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The modulation of neuroinflammation by inducible nitric oxide synthase
The accumulation and propagation of misfolded proteins in the brain is a pathological hallmark shared by many neurodegenerative diseases, such as the depositions of β-amyloid and hyperphosphorylated tau proteins in Alzheimer's disease. Initial evidence shows the role of nitric oxide synthases i...
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Published in: | Journal of cell communication and signaling 2022-06, Vol.16 (2), p.155-158 |
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description | The accumulation and propagation of misfolded proteins in the brain is a pathological hallmark shared by many neurodegenerative diseases, such as the depositions of β-amyloid and hyperphosphorylated tau proteins in Alzheimer's disease. Initial evidence shows the role of nitric oxide synthases in the development of neurodegenerative diseases. A recent, in an exciting paper (Bourgognon et al. in Proc Natl Acad Sci USA 118, 1–11, 2021. 10.1073/pnas.2009579118) it was shown that the inducible nitric oxide synthase plays an important role in promoting oxidative and nitrergic stress leading to neuroinflammation and consequently neuronal function impairments and decline in synaptic strength in mouse prion disease. In this context, we reviewed the possible mechanisms of nitric oxide synthase in the generation of neurodegenerative diseases. |
doi_str_mv | 10.1007/s12079-021-00663-x |
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The International CCN Society.</rights><rights>The International CCN Society 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5265-7101d30fe17375fca3dea5c24723f760e8f14ab9f2d756031950324ee3167e393</citedby><cites>FETCH-LOGICAL-c5265-7101d30fe17375fca3dea5c24723f760e8f14ab9f2d756031950324ee3167e393</cites><orcidid>0000-0001-5531-0485 ; 0000-0002-5942-4778</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8891402/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8891402/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35031946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Justo, Alberto Fernando Oliveira</creatorcontrib><creatorcontrib>Suemoto, Claudia Kimie</creatorcontrib><title>The modulation of neuroinflammation by inducible nitric oxide synthase</title><title>Journal of cell communication and signaling</title><addtitle>J. Cell Commun. Signal</addtitle><addtitle>J Cell Commun Signal</addtitle><description>The accumulation and propagation of misfolded proteins in the brain is a pathological hallmark shared by many neurodegenerative diseases, such as the depositions of β-amyloid and hyperphosphorylated tau proteins in Alzheimer's disease. Initial evidence shows the role of nitric oxide synthases in the development of neurodegenerative diseases. A recent, in an exciting paper (Bourgognon et al. in Proc Natl Acad Sci USA 118, 1–11, 2021. 10.1073/pnas.2009579118) it was shown that the inducible nitric oxide synthase plays an important role in promoting oxidative and nitrergic stress leading to neuroinflammation and consequently neuronal function impairments and decline in synaptic strength in mouse prion disease. 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subjects | Alzheimer's disease Biomedical and Life Sciences Biomedicine Bits and Bytes Cell Biology Inflammation iNOS Life Sciences Neurodegeneration Neurodegenerative diseases Neuromodulation Nitrergic stress Nitric oxide Nitric-oxide synthase Oxidative stress Prion model Protein folding Synaptic strength Tau protein β-Amyloid |
title | The modulation of neuroinflammation by inducible nitric oxide synthase |
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