Mechanism of Autonomic Exercise Improving Cognitive Function of Alzheimer’s Disease by Regulating lncRNA SNHG14

He, Yuchen; Yi, Qiang

doi:10.1177/15333175211027681

Cited by 15 publications

(6 citation statements)

References 34 publications

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“…The mechanism underlying exercise in AD has been explored by some authors. For example, the exercise meliorates MMSE and ADAS-Cog scores, and inhibits the raised expression of lncRNA SNHG14 [13]. In another investigation of AD patients, the levels of miR-129-5p were enhanced induced by physical exercise, and correlations were identified between miR-129-5p and ADAS-Cog and MMSE scores [17].…”

Section: Discussionmentioning

confidence: 98%

LncRNA HOTAIR in exercise-induced neuro-protective function in Alzheimer’s disease

Lü¹,

Liu²,

Chen³

et al. 2022

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Introduction: Exercise is effective in Alzheimer's disease (AD), which is characterized by neuro-degenerative progress with increasing morbidity. The present study aimed to explore whether HOTAIR participated in the regulation of exercise in AD. Material and methods: A relative expression of serum HOTAIR was detected using quantitative real-time polymerase chain reaction (PCR). The diagnostic significance of HOTAIR on distinguishing AD patients was evaluated by receiver operating characteristic (ROC) curve. Correlations between HOTAIR expression and Mini-Mental State Examination (MMSE) score or Alzheimer's Disease Assessment Scale-Cognitive (ADAS-Cog) score were analyzed with Pearson's test. Logistic regression analysis was applied to investigate factors as independent indicators for HOTAIR expression.Results: In AD patients, the expression of HOTAIR was increased, and it could function as a diagnostic marker in AD patients. The expression of HOTAIR was associated with MMSE score and ADAS-Cog score in AD patients before exercise. Exercise ameliorated the cognitive impairment and reduced the relative serum expression of HOTAIR. Exercise was proved to be an independent indicator of HOTAIR expression. Conclusions: HOTAIR was a possible biomarker for indicating AD patients, and it was correlated with MMSE scores and ADAS-Cog results. Exercise might moderate AD progress via controlling HOTAIR.

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Section: Discussionmentioning

confidence: 98%

LncRNA HOTAIR in exercise-induced neuro-protective function in Alzheimer’s disease

Lü¹,

Liu²,

Chen³

et al. 2022

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“…23 The researchers also found that in experimental mice with Alzheimer's disease, mice receiving exercise intervention could suppress inflammatory activity and improve their cognitive levels by reducing the level of lncRNA SNHG14. 24 Besides, Shi et al found that lncRNA SNHG14 activated the IL-1 receptor-associated kinase 4/nuclear factor-κB signaling pathway by binding to miR-93, which accelerated the inflammatory damage of septic induced AKI cells. 25 In this study, from the in vitro AGA cell model, it was noted that excessive lncRNA SNHG14 induced the inflammatory response of THP-1 cells, while silencing lncRNA SNHG14 significantly inhibited the production of IL-1β, IL-6, and TNFα.…”

Section: Discussionmentioning

confidence: 99%

“…For example, Zhang et al reported that lncRNA SNHG14 expression was increased in ischemic stroke, and that reducing lncRNA SNHG14 levels attenuated brain tissue damage and inflammation in a mouse model 23 . The researchers also found that in experimental mice with Alzheimer's disease, mice receiving exercise intervention could suppress inflammatory activity and improve their cognitive levels by reducing the level of lncRNA SNHG14 24 . Besides, Shi et al found that lncRNA SNHG14 activated the IL‐1 receptor‐associated kinase 4/nuclear factor‐κB signaling pathway by binding to miR‐93, which accelerated the inflammatory damage of septic induced AKI cells 25 .…”

Section: Discussionmentioning

confidence: 99%

Highly expressed long non‐coding RNA SNHG14 activated MSU‐induced inflammatory response in acute gout arthritis through targeting miR‐223‐3p

