인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
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지원사업
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커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Dear Editor,Alzheimer's disease (AD) is the most prevalent neurodegenerative disease without effective treatments. 1 Extracellular amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss are the characteristics of AD neuropathology.Amyloid protein (A), the major component of amyloid plaques, is produced through the sequential cleavage of the amyloid precursor protein (APP) by -secretase BACE1 and -secretase. 1Dysregulation of APP, BACE1, and -secretase increases A generation while dysfunction of microglia reduces A clearance, contributing to A deposition. 2 The increase in A deposition simultaneously activates microglia, promoting the secretion of a large number of pro-inflammatory cytokines.Dysregulation of gut microbiota and their metabolites plays a pivotal role in AD pathogenesis. 3Among the metabolites, butyrate has beneficial effects on AD.Increasing the bioavailability of butyrate is critical for its clinical application. 4To achieve consistent supplementation of butyrate, we have developed a strain of engineered butyrateproducing Saccharomyces cerevisiae (J17), a yeast probiotic, 5 which may mitigate AD phenotypes by the synergistic effect of butyrate supplementation and probiotic function of the chassis.We first investigated whether butyrate is deficient in the blood and brain of APP23/PS45 mice, a strain of AD model mice, and whether J17 has beneficial effects on AD.In APP23/PS45 mice, the butyrate levels were significantly decreased to 53.99 6.90% (blood, P < 0.05) and 28.92 2.92% (brain, P < 0.01) of those in the wild-type (WT) mice, respectively, which is consistent with that in AD patients and in the other two AD model mice, APP/PS1 mice and 3xTg mice.J17 administration rescued butyrate deficiency in the blood and brain of the AD mice, while the chassis strain BY4741 did not (Fig. 1a).Importantly, J17 rescued cognitive impairment in the AD mice.In the Morris water maze (MWM) test, no difference of escape latency was observed on the 1st day of visible platform trial among the four groups.From the 2nd day to the 5th day, the hidden platform trials were performed.The escape latency in the J17-treated AD mice was significantly reduced compared with that in the AD mice (e.g., 27.82 5.86 seconds vs. 50.20 6.64 seconds on the 5th day, P < 0.05), while it was comparable to that in the WT mice (30.01 4.70 seconds) (Fig. 1b).In the probe trial of the last day of MWM testing, the AD mice swam significantly shorter distances in the target quadrant compared with the WT mice (Fig. 1b).J17treated AD mice swam significantly longer distances in the target quadrant than the AD mice did, respectively (Fig. 1b).Notably, a trend of the increase of distance was observed in BY4741-treated AD mice, although the difference was not statistically significant.These results demonstrate that J17 rescues the learning and memory deficits of the AD mice, which may be attributed to the synergistic effect of butyrate supplementation and the probiotic function of the chassis.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
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