholar). We that the increase of Aβ in the brain of mice in the sucrose group be by a of cerebral which has been associated with insulin resistance and AD pathology (17Ho L. Qin W. Pompl P.N. Xiang Z. Wang J. Zhao Z. Peng Y. Cambareri G. Rocher A. Mobbs C.V. Hof P.R. Pasinetti G.M. FASEB J. 2004; 18: 902-904Crossref PubMed Scopus (538) Google Scholar, W. S. Y. L. M.P. D.J. S. S. A. 2003; PubMed Scopus Google Scholar). The of in the brain was by The results showed that the of in the sucrose group was by with that of the control group this did not We the of apoE in the brain. plays a role in the development of AD-like pathology in mouse models of AD T. R.C. Y. L. D.J. B. S.M. Nat. Genet. 1997; 17: PubMed Scopus Google Scholar). apoE is and aggregation and of Aβ B. T. L. S.M. K. Ann. Neurol. 2000; PubMed Scopus Google Scholar). Our results that the of apoE was 2.5-fold in the brain of mice in the sucrose group with that in the control group The brain however, was not the two In this study, we showed that consumption of sucrose-sweetened water to increased body glucose intolerance, insulin and in APP/PS1 mice fed a normal low fat rodent diet. These metabolic changes were associated with exacerbation of and memory impairment and cerebral Aβ deposition in this mouse model of AD. One of the mechanisms by which consumption of sugar-sweetened beverages body weight is to be the increase of intake Am. J. Clin. Nutr. 2006; PubMed Google Scholar). This to be the in the present The in intake was not to for the from sucrose-sweetened The sucrose group an of increase in which for the increase in body In the mice sucrose-sweetened water, of intake was provided by on a diet for this of consumption of sugar-sweetened beverages a this may to be on the of consumption in is that there is no sugar intake from In may not be to the data from mice to the metabolic of mice is higher that of J. 2004; Full Text Full Text PDF PubMed Scopus Google Scholar). Therefore, in is that a of sucrose consumption in effects as we in mice. is not to the effects by increased sucrose intake and increased intake from the present study, human studies have shown that of dietary with sucrose of changes in glucose and insulin S. Am. J. Clin. Nutr. PubMed Scopus Google Scholar, B. Am. J. Clin. Nutr. PubMed Scopus Google Scholar). in sucrose may be for the metabolic and is a that is to a of glucose and fructose in the glucose and fructose the and are to the the is more a major in and is to in the at a S.M. Am. J. Clin. Nutr. PubMed Scopus Google Scholar, Y. A. K. J. Nutr. PubMed Scopus Google Scholar). In glucose insulin and whereas fructose not insulin and (1Bray G.A. Nielsen S.J. Popkin B.M. Am. J. Clin. Nutr. 2004; 79: 537-543Crossref PubMed Scopus (1489) Google Scholar). the induced by fructose may intake. This in an increase in body of the of fructose an increased intake of sucrose has been shown to in an increase of levels in M.K. Am. J. Clin. Nutr. 2000; PubMed Scopus Google Scholar) and Cha J. Mol. 2003; PubMed Google Scholar). in this study, intake of sucrose-sweetened water did not affect levels in APP/PS1 mice was a for a of in the sucrose we did not the which be increased in the sucrose levels to were in these mice. with an increase of levels has been in A. A. 2000; Full Text PDF PubMed Scopus Google Scholar, D.R. S.J. 2006; PubMed Scopus Google Scholar) and Cha J. Mol. 2003; PubMed Google Scholar, J. Nutr. PubMed Scopus Google Scholar) with an increased intake of studies have shown that high fat high sucrose diets insulin resistance in (17Ho L. Qin W. Pompl P.N. Xiang Z. Wang J. Zhao Z. Peng Y. Cambareri G. Rocher A. Mobbs C.V. Hof P.R. Pasinetti G.M. FASEB J. 2004; 18: 902-904Crossref PubMed Scopus (538) Google Scholar, Cha J. Mol. 2003; PubMed Google Scholar, Y. J. Nutr. 2006; PubMed Scopus Google Scholar, D. K. B. S. V. S. Y. R. Pepe S. L. Mol. PubMed Scopus Google Scholar). The mechanisms by which high fat high sucrose diets insulin resistance are not fully understood. It has been shown that high fat and high sucrose diets may affect the of insulin and glucose Y. J. Nutr. 2006; PubMed Scopus Google Scholar). In this study, the mice were fed a regular low fat rodent diet. The of sucrose in water induced glucose intolerance and hyperinsulinemia, that chronic consumption of sugar-sweetened beverages lead to insulin resistance independent of dietary fat intake. the that type 2 diabetes mellitus is associated with cognitive impairment (11Craft S. Watson G.S. Lancet Neurol. 