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Research ArticleNew Research, Disorders of the Nervous System

Obesity Accelerates Alzheimer-Related Pathology in APOE4 but not APOE3 Mice

V. Alexandra Moser and Christian J. Pike
eNeuro 12 June 2017, 4 (3) ENEURO.0077-17.2017; DOI: https://doi.org/10.1523/ENEURO.0077-17.2017
V. Alexandra Moser
Neuroscience Graduate Program, Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089
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Christian J. Pike
Neuroscience Graduate Program, Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089
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  • Figure 1.
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    Figure 1.

    Metabolic outcomes associated with DIO in E3FAD and E4FAD mice. A, Body weights in male E3FAD and E4FAD mice maintained on control (CTL) and Western (WD) diets taken at baseline (week 0) and four-week intervals across the 12-week experimental period. Plasma levels of cholesterol (B) and triglyceride levels (C) in E3FAD and E4FAD mice on control and Western diets at the end of the experimental period. D, Weight of the gonadal fat pads across groups. Relative mRNA expression of macrophage markers (E) CD68 and (F) F4/80 in gonadal fat, as determined by real time PCR. Data show fold differences relative to the E3FAD + control diet group. G, GTT showing blood glucose levels over time after a glucose bolus. H, AUC for the GTT. I, Percentage change in fasting blood glucose levels relative to baseline after 12-weeks of control or Western diet. Data are presented as mean (±SEM) values; n = 7–11/group. E3FAD mice are shown as circles, E4FAD mice are shown as squares; control diet groups are indicated as open symbols or bars, whereas Western diet groups are filled symbols or bars. *, p < 0.05 relative to genotype-matched mice in control diet condition. #, p < 0.05 relative to E3FAD mice in same diet condition.

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    Figure 2.

    Accumulation of amyloidogenic deposits assessed by Thio-S staining in E3FAD and E4FAD mice across dietary treatments. A, Representative images of Thio-S staining in the subiculum of E3FAD and E4FAD males fed control and Western diets. Scale bar, 50 µm. Numbers of Thio-S positive plaque numbers in E3FAD and E4FAD mice maintained on control and Western diets were quantified in (B) entorhinal cortex, and hippocampal subregions (C) subiculum, (D) CA1, and (E) CA2/3. Data are presented as mean (±SEM) values; n = 7–11/group. E3FAD mice are shown as circles, E4FAD mice are shown as squares; control diet groups are indicated as open symbols, and Western diet groups as filled symbols. *, p < 0.05 relative to genotype-matched mice in control diet condition. #, p < 0.05 relative to E3FAD mice in same diet condition.

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    Figure 3.

    Accumulation of β-amyloid deposits assessed by immunohistochemistry in E3FAD and E4FAD mice across dietary treatments. A, Representative images of β-amyloid immunoreactivity in entorhinal cortex and hippocampus in E3FAD and E4FAD males maintained on control and Western diets. Scale bar, 100 µm. β-Amyloid burden was quantified as immunoreactivity load in E3FAD and E4FAD mice in control and Western diets groups in (B) entorhinal cortex, and hippocampal subregions (C) subiculum, (D) CA1, and (E) CA2/3. Data are presented as mean (±SEM) values; n = 7–11/group. E3FAD mice are shown as circles, E4FAD mice are shown as squares; control diet groups are indicated as open symbols, and Western diet groups as filled symbols. *, p < 0.05 relative to genotype-matched mice in control diet condition. #, p < 0.05 relative to E3FAD mice in same diet condition.

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    Figure 4.

