Evidence for involvement of dysfunctional teeth in the senile process in the hippocampus of SAMP8 mice

Watanabe, Kazuko; Tonosaki, Keiichi; Kawase, Toshio; Karasawa, Nobuyuki; Nagatsu, Ikuko; Fujita, Masafumi; Onozuka, Minoru

doi:10.1016/s0531-5565(00)00216-3

Cited by 58 publications

(71 citation statements)

References 26 publications

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“…In the CA4 area after task 2 and in the other hippocampal regions after task 3, the density decreased as the number of extracted teeth increased. The result of this report was in agreement with previous studies reporting that the loss of a tooth results in a decreased pyramidal cells within the hippocampal formation; this decreased density suggests impaired memory function (Kato et al, 1997;Watanabe et al, 2001). …”

supporting

confidence: 92%

“…The mechanism by which this occurs has been explored based on evaluations of the central cholinergic system (Kato et al, 1997;Terasawa et al, 2002) and the density of hippocampal cells, in relation to the cognitive and learning functions of aged rats (Watanabe et al, 2001). However, it has not yet been adequately defined, especially in relation to synaptic transmission in the signaling pathways from the trigeminal nerve area mediated by receptors located in mastication-associated tissues.…”

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confidence: 99%

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Effect of tooth loss on spatial memory and trkB‐mRNA levels in rats

et al. 2008

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The mechanism by which tooth loss accelerates spatial memory impairment is unknown. The purpose of this study was to test the hypothesis that tooth loss affects trkB-mRNA levels and leads to an accelerated decrease in the hippocampal cell density in rats. A radial maze was used to evaluate the spatial memory of male Wistar rats that were categorized based on the number of extracted molar teeth. Number of hippocampal pyramidal cells and the trkB-mRNA expressions in the amygdala, perirhinal cortex, thalamus, and the hippocampal CA1, CA3, and CA4 areas, were evaluated using molecular biological techniques. Seven weeks after tooth extraction, maze performance was significantly lower in each tooth loss group than in the control group, and the number of extracted teeth was inversely proportional to the induction of the trkB-mRNA and the hippocampal cell density. The average weight of rats increased by controlled feeding throughout the experiment without showing a significant difference between the control and experimental groups. The results indicated that, in rats, the spatial memory-linked trkB-mRNA was reduced in association with the tooth loss; this supports the hypothesis and suggests that teeth have a role in the prevention of spatial memory impairment.

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confidence: 92%

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confidence: 99%

Effect of tooth loss on spatial memory and trkB‐mRNA levels in rats

et al. 2008

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“…Among them senescenceaccelerated mice (SAM) strains are especially useful models to understand the mechanisms of the age-related mitochondrial decline. Behavioral studies showed that learning and memory deficits already started as early as 6 months and worsened with aging in SAMP8 mice (accelerated senescence-prone 8) (53,77). Moreover, Omata and collaborators showed agerelated changes in cerebral energy production in the 2-monthold SAMP8 followed by a decrease in mitochondrial function compared with SAMR1 mice (accelerated senescence-resistant 1) (51).…”

Section: Mitochondrial Aging-the Beginning Of the End In Ad?mentioning

confidence: 99%

Insights into Mitochondrial Dysfunction: Aging, Amyloid-β, and Tau–A Deleterious Trio

Schmitt

Grimm

Kaźmierczak

et al. 2012

Antioxidants & Redox Signaling

121

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Significance: Alzheimer's disease (AD) is an age-related progressive neurodegenerative disorder mainly affecting elderly individuals. The pathology of AD is characterized by amyloid plaques (aggregates of amyloid-b [Ab]) and neurofibrillary tangles (aggregates of tau), but the mechanisms underlying this dysfunction are still partially unclear. Recent Advances: A growing body of evidence supports mitochondrial dysfunction as a prominent and early, chronic oxidative stress-associated event that contributes to synaptic abnormalities and, ultimately, selective neuronal degeneration in AD. Critical Issues: In this review, we discuss on the one hand whether mitochondrial decline observed in brain aging is a determinant event in the onset of AD and on the other hand the close interrelationship of this organelle with Ab and tau in the pathogenic process underlying AD. Moreover, we summarize evidence from aging and Alzheimer models showing that the harmful trio ''aging, Ab, and tau protein'' triggers mitochondrial dysfunction through a number of pathways, such as impairment of oxidative phosphorylation (OXPHOS), elevation of reactive oxygen species production, and interaction with mitochondrial proteins, contributing to the development and progression of the disease. Future Directions: The aging process may weaken the mitochondrial OXPHOS system in a more general way over many years providing a basis for the specific and destructive effects of Ab and tau. Establishing strategies involving efforts to protect cells at the mitochondrial level by stabilizing or restoring mitochondrial function and energy homeostasis appears to be challenging, but very promising route on the horizon.

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“…In previous experimental studies, masticatory dysfunction has been shown to be involved in the senile process of hippocampal mechanisms, e.g. reduced spatial cognition [14,15,19], decreased input activities [18], enhanced neuronal degeneration [3,12,14,15,19] and the decline in the cholinergic system [13]. In addition, a soft diet from the weanling stage causes later impairment of avoidance performance in mice [4], and differences in neuronal density between the right and left cerebral hemispheres are seen in rats with unilateral mastication [2].…”

Section: Introductionmentioning

confidence: 97%