Expression Profiles of Long Noncoding RNAs in Intranasal LPS-Mediated Alzheimer’s Disease Model in Mice

Tang, Liang; Lan, Liu; Li, Guangyi; Jiang, Pengcheng; Wang, Yan; Li, Jianming

doi:10.1155/2019/9642589

Cited by 35 publications

(35 citation statements)

References 47 publications

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“…The relationship between CDC5L and some neurodegenerative and neuroimmune diseases is established in plenty researches, most of which operate with transcriptome analysis [23,24,25]. Adverse regulation of mRNA splicing in cerebral cortex through, inter alia, malfunction of CDC5L lead to a decrease of proliferative activity and disruption of the neuronal differentiation [26].…”

Section: Discussionmentioning

confidence: 99%

Perinatal changes in plasma of type 2 diabetes mellitus pregnancies who delivered newborns with cardiomyopathy, depression of the central nervous system, or hepatomegaly

Kopylov

Папышева

Gribova³

et al. 2020

Preprint

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Background Maternal diabetes either pregestational or gestational is the main risk factor contributing in development of diabetic fetopathy (DF) in newborns. There are no generalized signs of DF up to late gestational age due to insufficient sensitivity of the currently employed instrumental methods for diagnosis. Methods This is a cross-sectional prospective controlled study. Here, we reported proteomic investigation for several cases of severe types of diabetic fetopathy (cardiomyopathy (CRDM, n = 37), central nervous system depression (CNSD, n = 35) and hepatomegaly (HPMG, n = 35)) diagnosed during 30–35 gestational weeks and confirmed upon delivery by from patients with type 2 diabetes mellitus (T2DM). Control groups were comprised from women in whom T2DM had been ruled out (n = 40) and group of pregnancies with T2DM who delivered healthy newborns (n = 40). Results We found a composition of serum-based non-trivial markers capable that are strongly associated with the certain type of fetopathy or anatomical malfunctions in the affected newborns. Significant impact on mRNA splicing and DNA reparation has been determined by emerging alterations in CDCL5. Patients of CNSD groups were characterized by utmost depletion (ca. 7% of baseline) of DFP3 neurotrophic factor needed for the proper specialization of cardiomyocytes and oligodendrocytes. Corrupted regulation of non-canonical Wnt-signaling guided by PEDF (in CNSD and HPMG groups) and DAAM2 (in CRDM and HPMG groups) was also proposed. In addition, deficiency in retinoic acid and thyroxine transport was revealed by dramatic increase of TTHY in CNDS group. Conclusions We examined peripheral blood plasma and determined a small proportion of proteins indicating the pre-existing signs of DF. Most of the examined markers are participants of critical processes at different stages of embryogenesis and regulate various phases of morphogenesis. There are proteins regulating splicing and DNA repair, differentiation of neurons and their switching to the post-mitotic state. Therefore, reconstruction of the molecular interplay between the defined in proteins is decisive to appreciate cryptic violations in fetal development on the background of diabetic conditions

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Section: Discussionmentioning

confidence: 99%

Perinatal changes in plasma of type 2 diabetes mellitus pregnancies who delivered newborns with cardiomyopathy, depression of the central nervous system, or hepatomegaly

Kopylov

Папышева

Gribova³

et al. 2020

Preprint

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“…e LPS-induced AD mouse model was established according to our previous study [15]. A total of 40 LPS-induced AD mice were randomly divided into the following five groups:…”

Section: Animals and Drug Administrationmentioning

confidence: 99%

The Neuroprotective Effect of Byu d Mar 25 in LPS-Induced Alzheimer's Disease Mice Model

Liu

Zhang

Tang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Inflammatory factors play an important role in the pathogenesis of Alzheimer’s disease (AD). Byu d Mar 25 (BM25) has been suggested to have protective effects in the central nervous system. However, the effect of BM25 on AD has not been determined. This study aims to investigate the neuroprotective effect of BM25 in AD. A total of 40 AD model mice were randomly assigned to the following five groups (n = 8 per group): the AD + NS group, the AD + donepezil group, and three AD + BM25 groups treated with either 58.39 mg/kg (AD + BM25-L), 116.77 mg/kg (AD + BM25-M), or 233.54 mg/kg BM25 (AD + BM25-H). The Morris water maze test was performed to assess alterations in spatial learning and memory deficits. Nissl staining was performed to detect Nissl bodies and neuronal damage. The expression of IL-1β and TNF-α was evaluated by ELISA. The protein expression of P-P38, P38, P-IκBα, caspase 1, COX2, and iNOS was determined by western blotting. The expression of Aβ, p-Tau, and CD11b was measured by immunohistochemistry. The mRNA expression levels of IL-1β, TNF-α, COX2, and iNOS were measured by qRT-PCR. Spatial memory significantly improved in the AD + BM25-M and AD + BM25-H groups compared with the AD + NS group ( p < 0.05 ). The expression of Aβ and p-Tau significantly decreased in the AD + BM25-M and AD + BM25-H groups ( p < 0.05 ). The neuron density and hierarchy and number of pyramidal neurons significantly increased in the AD + BM25-M and AD + BM25-H groups ( p < 0.05 ). In addition, the expression levels of CD11b, IL-1β, TNF-α, COX2, iNOS, caspase 1, p-IκBα, and p-P38 significantly decreased in the AD + BM25-M and AD + BM25-H groups ( p < 0.05 ). In conclusion, our findings suggest that BM25 may exert anti-inflammatory and neuroprotective effects in AD model mice by suppressing the activity of microglia and inhibiting the phosphorylation of IκBα and p38 MAPK.

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“…XIST is a regulatory long non-coding RNA (lncRNA); XIST notably is involved in X-inactivation in females, possibly explaining why there are fairly consistent negative correlations between it and the Y-linked genes [38]. LncRNAs in general have been implicated in the pathogenesis of Alzheimer's disease that are both up and down regulated in the disease [39]. Another hub that is present in all three is a JARID1C splice variant.…”

Section: Under Expressed Regulatory Elementsmentioning

confidence: 99%

Network Medicine Approach for Analysis of Alzheimer’s Disease Gene Expression Data

Cohen

Pilozzi

Huang

2020

IJMS

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Alzheimer’s disease (AD) is the most widespread diagnosed cause of dementia in the elderly. It is a progressive neurodegenerative disease that causes memory loss as well as other detrimental symptoms that are ultimately fatal. Due to the urgent nature of this disease, and the current lack of success in treatment and prevention, it is vital that different methods and approaches are applied to its study in order to better understand its underlying mechanisms. To this end, we have conducted network-based gene co-expression analysis on data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. By processing and filtering gene expression data taken from the blood samples of subjects with varying disease states and constructing networks based on that data to evaluate gene relationships, we have been able to learn about gene expression correlated with the disease, and we have identified several areas of potential research interest.

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Expression Profiles of Long Noncoding RNAs in Intranasal LPS-Mediated Alzheimer’s Disease Model in Mice

Cited by 35 publications

References 47 publications

Perinatal changes in plasma of type 2 diabetes mellitus pregnancies who delivered newborns with cardiomyopathy, depression of the central nervous system, or hepatomegaly

Perinatal changes in plasma of type 2 diabetes mellitus pregnancies who delivered newborns with cardiomyopathy, depression of the central nervous system, or hepatomegaly

The Neuroprotective Effect of Byu d Mar 25 in LPS-Induced Alzheimer's Disease Mice Model

Network Medicine Approach for Analysis of Alzheimer’s Disease Gene Expression Data

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