    Microglia number and morphologic status assessed by IBA-1 immunohistochemistry in E3FAD and E4FAD mice across dietary treatments. A, Representative images of microglial morphology associated with resting (type 1) and reactive (types 2 and 3) phenotypes. Scale bar, 40 µm. B–E, Densities (cells/mm2) of IBA-1-immunoreactive cells in E3FAD and E4FAD mice on control and Western diets were quantified in (B) entorhinal cortex, and hippocampal subregions (C) subiculum, (D) CA1, and E) CA2/3. F–I) Percentages of all IBA-1-immunoreactive cells scored as having reactive phenotype (types 2 and 3) were quantified in (F) entorhinal cortex, and hippocampal subregions (G) subiculum, (H) CA1, and (I) CA2/3. Data are presented as mean (±SEM) values; n = 7–11/group. E3FAD mice are shown as circles, E4FAD mice are shown as squares; control diet groups are indicated as open symbols, and Western diet groups as filled symbols. *, p < 0.05 relative to genotype-matched mice in control diet condition. #, p < 0.05 relative to E3FAD mice in same diet condition.

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    Figure 5.

    Astrocyte number and morphologic status assessed by GFAP immunohistochemistry in E3FAD and E4FAD mice across dietary treatments. A, Representative images of astrocyte morphology associated with resting and reactive phenotypes. Scale bar, 50 µm. B–E, Densities (cells/mm2) of GFAP-immunoreactive cells in E3FAD and E4FAD mice on control and Western diets were quantified in (B) entorhinal cortex, and hippocampal subregions (C) subiculum, (D) CA1, and (E) CA2/3. F–I, Percentages of all GFAP-immunoreactive cells scored as having reactive phenotype (type 2) were quantified in (F) entorhinal cortex, and hippocampal subregions (G) subiculum, (H) CA1, and (I) CA2/3. Data are presented as mean (±SEM) values; n = 7–11/group. E3FAD mice are shown as circles, E4FAD mice are shown as squares; control diet groups are indicated as open symbols, and Western diet groups as filled symbols. *, p < 0.05 relative to genotype-matched mice in control diet condition. #, p < 0.05 relative to E3FAD mice in same diet condition.

Tables

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    Table 1.

    Gene targets for the PCR analyses are listed with their corresponding oligonucleotide sequences for the forward and reverse primers

    Target geneSequence
    CD68Forward: 5’-TTCTGCTGTGGAAATGCAAG-3’
    Reverse: 5’-AGAGGGGCTGGTAGGTTGAT-3’
    F4/80Forward: 5’-TGCATCTAGCAATGGACAGC-3’
    Reverse: 5’-GCCTTCTGGATCCATTTGAA-3’
    HPRTForward: 5’-AAGCTTGCTGGTGAAAAGGA-3’
    Reverse: 5’-TTGCGCTCATCTTAGGCTTT-3’
    SDHAForward: 5’-ACACAGACCTGGTGGAGACC-3’
    Reverse: 5’-GGATGGGCTTGGAGTAATCA-3’
    NeprilysinForward: 5’-GAGAAAAGCCCACTTGCTTG-3’
    Reverse: 5’-GAAAGACAAAATGGGGCAGA-3’
    BACE1Forward: 5’-TCGCTGTCTCACAGTCATCC-3’
    Reverse: 5’-AACAAACGGACCTTCCACTG-3’
    IDEForward: 5’-TGTTTCCACACACAGGCAAT-3’
    Reverse: 5’-ACCTGTGAAAAGCCGAGAGA-3’
    CD74Forward: 5’-CAAGTACGGCAACATGACCC-3’
    Reverse: 5’-GCACTTGGTCAGTACTTTAGGTG-3’
    GFAPForward: 5’-AACGACTATCGCCGCCAACTG-3’
    Reverse: 5’-CTCTTCCTGTTCGCGCATTTG-3’
    β-ActinForward: 5’-AGCCATGTACGTAGCCATCC-3’
    Reverse: 5’-CTCTCAGCTGTGGTGGTGAA-3’
    • View popup
    Table 2.

