Oxidative stress and pro-inflammatory cytokines may act as one of the signals for regulating microRNAs expression in Alzheimer’s disease
•On the basis of published data, this review has proposed a novel hypothesis that increased oxidative and chronic inflammation act as one of the signals that regulate the levels of microRNAs in Alzheimer’s disease (AD). Indirect and direct evidence on the effect of free radicals and pro-inflammatory...
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| Published in | Mechanisms of ageing and development Vol. 162; pp. 63 - 71 |
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| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
Ireland
Elsevier B.V
01.03.2017
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| Online Access | Get full text |
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| Abstract | •On the basis of published data, this review has proposed a novel hypothesis that increased oxidative and chronic inflammation act as one of the signals that regulate the levels of microRNAs in Alzheimer’s disease (AD). Indirect and direct evidence on the effect of free radicals and pro-inflammatory cytokines on changes in the expression levels of microRNA support the proposed hypothesis. This hypothesis is of particular importance, because increased oxidative stress and chronic inflammation represent one of the earliest biochemical defects that initiate and promote neurodegeneration in AD.•Antioxidants that protect neurons by reducing oxidative stress and chronic inflammation also influence the levels of microRNAs.•Uprregulation and downregulation of microRNAs in AD may be results of changes in their stability, transcription or processing by Drosa and Dicer in the nucleus and cytoplasm, respectively.
Oxidative stress and chronic inflammation are one of the earliest defects that initiate and promote Alzheimer’s disease (AD). Studies showed that expressions of microRNAs were upregulated or downregulated in AD. Therefore, these biochemical defects may influence the levels of microRNAs. The up-regulated microRNAs cause neurodegeneration by: (a) decreasing the levels of a nuclear transcriptional factor-2 (Nrf2), (b) reducing the levels of α-secretase ADM10; and (c) reducing the levels of phosphatases. The down-regulated microRNAs cause neurodegeneration by: (a) increasing the levels of β-secretase, (b) increasing the levels of tau kinase; (c) elevating the levels of tau proteins; (d) increasing the levels of APP; and (e) increasing the levels of nuclear factor-kappaB (NF-kB). Antioxidants protect neurons by reducing oxidative stress and chronic inflammation. Therefore, they may also influence the levels of microRNAs. This review briefly describes the studies on changes in the expressions of microRNAs in the pathogenesis of AD. It proposes a hypothesis that free radicals and pro-inflammatory cytokines act as one of the signals that upregulate or downregulate the levels of microRNAs by influencing their transcription, processing or stability leading to neurodegeneration in AD. Antioxidants that reduce oxidative stress and pro-inflammatory cytokines also regulate the levels of microRNAs. |
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| AbstractList | •On the basis of published data, this review has proposed a novel hypothesis that increased oxidative and chronic inflammation act as one of the signals that regulate the levels of microRNAs in Alzheimer’s disease (AD). Indirect and direct evidence on the effect of free radicals and pro-inflammatory cytokines on changes in the expression levels of microRNA support the proposed hypothesis. This hypothesis is of particular importance, because increased oxidative stress and chronic inflammation represent one of the earliest biochemical defects that initiate and promote neurodegeneration in AD.•Antioxidants that protect neurons by reducing oxidative stress and chronic inflammation also influence the levels of microRNAs.•Uprregulation and downregulation of microRNAs in AD may be results of changes in their stability, transcription or processing by Drosa and Dicer in the nucleus and cytoplasm, respectively.
Oxidative stress and chronic inflammation are one of the earliest defects that initiate and promote Alzheimer’s disease (AD). Studies showed that expressions of microRNAs were upregulated or downregulated in AD. Therefore, these biochemical defects may influence the levels of microRNAs. The up-regulated microRNAs cause neurodegeneration by: (a) decreasing the levels of a nuclear transcriptional factor-2 (Nrf2), (b) reducing the levels of α-secretase ADM10; and (c) reducing the levels of phosphatases. The down-regulated microRNAs cause neurodegeneration by: (a) increasing the levels of β-secretase, (b) increasing the levels of tau kinase; (c) elevating the levels of tau proteins; (d) increasing the levels of APP; and (e) increasing the levels of nuclear factor-kappaB (NF-kB). Antioxidants protect neurons by reducing oxidative stress and chronic inflammation. Therefore, they may also influence the levels of microRNAs. This review briefly describes the studies on changes in the expressions of microRNAs in the pathogenesis of AD. It proposes a hypothesis that free radicals and pro-inflammatory cytokines act as one of the signals that upregulate or downregulate the levels of microRNAs by influencing their transcription, processing or stability leading to neurodegeneration in AD. Antioxidants that reduce oxidative stress and pro-inflammatory cytokines also regulate the levels of microRNAs. Oxidative stress and chronic inflammation are one of the earliest defects that initiate and promote Alzheimer's disease (AD). Studies showed that expressions of microRNAs were upregulated or downregulated in AD. Therefore, these biochemical defects may influence the levels of microRNAs. The up-regulated microRNAs cause neurodegeneration by: (a) decreasing the levels of a nuclear transcriptional factor-2 (Nrf2), (b) reducing the levels of α-secretase ADM10; and (c) reducing the levels of phosphatases. The down-regulated microRNAs cause neurodegeneration by: (a) increasing the levels of β-secretase, (b) increasing the levels of tau kinase; (c) elevating the levels of tau proteins; (d) increasing the levels of APP; and (e) increasing the levels of nuclear factor-kappaB (NF-kB). Antioxidants protect neurons by reducing oxidative stress and chronic inflammation. Therefore, they may also influence the levels of microRNAs. This review briefly describes the studies on changes in the expressions of microRNAs in the pathogenesis of AD. It proposes a hypothesis that free radicals and pro-inflammatory cytokines act as one of the signals that upregulate or downregulate the levels of microRNAs by influencing their transcription, processing or stability leading to neurodegeneration in AD. Antioxidants that reduce oxidative stress and pro-inflammatory cytokines also regulate the levels of microRNAs. |
| Author | Prasad, Kedar N. |
| Author_xml | – sequence: 1 givenname: Kedar N. surname: Prasad fullname: Prasad, Kedar N. email: knprasad@comcast.net organization: 245 E-Faisan Drive, San Rafael, CA 94903, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27964992$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - pathology Animals Antioxidants Cytokines - genetics Cytokines - metabolism Dementia Gene Expression Regulation Humans Inflammation MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Oxidative Stress Signal Transduction |
| Title | Oxidative stress and pro-inflammatory cytokines may act as one of the signals for regulating microRNAs expression in Alzheimer’s disease |
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