P2X7 receptor/NLRP3 inflammasome complex and α‐synuclein in peripheral blood mononuclear cells: a prospective study in neo‐diagnosed, treatment‐naïve Parkinson’s disease
Background and purpose Neuroinflammation and probably systemic inflammation, with abnormal α‐synuclein deposition, participate in the development of Parkinson's disease (PD). The P2X7 receptor/NLRP3 inflammasome complex is upregulated in the brain of PD patients. By a prospective approach, the...
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| Veröffentlicht in: | European journal of neurology 2021-08, Vol.28 (8), p.2648-2656 |
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| creator | Solini, Anna Rossi, Chiara Santini, Eleonora Giuntini, Martina Raggi, Francesco Parolini, Federico Biancalana, Edoardo Del Prete, Eleonora Bonuccelli, Ubaldo Ceravolo, Roberto |
| description | Background and purpose
Neuroinflammation and probably systemic inflammation, with abnormal α‐synuclein deposition, participate in the development of Parkinson's disease (PD). The P2X7 receptor/NLRP3 inflammasome complex is upregulated in the brain of PD patients. By a prospective approach, the degree of systemic activation of such complex, and its regulatory mechanisms, were explored in treatment‐naïve PD individuals.
Methods
The expression and functional activity of the inflammasome were measured in peripheral blood mononuclear cells of 25 newly diagnosed PD patients and 25 controls at baseline and after 12 months of pharmacological treatment, exploring the intracellular signalling involved and its epigenetic regulation.
Results
De novo PD patients were characterized by a systemic hyper‐expression of the P2X7R/NLRP3 inflammasome platform, probably able to modulate lymphomonocyte α‐synuclein, whose brain deposits represent the main pathogenetic factor of PD. A reduced c‐Jun N‐terminal kinase (JNK) phosphorylation might be the intracellular signalling mediating this effect. miR‐7 and miR‐30, implied in the pathogenesis of PD and in the post‐transcriptional control of α‐synuclein and NLRP3 expression, were also increased in PD. After 1 year of usual anti‐Parkinson treatments, such inflammatory platform was significantly reduced.
Conclusions
Mononuclear cells of newly diagnosed PD subjects display a hyper‐expression of the P2X7R/NLRP3 inflammasome platform that seems to modulate cellular α‐synuclein content and is reduced after PD treatment; an impaired JNK phosphorylation might be the intracellular signalling mediating this effect, undergoing an epigenetic regulation by miR‐7 and miR‐30.
This study, performed in neo‐diagnosed Parkinson's disease patients, shows that a systemic hyper‐expression of the P2X7R/NLRP3 inflammasome platform is able to modulate circulating and lymphomonocyte α‐synuclein. This system is activated in an early phase of the disease, and undergoes a novel epigenetic regulation mediated by miRNAs showing a modulatory function in experimental models of the disease. A putative intracellular signalling responsible for this has also been identified. These results suggest a future use of the systemic evaluation of the P2X7R/NLRP3 complex in an integrated view of an early diagnosis and a correct identification of the main pathophysiological mechanisms of Parkinson's disease.
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| doi_str_mv | 10.1111/ene.14918 |
| format | Article |
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Neuroinflammation and probably systemic inflammation, with abnormal α‐synuclein deposition, participate in the development of Parkinson's disease (PD). The P2X7 receptor/NLRP3 inflammasome complex is upregulated in the brain of PD patients. By a prospective approach, the degree of systemic activation of such complex, and its regulatory mechanisms, were explored in treatment‐naïve PD individuals.
Methods
The expression and functional activity of the inflammasome were measured in peripheral blood mononuclear cells of 25 newly diagnosed PD patients and 25 controls at baseline and after 12 months of pharmacological treatment, exploring the intracellular signalling involved and its epigenetic regulation.
Results
De novo PD patients were characterized by a systemic hyper‐expression of the P2X7R/NLRP3 inflammasome platform, probably able to modulate lymphomonocyte α‐synuclein, whose brain deposits represent the main pathogenetic factor of PD. A reduced c‐Jun N‐terminal kinase (JNK) phosphorylation might be the intracellular signalling mediating this effect. miR‐7 and miR‐30, implied in the pathogenesis of PD and in the post‐transcriptional control of α‐synuclein and NLRP3 expression, were also increased in PD. After 1 year of usual anti‐Parkinson treatments, such inflammatory platform was significantly reduced.
Conclusions
Mononuclear cells of newly diagnosed PD subjects display a hyper‐expression of the P2X7R/NLRP3 inflammasome platform that seems to modulate cellular α‐synuclein content and is reduced after PD treatment; an impaired JNK phosphorylation might be the intracellular signalling mediating this effect, undergoing an epigenetic regulation by miR‐7 and miR‐30.
