Molar loss and powder diet leads to memory deficit and modifies the mRNA expression of brain-derived neurotrophic factor in the hippocampus of adult mice

Abstract

BackgroundIt is known that tooth loss is known to be a risk factor for Alzheimer’s disease and soft diet feeding induces memory impairment. Recent studies have shown that brain-derived neurotrophic factor (BDNF) is associated with tooth loss or soft diet in young animal model, and that BDNF expression is decreased in patients with Alzheimer’s disease. However, single or combined effect of tooth loss and/or soft diet on brain function has not fully understood. Here we examined the effect of molar loss and powder diet on memory ability and the expression of BDNF mRNA in the hippocampus of adult C57BL/6J mice. Twenty eight-weeks-old C57BL/6J mice were divided into intact molar group and extracted molar group. They were randomly divided into the I/S group (Intact upper molar teeth/Solid diet feeding), the E/S group (Extracted upper molar teeth/Solid diet feeding), the I/P group (Intact upper molar teeth/Powder diet feeding), and the E/P group (Extracted upper molar teeth/Powder diet feeding). The observation periods were 4 and 16-week. To analyze the memory ability, the step-through passive avoidance test was conducted. BDNF-related mRNA in the hippocampus was analyzed by real-time polymerase chain reaction (RT-PCR).ResultsAt 4 weeks later, we performed memory test and isolated brains to analyze. There were no differences in memory function and BDNF mRNA level between these four groups. However, at 16 weeks later, E/S and E/P group showed memory impairment, and decreased level of BDNF mRNA. Whereas, the powder diet had no effect on memory function and BDNF mRNA level even at 16 weeks later.ConclusionsThese results suggest that the effect of molar loss and powder diet on memory function and BDNF mRNA levels were different, molar loss may have a greater long-term effect on memory ability than powder diet does.

Tooth loss early in life induces hippocampal morphology remodeling in senescence-accelerated mouse prone 8 (SAMP8) mice

“…The hippocampal BDNF levels are involved in the regulation of the hippocampal neurogenesis and synaptic plasticity [11,33]. Animal studies indicated that tooth loss decreased hippocampal BDNF expression levels both in C57BL/6J and SAMP8 mice [11,33]. We consider that the effect of tooth loss on the hippocampus was similar for genetically different inbred murine strains.…”

“…Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family, which is widely expressed in the brain. The hippocampal BDNF levels are involved in the regulation of the hippocampal neurogenesis and synaptic plasticity [11,33]. Animal studies indicated that tooth loss decreased hippocampal BDNF expression levels both in C57BL/6J and SAMP8 mice [11,33].…”

Revisiting the link between cognitive decline and masticatory dysfunction

“…In general, these studies have supported the hypothesis that cognitive decline is associated with masticatory dysfunction. These studies have demonstrated that cognitive decline is related to cellular and neurochemical change in the hippocampus, including decreased cellular proliferation [ 47 , 48 , 50 ], decreased levels of brain-derived neurotrophic factor [ 44 , 47 , 59 ], as well as increased nitrous oxide levels [ 55 ] and extracellular dopamine levels [ 52 ]. These findings suggested that the hippocampus-dependent deficits in learning and memory may contribute to the association between cognitive decline and masticatory dysfunction [ 10 ].…”

“…These findings suggested that the hippocampus-dependent deficits in learning and memory may contribute to the association between cognitive decline and masticatory dysfunction [ 10 ]. Importantly, using animal models, researchers were able to investigate the interactional effect between masticatory dysfunction and other factors, such as the type of diet [ 46 , 59 ], environmental stimuli [ 47 ], and stress [ 52 ]. These factors can partially ameliorate the cognitive deficits induced by masticatory dysfunction [ 46 , 47 ].…”

Preceding functional tooth loss delays recovery from acute cerebral hypoxia and locomotor hypoactivity after murine subarachnoid haemorrhage

“…Second, this study does not answer age‐related deficits in learning and memory similar to those seen in elderly humans, since we created disease models in intact mice and the behavioural test battery was consisted of a single open‐field test. To understand clinically relevant situations, more specific experimental settings such as experimental murine model for human senile dementia, longer neurobehavioural assessments of spatial learning ability to cause cognitive impairment, and pathological/molecular‐based preparations to validate hippocampal neuron loss should be proposed in future studies.…”