2004; 3: 169-178Abstract Full Text Full Text PDF PubMed Scopus (687) Google Scholar), this study showed that insulin resistance exacerbated and memory in APP/PS1 mice. In with a high fat insulin resistance was associated with and memory in a mouse model of AD (17Ho L. Qin W. Pompl P.N. Xiang Z. Wang J. Zhao Z. Peng Y. Cambareri G. Rocher A. Mobbs C.V. Hof P.R. Pasinetti G.M. FASEB J. 2004; 18: 902-904Crossref PubMed Scopus (538) Google Scholar). The mechanisms by which insulin affects memory may the of insulin in the brain Mol. 2001; PubMed Scopus Google Scholar). an increase of insulin the insulin in the chronic insulin and insulin the brain D. L. D. J. Clin. PubMed Scopus Google Scholar). It has been shown that insulin is in the of mice with a high fat insulin resistance (17Ho L. Qin W. Pompl P.N. Xiang Z. Wang J. Zhao Z. Peng Y. Cambareri G. Rocher A. Mobbs C.V. Hof P.R. Pasinetti G.M. FASEB J. 2004; 18: 902-904Crossref PubMed Scopus (538) Google Scholar). In insulin by and memory in a mouse model of AD W.A. P.J. Leverenz J.B. S. Neurol. 2006; PubMed Scopus Google Scholar). the exacerbation of cognitive the deposition was increased in the brain of APP/PS1 mice sucrose-sweetened cerebral Aβ deposition may be by increased increased aggregation of Our results showed that the expression of the APP transgene did not The levels of and of by were not In the levels of and in the of the brain did not the two of mice. These results suggest that the of Aβ from APP was not affected by excess sucrose studies have shown that high fat insulin resistance is associated with a of cerebral (17Ho L. Qin W. Pompl P.N. Xiang Z. Wang J. Zhao Z. Peng Y. Cambareri G. Rocher A. Mobbs C.V. Hof P.R. Pasinetti G.M. FASEB J. 2004; 18: 902-904Crossref PubMed Scopus (538) Google Scholar), a that insulin and In this study, there was a for a of in the sucrose the of not for a increase in Aβ deposition in these mice. with there was no change in Aβ that there were no effects from Aβ W. S. Y. L. M.P. D.J. S. S. A. 2003; PubMed Scopus Google Scholar). increase of Aβ deposition that aggregation of Aβ be increased in the mice sucrose-sweetened In this of APP/PS1 the levels of are higher the levels of in and mice of the of transgene that the of J.L. Fadale D.J. Anderson J. Xu G.M. Gonzales V. Jenkins N.A. Copeland N.G. Lee M.K. Younkin L.H. Wagner S.L. Younkin S.G. Borchelt D.R. Hum. Mol. Genet. 2004; 13: 159-170Crossref PubMed Scopus (1143) Google Scholar). Our results showed that the of insoluble increased in the of sucrose-treated APP/PS1 mice. is more leading to more Aβ deposition J.L. Fadale D.J. Anderson J. Xu G.M. Gonzales V. Jenkins N.A. Copeland N.G. Lee M.K. Younkin L.H. Wagner S.L. Younkin S.G. Borchelt D.R. Hum. Mol. Genet. 2004; 13: 159-170Crossref PubMed Scopus (1143) Google Scholar). In there was a increase in the of apoE in the of these mice. apoE has been shown to promote aggregation and of Aβ B. T. L. S.M. K. Ann. Neurol. 2000; PubMed Scopus Google Scholar). apoE in the brain is in these mice is not studies have shown that a sucrose diet apoE W. G.A. W. J. Full Text PDF PubMed Google Scholar). It that brain apoE expression is by sucrose intake as we in this 2.5-fold increase of apoE well with a increase of Aβ deposition in the brain. Therefore, these results suggest that the exacerbation of cerebral amyloidosis in sucrose-treated APP/PS1 mice mainly from increased aggregation of Aβ induced by the up-regulation of In we have shown that consumption of sucrose-sweetened water increase of more weight insulin and AD-like cognitive impairment and cerebral deposition independent of dietary fat intake in a mouse model of AD. Our are of that the consumption of sugar-sweetened beverages has increased in the and high in modern the consumption of sugar-sweetened beverages may be an effective way to curtail the risk of developing AD. We A. and J. for on this
Cao et al. (Wed,) studied this question.