Effects of apoE Deficiency and Occlusal Disharmony on Amyloid-Beta Production and Spatial Memory in Rats

Ekuni, Daisuke; Endo, Yoshikatsu; Tomofuji, Takaaki; Azuma, Tetsuji; Irie, Koichiro; Kasuyama, Kenta; Morita, Manabu

doi:10.1371/journal.pone.0074966

Cited by 14 publications

(21 citation statements)

References 54 publications

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“…14 These findings also corroborate to another study by Okihara, et al 7 (2014), which found a memory impairment accompanied by low number of neuron cells in the hippocampus after long-term soft diet. 7 Previous studies on mastication impaired animal models through tooth extraction 22 , 23 , bite-raise 24 , 25 and long-term soft diets 7 , 26 found that these aspects may alter hippocampus learning and memory function. Other studies also proved that impaired function of the hippocampus due to long-term soft diet could be improved by providing a hard diet.…”

Section: Discussionmentioning

confidence: 99%

Difference of brain-derived neurotrophic factor expression and pyramid cell count during mastication of food with varying hardness

2019

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Previous studies suggested that mastication activity can affect learning and memory function. However, most were focused on mastication impaired models by providing long-term soft diet. The effects of chewing food with various hardness, especially during the growth period, remain unknown. Objective: To analyze the difference of hippocampus function and morphology, as characterized by pyramidal cell count and BDNF expression in different mastication activities. Materials and Methods: 28-day old, post-weaned, male-Wistar rats were randomly divided into three groups (n=7); the first (K0) was fed a standard diet using pellets as the control, the second (K1) was fed soft food and the third (K2) was fed hard food. After eight weeks, the rats were decapitated, their brains were removed and placed on histological plates made to count the pyramid cells and quantify BDNF expression in the hippocampus. Data collected were compared using one-way ANOVA. Results: Results confirmed the pyramid cell count (K0=169.14±27.25; K1=130.14±29.32; K2=128.14±39.02) and BDNF expression (K0=85.27±19.78; K1=49.57±20.90; K2=36.86±28.97) of the K0 group to be significantly higher than that of K1 and K2 groups (p<0.05); no significant difference in the pyramidal cell count and BNDF expression was found between K1 and K2 groups (p>0.05). Conclusion: A standard diet leads to the optimum effect on hippocampus morphology. Food consistency must be appropriately suited to each development stage, in this case, hippocampus development in post-weaned period.

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Section: Discussionmentioning

confidence: 99%

Difference of brain-derived neurotrophic factor expression and pyramid cell count during mastication of food with varying hardness

2019

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“…Reduced masticatory abilities due to periodontal disease may result in dietary deficiencies and increased stress response, and these may lead to increased amyloid beta (Ekuni, et al, 2013). It is also possible that the relationship between CAL and amyloid load is related to a relationship between CAL and cognitive dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Periodontal disease associates with higher brain amyloid load in normal elderly

Kamer¹,

Pirraglia²,

Tsui³

et al. 2015

Neurobiology of Aging

209

150

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Background The accumulation of amyloid β plaques (Aβ) is a central feature of Alzheimer’s disease (AD). First reported in animal models, it remains uncertain if peripheral inflammatory/infectious conditions in humans can promote Aβ brain accumulation. Periodontal disease, a common chronic infection, has been previously reported to be associated with AD. Methods Thirty-eight cognitively normal, healthy, community residing elderly (mean age 61; 68% female) were examined in an Alzheimer’s Disease research center and a University-based Dental School. Linear regression models (adjusted for age, ApoE and smoking) were used to test the hypothesis that periodontal disease assessed by clinical attachment loss was associated with brain Aβ load using 11C-PIB PET imaging. Results After adjusting for confounders, clinical attachment loss (≥ 3mm), representing a history of periodontal inflammatory/infectious burden, was associated with increased 11C-PIB uptake in Aβ vulnerable brain regions (p=0.002). Conclusion We show for the first time in humans an association between periodontal disease and brain Aβ load. These data are consistent with prior animal studies showing that peripheral inflammation/infections are sufficient to produce brain Aβ accumulations.

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“…Aged ApoE −/− mice showed significantly impaired cognitive function, which may be caused by a decreased neuronal excitability in hippocampus [15]. However, other studies did not detect learning and behavioral defects in ApoE −/− mice [16] and rats [17]. …”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Genistein against Neuronal Degeneration in ApoE−/− Mice Fed a High-Fat Diet

Park

Jeon

et al. 2016

Nutrients

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Altered cholesterol metabolism is believed to play a causal role in major pathophysiological changes in neurodegeneration. Several studies have demonstrated that the absence of apolipoprotein E (ApoE), a predominant apolipoprotein in the brain, leads to an increased susceptibility to neurodegeneration. Previously, we observed that genistein, a soy isoflavone, significantly alleviated apoptosis and tau hyperphosphorylation in SH-SY5Y cells. Therefore, we investigated the neuroprotective effects of dietary genistein supplementation (0.5 g/kg diet) in the cortex and hippocampus of wild-type C57BL/6 (WT) and ApoE knockout (ApoE−/−) mice fed a high-fat diet (HFD) for 24 weeks. Genistein supplementation alleviated neuroinflammation and peripheral and brain insulin resistance. Reductions in oxidative and endoplasmic reticulum stress were also observed in ApoE−/− mice fed a genistein-supplemented diet. Beta-secretase 1 and presenilin 1 mRNA levels and beta-amyloid peptide (Aβ) protein levels were reduced in response to genistein supplementation in ApoE−/− mice but not in WT mice. Although the absence of ApoE did not increase tau hyperphosphorylation, genistein supplementation reduced tau hyperphosphorylation in both WT and ApoE−/− mice. Consistent with this result, we also observed that genistein alleviated activity of c-Jun N-terminal kinase and glycogen synthase kinase 3β, which are involved in tau hyperphosphorylation. Taken together, these results demonstrate that genistein alleviated neuroinflammation, Aβ deposition, and hyperphosphorylation in ApoE−/− mice fed an HFD.

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Effects of apoE Deficiency and Occlusal Disharmony on Amyloid-Beta Production and Spatial Memory in Rats

Cited by 14 publications

References 54 publications

Difference of brain-derived neurotrophic factor expression and pyramid cell count during mastication of food with varying hardness

Difference of brain-derived neurotrophic factor expression and pyramid cell count during mastication of food with varying hardness

Periodontal disease associates with higher brain amyloid load in normal elderly

Protective Effect of Genistein against Neuronal Degeneration in ApoE−/− Mice Fed a High-Fat Diet

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