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1.

Fig 4. From: HIGH CHOLESTEROL-INDUCED NEUROINFLAMMATION AND AMYLOID PRECURSOR PROTEIN PROCESSING CORRELATE WITH LOSS OF WORKING MEMORY IN MICE.

qPCR analysis of high fat/cholesterol-induced proinflammatory mediator expression. A. Relative levels of cytokine/mediator mRNAs in C57BL/6 mice fed either normal or high fat diet. B. Relative cytokine/mediator mRNA levels in normally fed C57BL/6 and LDLR−/− mice. * p < 0.05 versus the normally fed control group. # represents significant (p < 0.05) difference of normally fed LDLR−/− group from normally fed C57BL/6 (control) group. C. Relative levels of cytokine/mediator mRNAs in LDLR−/− mice fed either normal or high fat diet.

Lakshmi Thirumangalakudi, et al. J Neurochem. ;106(1):475-485.
2.
Fig 6

Fig 6. From: HIGH CHOLESTEROL-INDUCED NEUROINFLAMMATION AND AMYLOID PRECURSOR PROTEIN PROCESSING CORRELATE WITH LOSS OF WORKING MEMORY IN MICE.

Western blot analysis of APP processing. A. Representative blots of APP/CTFs in tissue samples from C57BL/6, LDLR−/− and APPTg mice fed either a normal chow or the high fat/cholesterol diet. B. Densitometric analysis of CTF relative to APP. All three strains of high fat/cholesterol fed mice showed significantly higher CTF:APP ratio compared to normal chow fed counter part animals.**p<0.01; *P<0.05

Lakshmi Thirumangalakudi, et al. J Neurochem. ;106(1):475-485.
3.
Fig 5

Fig 5. From: HIGH CHOLESTEROL-INDUCED NEUROINFLAMMATION AND AMYLOID PRECURSOR PROTEIN PROCESSING CORRELATE WITH LOSS OF WORKING MEMORY IN MICE.

High fat/cholesterol-induced expression of BACE1. A. Total RNA was isolated from the corteces of C57BL/6 and LDLR−/− mice fed the two diet regimen and analysed by qPCR for BACE1 mRNA. * p < 0.05 versus the normally fed control group. # represents significant (p < 0.05) difference of normally fed LDLR−/− group from normally fed C57BL/6 (control) group. B. Corresponding tissue extracts were analysed by immunoblot for BACE1 protein levels using BACE1-specific antibodies. The line graphs below show the relative BACE1 protein levels.

Lakshmi Thirumangalakudi, et al. J Neurochem. ;106(1):475-485.
4.
Fig 7

Fig 7. From: HIGH CHOLESTEROL-INDUCED NEUROINFLAMMATION AND AMYLOID PRECURSOR PROTEIN PROCESSING CORRELATE WITH LOSS OF WORKING MEMORY IN MICE.

Aβ generation in LDLR−/− mice (A) and hAPP tg mice (B) fed either the normal chow or the high fat/cholesterol diet. The tissue extracts were prepared as described under Methods and analysed for Abet species using a sensitive ELISA. The levels of Ab42 were very low in the LDLR−/− mice. The levels of AB40 as well as 42 were very low in the normal C57BL/6 mice. * p < 0.05 versus the normally fed control group.

Lakshmi Thirumangalakudi, et al. J Neurochem. ;106(1):475-485.
5.
Fig 2

Fig 2. From: HIGH CHOLESTEROL-INDUCED NEUROINFLAMMATION AND AMYLOID PRECURSOR PROTEIN PROCESSING CORRELATE WITH LOSS OF WORKING MEMORY IN MICE.

Behavioral analysis of working memory. Mean (± SE) number of working memory incorrect errors for each trial committed on the water radial maze for normally fed and high fat fed C57BL/6 mice were determined as described under Methods. B. Working memory incorrect ± SE for each treatment group i.e., C57BL/6 and LDLR−/− mice fed either normal or high fat diet. * p < 0.05 versus the normally (basal diet) fed control group. # represents significant (p < 0.05) difference of normally fed LDLR−/− group from normally fed C57BL/6 (control) group.

Lakshmi Thirumangalakudi, et al. J Neurochem. ;106(1):475-485.
6.

Fig 3. From: HIGH CHOLESTEROL-INDUCED NEUROINFLAMMATION AND AMYLOID PRECURSOR PROTEIN PROCESSING CORRELATE WITH LOSS OF WORKING MEMORY IN MICE.

Immunohistochemical analysis of high fat/cholesterol diet-induced glial activation. A shows CD45 staining of microglia in the hippocampus of C57BL/6 and LDLR−/− mice fed normal chow or the high fat/cholesterol diet. B. GFAP-immunoreactive astrocytes in the hippocampus of C57BL/6 and LDLR−/− mice fed normal chow or the high fat/cholesterol diet. C. Quantitation of CD45 and GFAP stainings of C57BL/6 (left panel) and LDLR−/− (right panel) mice fed normal and high fat diet. The images (4 sections per animal) were captured and quantified using the NIH Image software package. * p < 0.05 versus the normally (basal diet) fed control group. ** p < 0.01 versus the normally (basal diet) fed control group.

Lakshmi Thirumangalakudi, et al. J Neurochem. ;106(1):475-485.
7.
Fig 1

Fig 1. From: HIGH CHOLESTEROL-INDUCED NEUROINFLAMMATION AND AMYLOID PRECURSOR PROTEIN PROCESSING CORRELATE WITH LOSS OF WORKING MEMORY IN MICE.

Plasma cholesterol and triglyceride levels in C57BL/6 and LDLR−/− mice fed a normal chow vs. a high fat/high cholesterol diet. The plasma lipid profiles of different treatment groups were determined in the GCRC facility at MUSC. A. Total cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride levels of plasma samples from C57BL/6 mice fed either normal chow or a high fat diet. B. Total cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride levels of plasma from LDLR−/− on either normal chow or the high fat diet. C. A comparison of total cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride levels of plasma derived from normally fed C57BL/6 and LDLR−/− mice. * p < 0.05 versus the normally fed control group. # represents significant (p < 0.05) difference of normally fed LDLR−/− group from normally fed C57BL/6 (control) group.

Lakshmi Thirumangalakudi, et al. J Neurochem. ;106(1):475-485.

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