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
Takeda et al. BMC Neurosci
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
Yosuke Takeda 0
Hiroshi Oue 0
Shinsuke Okada 0
Akira Kawano 0
Katsunori Koretake 0
Makoto Michikawa 1
Yasumasa Akagawa 0
Kazuhiro Tsuga 0
0 Department of Advanced Prosthodontics, Hiroshima University Graduate School of Biomedical and Health Sciences , Hiroshima , Japan
1 Department of Biochemistry, Nagoya City University Graduate School of Medical Sciences , Nagoya , Japan
Background: It 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. BDNFrelated mRNA in the hippocampus was analyzed by real-time polymerase chain reaction (RT-PCR). Results: At 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. Conclusions: These 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.
Molar loss; Powder diet; Memory deficit; Brain-derived neurotrophic factor
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Maintenance of healthy dental conditions and
mastication has been believed to play a crucial role not only in
oral function, but also in systemic conditions and brain
function [1–3]. Retrospective studies have reported
the relationship between oral health and cognitive
impairment [4–6]. Community-dwelling persons with
tooth loss are more likely to have impaired cognitive test
performance, with those older than 45 years being more
significantly affected [5]. Another study reported that
the possession of fewer teeth in adulthood was
significantly associated with incident of dementia [6] or tooth
loss has been suggested as a possible epidemiological risk
factor for Alzheimer’s disease (AD) [7]. Additionally,
animal studies suggested that impairment of oral condition,
including tooth loss, could lead to memory impairment
[8–10].
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Brain-derived neurotrophic factor (BDNF), a member
of the neurotrophic family, is widely expressed in the
central nervous system and plays an important role in the
regulation of hippocampal learning and memory
processes [11]. Also, BDNF is a key molecule involved in the
structural and functional plasticity of the hippocampal
synapse. In addition, decreased BDNF levels may result
in decreased hippocampal neurogenesis; BDNF
expression is decreased in patients with AD and Parkinson’s
disease [12–14]. BDNF actions include activation of insulin
receptor substrate-1 (IRS-1/2), Pl-3K, and protein kinase
B (Akt). BDNF binds to tyrosine kinase B (TrkB), which
is a high affinity receptor of BDNF and activates a signal
transduction cascade [15]. BDNF and its tyrosine kinase
receptor, TrkB, are expressed in hypothalamic nuclei
associated with satiety and locomotor activity [26].
Some reports suggest that BDNF might be associated with
molar loss or soft diet [16, 17]. TrkB was also reduced in
association with molar loss [16, 17]. Molar loss is associated
with a reduction in t (...truncated)