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Contribution of genetic and dietary insulin resistance to Alzheimer phenotype in APP/PS1 transgenic mice.

Hiltunen M, Khandelwal VK, Yaluri N, Tiilikainen T, Tusa M, Koivisto H, Krzisch M, Vepsäläinen S, Mäkinen P, Kemppainen S, Miettinen P, Haapasalo A, Soininen H, Laakso M, Tanila H - J. Cell. Mol. Med. (2012)

Bottom Line: According to epidemiological studies, type-2 diabetes increases the risk of Alzheimer's disease.Neither high-fat diet nor IGF-2 increased β-amyloid burden in the brain.These findings provide evidence for new regulatory mechanisms that link type-2 diabetes and Alzheimer pathology.

View Article: PubMed Central - PubMed

Affiliation: Institute of Clinical Medicine - Neurology, University of Eastern Finland, Kuopio, Finland. mikko.hiltunen@uef.fi

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Related in: MedlinePlus

Aβ levels in the cortex of female and male APdE9 mice without (Iw) or with (I+) IFG2 transgene and on standard diet (STD) or typical Western diet (TWD). ELISA results (mean + S.E.M.) are shown separately for Aβ1-40 (A and B), Aβ1-42 (C and D) and the Aβ42/40 ratio (E and F). *Different from the Iw genotype mouse on the same diet (P < 0.05, t-test). #Main effect of IGF-2 (P < 0.05, ANOVA); n ∇ 4–6 mice/group.
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fig05: Aβ levels in the cortex of female and male APdE9 mice without (Iw) or with (I+) IFG2 transgene and on standard diet (STD) or typical Western diet (TWD). ELISA results (mean + S.E.M.) are shown separately for Aβ1-40 (A and B), Aβ1-42 (C and D) and the Aβ42/40 ratio (E and F). *Different from the Iw genotype mouse on the same diet (P < 0.05, t-test). #Main effect of IGF-2 (P < 0.05, ANOVA); n ∇ 4–6 mice/group.

Mentions: In addition, insoluble Aβ1–40 (Fig. 5A and B) and Aβ1–42 (Fig. 5C and D) levels were measured from the same protein lysates. Among female mice, Aβ levels did not differ between the genotypes or diet groups. However, IGF-2 χ diet interaction revealed a borderline significance for increased Aβ1–40 levels in A+I+ female mice on TWD [F(1,26) ∇ 4.0, P ∇ 0.06] (Fig. 5A). In contrast, male A+I+ mice on STD or TWD had lower Aβ1–40 [F(1,32) ∇ 5.6, P ∇ 0.03] levels as compared to A+Iw mice on STD or TWD (Fig. 5B). Insoluble Aβ1–42 levels did not differ between the genotypes or diet groups in either female or male mice (Fig. 5C and D). However, male A+I+ mice showed a higher Aβ 42/40 ratio than A+Iw mice (F ∇ 8.6, P ∇ 0.006; Fig. 5F), while neither the IGF-2 transgene nor the diet modulated this ratio in female mice (Fig. 5E).


Contribution of genetic and dietary insulin resistance to Alzheimer phenotype in APP/PS1 transgenic mice.

Hiltunen M, Khandelwal VK, Yaluri N, Tiilikainen T, Tusa M, Koivisto H, Krzisch M, Vepsäläinen S, Mäkinen P, Kemppainen S, Miettinen P, Haapasalo A, Soininen H, Laakso M, Tanila H - J. Cell. Mol. Med. (2012)

Aβ levels in the cortex of female and male APdE9 mice without (Iw) or with (I+) IFG2 transgene and on standard diet (STD) or typical Western diet (TWD). ELISA results (mean + S.E.M.) are shown separately for Aβ1-40 (A and B), Aβ1-42 (C and D) and the Aβ42/40 ratio (E and F). *Different from the Iw genotype mouse on the same diet (P < 0.05, t-test). #Main effect of IGF-2 (P < 0.05, ANOVA); n ∇ 4–6 mice/group.
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Related In: Results  -  Collection

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fig05: Aβ levels in the cortex of female and male APdE9 mice without (Iw) or with (I+) IFG2 transgene and on standard diet (STD) or typical Western diet (TWD). ELISA results (mean + S.E.M.) are shown separately for Aβ1-40 (A and B), Aβ1-42 (C and D) and the Aβ42/40 ratio (E and F). *Different from the Iw genotype mouse on the same diet (P < 0.05, t-test). #Main effect of IGF-2 (P < 0.05, ANOVA); n ∇ 4–6 mice/group.
Mentions: In addition, insoluble Aβ1–40 (Fig. 5A and B) and Aβ1–42 (Fig. 5C and D) levels were measured from the same protein lysates. Among female mice, Aβ levels did not differ between the genotypes or diet groups. However, IGF-2 χ diet interaction revealed a borderline significance for increased Aβ1–40 levels in A+I+ female mice on TWD [F(1,26) ∇ 4.0, P ∇ 0.06] (Fig. 5A). In contrast, male A+I+ mice on STD or TWD had lower Aβ1–40 [F(1,32) ∇ 5.6, P ∇ 0.03] levels as compared to A+Iw mice on STD or TWD (Fig. 5B). Insoluble Aβ1–42 levels did not differ between the genotypes or diet groups in either female or male mice (Fig. 5C and D). However, male A+I+ mice showed a higher Aβ 42/40 ratio than A+Iw mice (F ∇ 8.6, P ∇ 0.006; Fig. 5F), while neither the IGF-2 transgene nor the diet modulated this ratio in female mice (Fig. 5E).

Bottom Line: According to epidemiological studies, type-2 diabetes increases the risk of Alzheimer's disease.Neither high-fat diet nor IGF-2 increased β-amyloid burden in the brain.These findings provide evidence for new regulatory mechanisms that link type-2 diabetes and Alzheimer pathology.

View Article: PubMed Central - PubMed

Affiliation: Institute of Clinical Medicine - Neurology, University of Eastern Finland, Kuopio, Finland. mikko.hiltunen@uef.fi

Show MeSH
Related in: MedlinePlus