This study, performed in neo‐diagnosed Parkinson's disease patients, shows that a systemic hyper‐expression of the P2X7R/NLRP3 inflammasome platform is able to modulate circulating and lymphomonocyte α‐synuclein. This system is activated in an early phase of the disease, and undergoes a novel epigenetic regulation mediated by miRNAs showing a modulatory function in experimental models of the disease. A putative intracellular signalling responsible for this has also been identified. These results suggest a future use of the systemic evaluation of the P2X7R/NLRP3 complex in an integrated view of an early diagnosis and a correct identification of the main pathophysiological mechanisms of Parkinson's disease.
</description><identifier>ISSN: 1351-5101</identifier><identifier>EISSN: 1468-1331</identifier><identifier>DOI: 10.1111/ene.14918</identifier><identifier>PMID: 33991356</identifier><language>eng</language><publisher>HOBOKEN: Wiley</publisher><subject>Blood ; Brain ; Brain diseases ; Clinical Neurology ; Drug therapy ; Epigenetics ; Inflammasomes ; Inflammation ; Intracellular ; Intracellular signalling ; JNK protein ; Kinases ; Leukocytes (mononuclear) ; Life Sciences & Biomedicine ; Movement disorders ; Neurodegenerative diseases ; Neurosciences ; Neurosciences & Neurology ; NLRP3 inflammasome ; P2X7 receptor ; Parkinson's disease ; Parkinson's disease/parkinsonism ; Pathogenesis ; Patients ; Peripheral blood mononuclear cells ; Phosphorylation ; Receptors ; Regulatory mechanisms (biology) ; Science & Technology ; Signaling ; Synuclein ; Transcription ; α‐synuclein</subject><ispartof>European journal of neurology, 2021-08, Vol.28 (8), p.2648-2656</ispartof><rights>2021 European Academy of Neurology</rights><rights>This article is protected by copyright. All rights reserved.</rights><rights>Copyright © 2021 European Academy of Neurology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>11</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000656809500001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c3538-7db5f57244652bc1e340afeb78b24579d846db5178c4c463add74cbb078b6c1a3</citedby><cites>FETCH-LOGICAL-c3538-7db5f57244652bc1e340afeb78b24579d846db5178c4c463add74cbb078b6c1a3</cites><orcidid>0000-0002-7855-8253 ; 0009-0007-5792-4393 ; 0000-0002-1410-4375 ; 0000-0002-4690-1387</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fene.14918$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fene.14918$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,39263,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33991356$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Solini, Anna</creatorcontrib><creatorcontrib>Rossi, Chiara</creatorcontrib><creatorcontrib>Santini, Eleonora</creatorcontrib><creatorcontrib>Giuntini, Martina</creatorcontrib><creatorcontrib>Raggi, Francesco</creatorcontrib><creatorcontrib>Parolini, Federico</creatorcontrib><creatorcontrib>Biancalana, Edoardo</creatorcontrib><creatorcontrib>Del Prete, Eleonora</creatorcontrib><creatorcontrib>Bonuccelli, Ubaldo</creatorcontrib><creatorcontrib>Ceravolo, Roberto</creatorcontrib><title>P2X7 receptor/NLRP3 inflammasome complex and α‐synuclein in peripheral blood mononuclear cells: a prospective study in neo‐diagnosed, treatment‐naïve Parkinson’s disease</title><title>European journal of neurology</title><addtitle>EUR J NEUROL</addtitle><addtitle>Eur J Neurol</addtitle><description>Background and purpose
Neuroinflammation and probably systemic inflammation, with abnormal α‐synuclein deposition, participate in the development of Parkinson's disease (PD). The P2X7 receptor/NLRP3 inflammasome complex is upregulated in the brain of PD patients. By a prospective approach, the degree of systemic activation of such complex, and its regulatory mechanisms, were explored in treatment‐naïve PD individuals.
Methods
The expression and functional activity of the inflammasome were measured in peripheral blood mononuclear cells of 25 newly diagnosed PD patients and 25 controls at baseline and after 12 months of pharmacological treatment, exploring the intracellular signalling involved and its epigenetic regulation.
Results
De novo PD patients were characterized by a systemic hyper‐expression of the P2X7R/NLRP3 inflammasome platform, probably able to modulate lymphomonocyte α‐synuclein, whose brain deposits represent the main pathogenetic factor of PD. A reduced c‐Jun N‐terminal kinase (JNK) phosphorylation might be the intracellular signalling mediating this effect. miR‐7 and miR‐30, implied in the pathogenesis of PD and in the post‐transcriptional control of α‐synuclein and NLRP3 expression, were also increased in PD. After 1 year of usual anti‐Parkinson treatments, such inflammatory platform was significantly reduced.