Yang,

Liu,

Yan

et al. 2023

Int J of Rheum Dis

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AimAccording to reports, long non‐coding RNAs (lncRNAs) are involved in the regulation of many inflammatory diseases. Here, our main purpose was to ascertain the expression data of lncRNA SNHG14 in acute gouty arthritis (AGA) and to explore its possible mechanism in the regulation of AGA.MethodReverse transcription quantitative polymerase chain reaction technology was supplied to detect the lncRNA SNHG14 expression. A receiver operating characteristics curve was drawn to estimate the accuracy of lncRNA SNHG14 in AGA diagnosis. An in vitro AGA cell model was constructed by inducing THP‐1 cells with monosodium urate (MSU). The concentrations of inflammatory factors such as interleukin‐1β, interleukin‐6, and tumor necrosis factor‐α were measured by enzyme‐linked immunosorbent assay. The luciferase reporter gene was used to verify the relationship between lncRNA SNHG14 and miR‐223‐3p.ResultsIn clinical analysis, the levels of serum lncRNA SNHG14 in AGA patients were significantly higher than those in the control group. Abnormally elevated lncRNA SNHG14 has high sensitivity and specificity for AGA diagnosis. In in vitro cell experiments, silencing lncRNA SNHG14 inhibited the inflammatory response of THP‐1 cells stimulated by MSU, and the luciferase reporter gene proved that lncRNA SNHG14 could bind to miR‐223‐3p. In addition, the level of miR‐223‐3p declined in AGA patients and the AGA cell model. Overexpression of miR‐223‐3p is helpful to alleviate an MSU‐induced inflammatory response.ConclusionIn the AGA cell model, lncRNA SNHG14, as an miR‐223‐3p sponge, induces a cellular inflammatory response by controlling the level of miR‐223‐3p, so aggravating the disease progress of AGA.

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“…In this model, angiotensin analogs inhibit inflammation and prevent cognitive impairment by inhibiting SNHG14, thus restoring miR-223-3p function [ 74 ]. Exercise that improves cognition and reduces inflammation markers can also reduce SNG14 levels, in mice models and AD patients [ 75 ].…”

Section: Long Non-coding Rnas In Alzheimer’s Disease Related To Infla...mentioning

confidence: 99%

Long Non-Coding RNAs, Extracellular Vesicles and Inflammation in Alzheimer’s Disease

Canseco-Rodriguez

Masola

Aliperti

et al. 2022

IJMS

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Alzheimer’s Disease (AD) has currently no effective treatment; however, preventive measures have the potential to reduce AD risk. Thus, accurate and early prediction of risk is an important strategy to alleviate the AD burden. Neuroinflammation is a major factor prompting the onset of the disease. Inflammation exerts its toxic effect via multiple mechanisms. Amongst others, it is affecting gene expression via modulation of non-coding RNAs (ncRNAs), such as miRNAs. Recent evidence supports that inflammation can also affect long non-coding RNA (lncRNA) expression. While the association between miRNAs and inflammation in AD has been studied, the role of lncRNAs in neurodegenerative diseases has been less explored. In this review, we focus on lncRNAs and inflammation in the context of AD. Furthermore, since plasma-isolated extracellular vesicles (EVs) are increasingly recognized as an effective monitoring strategy for brain pathologies, we have focused on the studies reporting dysregulated lncRNAs in EVs isolated from AD patients and controls. The revised literature shows a positive association between pro-inflammatory lncRNAs and AD. However, the reports evaluating lncRNA alterations in EVs isolated from the plasma of patients and controls, although still limited, confirm the value of specific lncRNAs associated with AD as reliable biomarkers. This is an emerging field that will open new avenues to improve risk prediction and patient stratification, and may lead to the discovery of potential novel therapeutic targets for AD.

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Mechanism of Autonomic Exercise Improving Cognitive Function of Alzheimer’s Disease by Regulating lncRNA SNHG14

Cited by 15 publications

References 34 publications

LncRNA HOTAIR in exercise-induced neuro-protective function in Alzheimer’s disease

LncRNA HOTAIR in exercise-induced neuro-protective function in Alzheimer’s disease

Highly expressed long non‐coding RNA SNHG14 activated MSU‐induced inflammatory response in acute gout arthritis through targeting miR‐223‐3p

Long Non-Coding RNAs, Extracellular Vesicles and Inflammation in Alzheimer’s Disease

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