    Statistical table

    FigureKolmogorov-Smirnov test for normality (p value)Statistical significance
    Figure 1A
    body weight
    All groups at all time points are normally distributed (p > 0.05).Genotype: F(1,29) = 0.10, p = 0.759
    diet: F(1,29) = 10.51, p = 0.003
    interaction: F(1,29) = 2.68, p = 0.112
    Figure 1B
    plasma cholesterol
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,29) = 2.86, p = 0.103
    diet: F(1,29) = 1.58, p = 0.221
    interaction: F(1,29) = 2.60, p = 0.119
    Figure 1C
    plasma triglycerides
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,29) = 0.56, p = 0.46
    diet: F(1,29) = 2.87, p = 0.102
    interaction: F(1,29) = 1.91, p = 0.179
    Figure 1D
    gonadal fat weight
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,29) = 0.18, p = 0.673
    diet: F(1,29) = 37.04, p < 0.001
    interaction: F(1,29) = 5.01, p = 0.033
    Figure 1E
    CD68
    E3FAD CTL N/A
    E3FAD WD > 0.10
    E4FAD CTL = 0.004
    E4FAD WD > 0.10
    Genotype: F(1,21) = 0.90, p = 0.353
    diet: F(1,21) = 11.54, p = 0.003
    interaction: F(1,21) = 0.85, p = 0.366
    Figure 1F
    F4/80
    E3FAD CTL N/A
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,21) = .09, p = .768
    diet: F(1,21) = 7.02, p = 0.015
    interaction: F(1,21) = 1.19, p = 0.288
    Figure 1G
    glucose (GTT)
    All groups at all time points are normally distributed (p > 0.05), except: E4FAD CTL 0 min = 0.002 E4FADWD 15 min = 0.025 E3FAD WD 30 min = 0.011 E4FAD WD 30 min = 0.008Genotype: F(1,29) = 0.02, p = 0.886
    diet: F(1,29) = 5.03, p = 0.033
    interaction: F(1,29) = 0.10, p = 0.750
    Figure 1H
    GTT AUC
    E3FAD CTL = 0.07
    E3FAD WD = 0.097
    E4FAD CTL > 0.10
    E4FAD WD = 0.033
    Genotype: F(1,29) = .06, p = 0.817
    diet: F(1,29) = 5.73, p = 0.023
    interaction: F(1,29) = 0.12, p = 0.737
    Figure 1I
    percent glucose change
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,29) = .83, p = 0.371
    diet: F(1,29) = 3.84, p = 0.059
    interaction: F(1,29) = 0.90, p = 0.352
    Figure 2B
    Thio-S: entorhinal cortex
    E3FAD CTL > 0.10
    E3FAD WD = 0.049
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,29) = 50.30, p < 0.001
    diet: F(1,29) = 6.62, p = 0.016
    interaction: F(1,29) = 4.09, p = 0.053
    Figure 2C
    Thio-S: subiculum
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,29) = 59.40, p < 0.001
    diet: F(1,29) = 2.98, p = 0.095
    interaction: F(1,29) = 9.75, p = 0.004
    Figure 2D
    Thio-S: CA1
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,29) = 80.58, p < 0.001
    diet: F(1,29) = 4.95, p = 0.034
    interaction: F(1,29) = 8.41, p = 0.007
    Figure 2E
    Thio-S: CA2/3
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 46.39, p < 0.001
    diet: F(1,29) = 7.41, p = 0.011
    interaction: F(1,29) = 7.32, p = 0.011
    Figure 3B
    Aβ load:
    entorhinal cortex
    E3FAD CTL > 0.10
    E3FAD WD = 0.002
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 21.38, p < 0.001
    diet: F(1,29) = 7.83, p = 0.009
    interaction: F(1,29) = 4.91, p = 0.035
    Figure 3C
    Aβ load:
    subiculum
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 25.40, p < 0.001
    diet: F(1,29) = 11.19, p = 0.002
    interaction: F(1,29) = 0.11, p = 0.742
    Figure 3D
    Aβ load:
    CA1
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD = 0.036
    Genotype F(1,29) = 37.66, p < 0.001
    diet: F(1,29) = 2.91, p = 0.099
    interaction: F(1,29) = 2.71, p = 0.110
    Figure 3E
    Aβ load:
    CA2/3
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 47.27, p < 0.001
