Impact of different saturated fatty acid, polyunsaturated fatty acid and cholesterol containing diets on beta-amyloid accumulation in APP/PS1 transgenic mice

Oksman, Mari; Iivonen, H.; Hogyes, E.; Amtul, Zareen; Penke, Botond; Leenders, Inge; Broersen, Laus M.; Lütjohann, Dieter; Hartmann, Tobias; Tanila, Heikki

doi:10.1016/j.nbd.2006.04.013

Cited by 278 publications

(208 citation statements)

References 37 publications

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“…This presumption is supported by the presence of only mature fibrillary plaques, without new inflammatory plaques, in the hippocampus of 24-month-old APP/PS1 mice. Similar to adult APP/PS1 mice, the deposition of Aβ plaques was mainly present in the molecular layer and stratum lacunosum moleculare, while being virtually absent in the pyramidal cell layer and the granule cell layer (Bas Orth et al 2005;Oksman et al 2006;Donkin et al 2010;Scott et al 2012;Xu et al 2012Xu et al , 2016. Furthermore, our previous and present results suggest that laminar heterogeneity and Aβ load is correlated with laminar variability in expression of APP secretases (Xu et al 2016).…”

Section: Discussionsupporting

confidence: 70%

Characterization of AD-like phenotype in aged APPSwe/PS1dE9 mice

Huang

Nie

Cao

et al. 2016

AGE

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Transgenic APPSwe/PS1dE9 (APP/PS1) mice that overproduce amyloid beta (Aβ) are extensively used in the studies of pathogenesis and experimental therapeutics and new drug screening for Alzheimer's disease (AD). However, most of the current literature uses young or adult APP/PS1 mice. In order to provide a broader view of AD-like phenotype of this animal model, in this study, we systematically analyzed behavioral and pathological profiles of 24-month-old male APP/ PS1 mice. Aged APP/PS1 mice had reference memory deficits as well as anxiety, hyperactivity, and social interaction impairment. Consistently, there was obvious deposition of amyloid plaques in the dorsal hippocampus with decreased expression of insulin-degrading enzyme, a proteolytic enzyme responsible for degradation of intracellular Aβ. Furthermore, decreases in hippocampal volume, neuronal number and synaptophysin expression, and astrocyte atrophy were also observed in aged APP/PS1 mice. This finding suggests that aged APP/PS1 mice can well replicate cognitive and noncognitive behavioral abnormalities, hippocampal atrophy, and neuronal and astrocyte degeneration in AD patients, to enable more objective and refined preclinical evaluation of therapeutic drugs and strategies for AD treatment.

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Section: Discussionsupporting

confidence: 70%

Characterization of AD-like phenotype in aged APPSwe/PS1dE9 mice

Huang

Nie

Cao

et al. 2016

AGE

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“…DHA, an important dietary n-3 (omega-3) fatty acid was the plasma lipid most predictive of AD risk in the Framingham study in which higher blood levels of DHA correlated with reduced AD assessed 10 years later (Johnson and Schaefer, 2006). Our own and previous work from other groups indicate that dietary DHA significantly improves cognitive deficits, protects from synaptic protein loss, and lowers insoluble A␤ in transgenic AD mouse models (Calon et al, 2004;Lim et al, 2005;Oksman et al, 2006;Ma et al, 2007). Our current data are consistent with a report that algal DHA reduced A␤ accumulation, suggesting this effect may have reduced JNK activation and ptau in 3xTg-AD mice (Green et al, 2007), but the effects we observed need not be secondary to A␤ reduction because we show that DHA reduces the JNK, IRS-1, and tau phosphorylation response to exogenous A␤ oligomers.…”

Section: Discussionmentioning

confidence: 63%

-Amyloid Oligomers Induce Phosphorylation of Tau and Inactivation of Insulin Receptor Substrate via c-Jun N-Terminal Kinase Signaling: Suppression by Omega-3 Fatty Acids and Curcumin

Yang²,

Rosario³

et al. 2009

Journal of Neuroscience

481

332

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“…Similarly, DHA reduced amyloid ␤ 42 (A␤42) in AD mice (Lim et al, 2005;Oksman et al, 2006;Green et al, 2007;Hooijmans et al, 2007) and production by cultured human neurons (Lukiw et al, 2005). The mechanism involved in the DHAinduced reductions in A␤42 may be due to multiple effects, such as: changes in lipid raft structure (Stillwell et al, 2005), alterations in APP processing (Ehehalt et al, 2003), induction of antiamyloidogenic chaperones for APP , and A␤ transthyretin (Schwarzman et al, 1994;Puskás et al, 2003).…”

Section: Walnut and Fish Polyunsaturated Fatty Acidsmentioning

confidence: 99%

Nutrition, Brain Aging, and Neurodegeneration: Table 1.

Joseph¹,

Cole²,

Head³

et al. 2009

J. Neurosci.

236

129

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The onset of age-related neurodegenerative diseases superimposed on a declining nervous system could enhance the motor and cognitive behavioral deficits that normally occur in senescence. It is likely that, in cases of severe deficits in memory or motor function, hospitalization and/or custodial care would be a likely outcome. This means that unless some way is found to reduce these age-related decrements in neuronal function, health care costs will continue to rise exponentially. Applying molecular biological approaches to slow aging in the human condition may be years away. So, it is important to determine what methods can be used today to increase healthy aging, forestall the onset of these diseases, and create conditions favorable to obtaining a "longevity dividend" in both financial and human terms. Recent studies suggest that consumption of diets rich in antioxidants and anti-inflammatory components such as those found in fruits, nuts, vegetables, and spices, or even reduced caloric intake, may lower age-related cognitive declines and the risk of developing neurodegenerative disease.

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Impact of different saturated fatty acid, polyunsaturated fatty acid and cholesterol containing diets on beta-amyloid accumulation in APP/PS1 transgenic mice

Cited by 278 publications

References 37 publications

Characterization of AD-like phenotype in aged APPSwe/PS1dE9 mice

Characterization of AD-like phenotype in aged APPSwe/PS1dE9 mice

-Amyloid Oligomers Induce Phosphorylation of Tau and Inactivation of Insulin Receptor Substrate via c-Jun N-Terminal Kinase Signaling: Suppression by Omega-3 Fatty Acids and Curcumin

Nutrition, Brain Aging, and Neurodegeneration: Table 1.

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