Impaired Hippocampal Neurogenesis and its Enhancement with Ghrelin in 5XFAD Mice

Moon, Minho; Moon, Yong; Mook‐Jung, Inhee

doi:10.3233/jad-132417

Cited by 102 publications

(83 citation statements)

References 57 publications

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“…Immunohistochemistry against DCX, a commonly used neuroblast marker that correlates well with the number of newly generated neurons in the hippocampus (Brown et al, 2003), supported these observations. Our data are in line with previously published studies demonstrating altered neurogenesis in AD (Baglietto-Vargas et al, 2010;Moon et al, 2014;Tatebayashi, 2003).…”

Section: Calretinin Immunoreactivitysupporting

confidence: 95%

Vulnerability of calbindin, calretinin and parvalbumin in a transgenic/knock-in APPswe/PS1dE9 mouse model of Alzheimer disease together with disruption of hippocampal neurogenesis

Verdaguer

Brox

Петров

et al. 2015

Experimental Gerontology

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Section: Calretinin Immunoreactivitysupporting

confidence: 95%

Vulnerability of calbindin, calretinin and parvalbumin in a transgenic/knock-in APPswe/PS1dE9 mouse model of Alzheimer disease together with disruption of hippocampal neurogenesis

Verdaguer

Brox

Петров

et al. 2015

Experimental Gerontology

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“…The survival and proliferation of hippocampal cells in patients with AD is significantly suppressed; thus, promoting their survival and proliferation is critical for the treatment of AD (21). In the present in vitro study, it was revealed that the overexpression of miR-135b significantly promotes the proliferation of hippocampal cells.…”

Section: Discussionmentioning

confidence: 62%

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

Zhang

Xing

Guo

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRs) are a class of endogenous small non-coding RNAs that have been revealed to negatively mediate the expression of their target genes at the post-transcriptional level. Recently, particular miRs have demonstrated an involvement in the pathogenesis of Alzheimer's disease (AD). However, the specific role of miR-135b in AD has yet to be elucidated. The present study aimed to investigate the neuroprotective role of miR-135b, in addition to its underlying mechanism. Herein, reverse transcription-quantitative polymerase chain reaction was conducted to determine miR-135b expression levels in the peripheral blood samples of patients with AD and age-matched normal controls. The data of the present study revealed that the expression levels of miR-135b were significantly reduced in the peripheral blood of AD patients compared with normal controls (P<0.01). In vitro MTT analyses identified that the overexpression of miR-135b significantly enhanced the proliferation of hippocampal cells (P<0.01). Furthermore, in vivo analysis using a Y-maze test indicated that injection with miR-135b mimics into the third ventricle of anesthetized SAMP8 mice significantly enhanced their learning and memory capacities (P<0.01). Molecular mechanism investigations identified β-site APP-cleaving enzyme 1 (BACE1) as a direct target gene of miR-135b, and the latter was identified to negatively mediate the protein expression levels of BACE1 in hippocampal cells, in addition to hippocampal tissues, of SAMP8 mice. Based on the aforementioned findings, we propose that miR-135b has a neuroprotective role via direct targeting of BACE1 and, thus, may be used for the treatment of AD.

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“…The generation of 5xFAD mice has been described previously [Moon et al, 2014]. We used female 5xFAD mice and assigned the mice to two groups: 5xFAD sham exposure ( n = 8) and 5xFAD RF exposure ( n = 8).…”

Section: Methodsmentioning

confidence: 99%

1950 MHz radiofrequency electromagnetic fields do not aggravate memory deficits in 5xFAD mice

Son

Jeong

Kwon³

et al. 2016

Bioelectromagnetics

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The increased use of mobile phones has generated public concern about the impact of radiofrequency electromagnetic fields (RF‐EMF) on health. In the present study, we investigated whether RF‐EMFs induce molecular changes in amyloid precursor protein (APP) processing and amyloid beta (Aβ)‐related memory impairment in the 5xFAD mouse, which is a widely used amyloid animal model. The 5xFAD mice at the age of 1.5 months were assigned to two groups (RF‐EMF‐ and sham‐exposed groups, eight mice per group). The RF‐EMF group was placed in a reverberation chamber and exposed to 1950 MHz electromagnetic fields for 3 months (SAR 5 W/kg, 2 h/day, 5 days/week). The Y‐maze, Morris water maze, and novel object recognition memory test were used to evaluate spatial and non‐spatial memory following 3‐month RF‐EMF exposure. Furthermore, Aβ deposition and APP and carboxyl‐terminal fragment β (CTFβ) levels were evaluated in the hippocampus and cortex of 5xFAD mice, and plasma levels of Aβ peptides were also investigated. In behavioral tests, mice that were exposed to RF‐EMF for 3 months did not exhibit differences in spatial and non‐spatial memory compared to the sham‐exposed group, and no apparent change was evident in locomotor activity. Consistent with behavioral data, RF‐EMF did not alter APP and CTFβ levels or Aβ deposition in the brains of the 5xFAD mice. These findings indicate that 3‐month RF‐EMF exposure did not affect Aβ‐related memory impairment or Aβ accumulation in the 5xFAD Alzheimer's disease model. Bioelectromagnetics. 37:391–399, 2016. © 2016 The Authors Bioelectromagnetics published by Wiley Periodicals, Inc. on behalf of Bioelectromagnetics Society.

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Impaired Hippocampal Neurogenesis and its Enhancement with Ghrelin in 5XFAD Mice

Cited by 102 publications

References 57 publications

Vulnerability of calbindin, calretinin and parvalbumin in a transgenic/knock-in APPswe/PS1dE9 mouse model of Alzheimer disease together with disruption of hippocampal neurogenesis

Vulnerability of calbindin, calretinin and parvalbumin in a transgenic/knock-in APPswe/PS1dE9 mouse model of Alzheimer disease together with disruption of hippocampal neurogenesis

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

1950 MHz radiofrequency electromagnetic fields do not aggravate memory deficits in 5xFAD mice

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