    diet: F(1,29) = 10.36, p = 0.003
    interaction: F(1,29) = 4.48, p = 0.043
    Figure 4B
    microglia number:
    entorhinal cortex
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,27) = 9.78, p = 0.004
    diet: F(1,27) = 2.31, p = 0.141
    interaction: F(1,27) = 1.05, p = 0.316
    Figure 4C
    microglia number:
    subiculum
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,27) = 42.77, p < 0.001
    diet: F(1,27) = 4.20, p = 0.050
    interaction: F(1,27) = 4.75, p = 0.038
    Figure 4D
    microglia number:
    CA1
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,27) = 51.42, p < 0.001
    diet: F(1,27) = 10.78, p = 0.003
    interaction: F(1,27) = 7.97, p = 0.009
    Figure 4E
    microglia number:
    CA2/3
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,27) = 21.64, p < 0.001
    diet: F(1,27) = 1.97, p = 0.172
    interaction: F(1,27) = 1.90, p = 0.180
    Figure 4F
    microglia reactivity:
    entorhinal cortex
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,27) = 109.10, p < 0.001
    diet: F(1,27) = 1.64, p = 0.212
    interaction: F(1,27) = 5.52, p = 0.027
    Figure 4G
    microglial reactivity:
    subiculum
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL = 0.07
    E4FAD WD < 0.001
    Genotype F(1,27) = 19.70, p < 0.001
    diet: F(1,27) = 0.00, p = 0.995
    interaction: F(1,27) = 0.51, p = 0.480
    Figure 4H
    microglial reactivity:
    CA1
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD = 0.04
    Genotype F(1,27) = 78.70, p < 0.001
    diet: F(1,27) = 5.00, p = 0.034
    interaction: F(1,27) = 11.58, p = 0.002
    Figure 4I
    microglial reactivity:
    CA2/3
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,27) = 165.70, p < 0.001
    diet: F(1,27) = 21.04, p < 0.001
    interaction: F(1,27) = 32.66, p < 0.001
    Figure 5B
    astrocyte number:
    entorhinal cortex
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 3.82, p = 0.060
    diet: F(1,29) = 0.29, p = 0.593
    interaction: F(1,29) = 0.41, p = 0.528
    Figure 5C
    astrocyte number:
    subiculum
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 9.95, p = 0.004
    diet: F(1,29) = 4.79, p = 0.037
    interaction: F(1,29) = 1.04, p = 0.316
    Figure 5D
    astrocyte number:
    CA1
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 5.88, p = 0.022
    diet: F(1,29) = 3.55, p = 0.069
    interaction: F(1,29) = 0.49, p = 0.489
    Figure 5E
    astrocyte number:
    CA2/3
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 1.82, p = 0.188
    diet: F(1,29) = 4.26, p = 0.048
    interaction: F(1,29) = 0.02, p = 0.894
    Figure 5F
    astrocyte reactivity:
    entorhinal cortex
    E3FAD CTL > 0.10
    E3FAD WD = 0.004
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 46.97, p < 0.001
    diet: F(1,29) = 5.75, p = 0.023
    interaction: F(1,29) = 4.82, p = 0.036
    Figure 5G
    astrocyte reactivity:
    subiculum
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL = 0.045
    E4FAD WD > 0.10
    Genotype F(1,29) = 27.72, p < 0.001
    diet: F(1,29) = 3.13, p = 0.088
    interaction: F(1,29) = 0.00, p = 0.989
    Figure 5H
    astrocyte reactivity:
    CA1
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 87.49, p < 0.001
    diet: F(1,29) = 23.82, p < 0.001
    interaction: F(1,29) = 2.08, p = 0.160
    Figure 5I
    astrocyte reactivity:
    CA2/3
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype F(1,29) = 11.68, p = 0.002
    diet: F(1,29) = 7.83, p = 0.009
    interaction: F(1,29) = 2.405, p = 0.132
    • View popup
    Table 3.

    Relative gene expression in hippocampus

    GeneMean ± SEMKolmogorov-Smirnov test for normality (p value)Statistical significance
    BACE1E3FAD CTL = 1 ± N/A
    E3FAD WD = 1.53 ± 0.31
    E4FAD CTL = 1.32 ± 0.19
    E4FAD WD = 1.76 ± 0.41
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,28) = 1.10, p = 0.304
    diet: F(1,28) = 3.44, p = 0.074
    interaction: F(1,28) = 0.03, p = 0.874
    NeprilysinE3FAD CTL = 1 ± N/A
    E3FAD WD = 1.61 ± 0.79
    E4FAD CTL = 0.94 ± 0.30
    E4FAD WD = 1.79 ± 0.63
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,28) = 0.02, p = 0.902
    diet: F(1,28) = 2.49, p = 0.126
    interaction: F(1,28) = 0.06, p = 0.802
    IDEE3FAD CTL = 1 ± N/A
    E3FAD WD = 1.27 ± 0.39
    E4FAD CTL = 1.30 ± 0.39
    E4FAD WD = 1.12 ± 0.35
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL = 0.01
    E4FAD WD > 0.10
    Genotype: F(1,28) = 0.08, p = 0.785
    diet: F(1,28) = 0.00, p = 0.955
    interaction: F(1,28) = 0.49, p = 0.489
    CD68E3FAD CTL = 1 ± N/A
    E3FAD WD = 1.21 ± 0.29
    E4FAD CTL = 1.74 ± 0.30
    E4FAD WD = 2.30 ± 0.29
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,28) = 10.75, p = 0.003
    diet: F(1,28) = 1.91, p = 0.178
    interaction: F(1,28) = 0.40, p = 0.532
    GFAPE3FAD CTL = 1 ± N/A
    E3FAD WD = 1.02 ± 0.11
    E4FAD CTL = 1.56 ± 0.21
    E4FAD WD = 2.70 ± 0.04
    E3FAD CTL > 0.10
    E3FAD WD > 0.10
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,28) = 14.26, p < 0.001
    diet: F(1,28) = 0.23, p = 0.634
    interaction: F(1,28) = 0.14, p = 0.712
    CD74E3FAD CTL = 1 ± N/A
    E3FAD WD = 1.28 ± 0.28
    E4FAD CTL = 3.32 ± 0.62
    E4FAD WD = 5.04 ± 1.30
    E3FAD CTL > 0.10
    E3FAD WD = 0.01
    E4FAD CTL > 0.10
    E4FAD WD > 0.10
    Genotype: F(1,28) = 16.98, p < 0.001
    diet: F(1,28) = 1.86, p = 0.184
    interaction: F(1,28) = 0.96, p = 0.335
    • Data are presented as mean fold differences (±SEM) relative to E3FAD mice on a control diet. The Kolmogorov-Smirnov test for normality was performed, with p > 0.05 indicating a normal distribution. Genes related to β-amyloid production (BACE-1) and clearance (neprilysin, IDE) showed no significant changes with either diet or genotype, while genes related to glial activation (CD68, GFAP, and CD74) were increased in E4FAD mice on both control and Western diets.

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Obesity Accelerates Alzheimer-Related Pathology in APOE4 but not APOE3 Mice
V. Alexandra Moser, Christian J. Pike
eNeuro 12 June 2017, 4 (3) ENEURO.0077-17.2017; DOI: 10.1523/ENEURO.0077-17.2017

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Obesity Accelerates Alzheimer-Related Pathology in APOE4 but not APOE3 Mice
V. Alexandra Moser, Christian J. Pike
eNeuro 12 June 2017, 4 (3) ENEURO.0077-17.2017; DOI: 10.1523/ENEURO.0077-17.2017
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Keywords

  • Alzheimer’s disease
  • apolipoprotein E
  • β-amyloid
  • Gliosis
  • obesity
  • transgenic

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