Conclusions
Mononuclear cells of newly diagnosed PD subjects display a hyper‐expression of the P2X7R/NLRP3 inflammasome platform that seems to modulate cellular α‐synuclein content and is reduced after PD treatment; an impaired JNK phosphorylation might be the intracellular signalling mediating this effect, undergoing an epigenetic regulation by miR‐7 and miR‐30.
This study, performed in neo‐diagnosed Parkinson's disease patients, shows that a systemic hyper‐expression of the P2X7R/NLRP3 inflammasome platform is able to modulate circulating and lymphomonocyte α‐synuclein. This system is activated in an early phase of the disease, and undergoes a novel epigenetic regulation mediated by miRNAs showing a modulatory function in experimental models of the disease. A putative intracellular signalling responsible for this has also been identified. These results suggest a future use of the systemic evaluation of the P2X7R/NLRP3 complex in an integrated view of an early diagnosis and a correct identification of the main pathophysiological mechanisms of Parkinson's disease.
</description><subject>Blood</subject><subject>Brain</subject><subject>Brain diseases</subject><subject>Clinical Neurology</subject><subject>Drug therapy</subject><subject>Epigenetics</subject><subject>Inflammasomes</subject><subject>Inflammation</subject><subject>Intracellular</subject><subject>Intracellular signalling</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Leukocytes (mononuclear)</subject><subject>Life Sciences & Biomedicine</subject><subject>Movement disorders</subject><subject>Neurodegenerative diseases</subject><subject>Neurosciences</subject><subject>Neurosciences & Neurology</subject><subject>NLRP3 inflammasome</subject><subject>P2X7 receptor</subject><subject>Parkinson's disease</subject><subject>Parkinson's disease/parkinsonism</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Peripheral blood mononuclear cells</subject><subject>Phosphorylation</subject><subject>Receptors</subject><subject>Regulatory mechanisms (biology)</subject><subject>Science & Technology</subject><subject>Signaling</subject><subject>Synuclein</subject><subject>Transcription</subject><subject>α‐synuclein</subject><issn>1351-5101</issn><issn>1468-1331</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>HGBXW</sourceid><recordid>eNqNkU-KFDEUxgtRnHF04QUk4EbRnk4qSVXKnTTtH2jGRhTcFanklWasSsqkSu3dHMGtpxDxCO49xJzE19PtLATBQMgj7_c9vuTLstuMHjNcc_BwzETF1JXskIlCzRjn7CrWXLKZZJQdZDdSOqWU5mVOr2cHnFcVNovD7Mc6f1OSCAaGMcT5yerlmhPn2073vU6hB2JCP3TwmWhvya_v52df0sZPpgPnkSMDRDe8g6g70nQhWNIHHy76OhIDXZceEU2GGNIAZnQfgaRxsput1EPAadbptz4ksA_JGEGPPfgRr73--Q3htY7vnU_Bn599TcS6BDrBzexaq7sEt_bnUfb6yfLV4tls9eLp88Xj1cxwydWstI1sZZkLUci8MQy4oLqFplRNLmRZWSUKRFipjDCi4NraUpimoQgUhml-lN3bzUX7HyZIY927tH2TRutTqnOZK6ZwV4je_Qs9DVP06A4pyQtBq5IidX9HGfyPFKGth-h6HTc1o_U2yRqTrC-SRPbOfuLU9GAvyT_RIaB2wCdoQpuMA2_gEsOsC1koWkmsKFu4UY8u-EWY_IjSB_8vRXq-p10Hm39brpcny5333x7y0Iw</recordid><startdate>202108</startdate><enddate>202108</enddate><creator>Solini, Anna</creator><creator>Rossi, Chiara</creator><creator>Santini, Eleonora</creator><creator>Giuntini, Martina</creator><creator>Raggi, Francesco</creator><creator>Parolini, Federico</creator><creator>Biancalana, Edoardo</creator><creator>Del Prete, Eleonora</creator><creator>Bonuccelli, Ubaldo</creator><creator>Ceravolo, Roberto</creator><general>Wiley</general><general>John Wiley & Sons, Inc</general><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7855-8253</orcidid><orcidid>https://orcid.org/0009-0007-5792-4393</orcidid><orcidid>https://orcid.org/0000-0002-1410-4375</orcidid><orcidid>https://orcid.org/0000-0002-4690-1387</orcidid></search><sort><creationdate>202108</creationdate><title>P2X7 receptor/NLRP3 inflammasome complex and α‐synuclein in peripheral blood mononuclear cells: a prospective study in neo‐diagnosed, treatment‐naïve Parkinson’s disease</title><author>Solini, Anna ; Rossi, Chiara ; Santini, Eleonora ; Giuntini, Martina ; Raggi, Francesco ; Parolini, Federico ; Biancalana, Edoardo ; Del Prete, Eleonora ; Bonuccelli, Ubaldo ; Ceravolo, Roberto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3538-7db5f57244652bc1e340afeb78b24579d846db5178c4c463add74cbb078b6c1a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Blood</topic><topic>Brain</topic><topic>Brain diseases</topic><topic>Clinical Neurology</topic><topic>Drug therapy</topic><topic>Epigenetics</topic><topic>Inflammasomes</topic><topic>Inflammation</topic><topic>Intracellular</topic><topic>Intracellular signalling</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Leukocytes (mononuclear)</topic><topic>Life Sciences & Biomedicine</topic><topic>Movement disorders</topic><topic>Neurodegenerative diseases</topic><topic>Neurosciences</topic><topic>Neurosciences & Neurology</topic><topic>NLRP3 inflammasome</topic><topic>P2X7 receptor</topic><topic>Parkinson's disease</topic><topic>Parkinson's disease/parkinsonism</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Peripheral blood mononuclear cells</topic><topic>Phosphorylation</topic><topic>Receptors</topic><topic>Regulatory mechanisms (biology)</topic><topic>Science & Technology</topic><topic>Signaling</topic><topic>Synuclein</topic><topic>Transcription</topic><topic>α‐synuclein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Solini, Anna</creatorcontrib><creatorcontrib>Rossi, Chiara</creatorcontrib><creatorcontrib>Santini, Eleonora</creatorcontrib><creatorcontrib>Giuntini, Martina</creatorcontrib><creatorcontrib>Raggi, Francesco</creatorcontrib><creatorcontrib>Parolini, Federico</creatorcontrib><creatorcontrib>Biancalana, Edoardo</creatorcontrib><creatorcontrib>Del Prete, Eleonora</creatorcontrib><creatorcontrib>Bonuccelli, Ubaldo</creatorcontrib><creatorcontrib>Ceravolo, Roberto</creatorcontrib><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 2021</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Solini, Anna</au><au>Rossi, Chiara</au><au>Santini, Eleonora</au><au>Giuntini, Martina</au><au>Raggi, Francesco</au><au>Parolini, Federico</au><au>Biancalana, Edoardo</au><au>Del Prete, Eleonora</au><au>Bonuccelli, Ubaldo</au><au>Ceravolo, Roberto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P2X7 receptor/NLRP3 inflammasome complex and α‐synuclein in peripheral blood mononuclear cells: a prospective study in neo‐diagnosed, treatment‐naïve Parkinson’s disease</atitle><jtitle>European journal of neurology</jtitle><stitle>EUR J NEUROL</stitle><addtitle>Eur J Neurol</addtitle><date>2021-08</date><risdate>2021</risdate><volume>28</volume><issue>8</issue><spage>2648</spage><epage>2656</epage><pages>2648-2656</pages><issn>1351-5101</issn><eissn>1468-1331</eissn><abstract>Background and purpose
Neuroinflammation and probably systemic inflammation, with abnormal α‐synuclein deposition, participate in the development of Parkinson's disease (PD). The P2X7 receptor/NLRP3 inflammasome complex is upregulated in the brain of PD patients. By a prospective approach, the degree of systemic activation of such complex, and its regulatory mechanisms, were explored in treatment‐naïve PD individuals.
Methods
The expression and functional activity of the inflammasome were measured in peripheral blood mononuclear cells of 25 newly diagnosed PD patients and 25 controls at baseline and after 12 months of pharmacological treatment, exploring the intracellular signalling involved and its epigenetic regulation.
Results
De novo PD patients were characterized by a systemic hyper‐expression of the P2X7R/NLRP3 inflammasome platform, probably able to modulate lymphomonocyte α‐synuclein, whose brain deposits represent the main pathogenetic factor of PD. A reduced c‐Jun N‐terminal kinase (JNK) phosphorylation might be the intracellular signalling mediating this effect. miR‐7 and miR‐30, implied in the pathogenesis of PD and in the post‐transcriptional control of α‐synuclein and NLRP3 expression, were also increased in PD. After 1 year of usual anti‐Parkinson treatments, such inflammatory platform was significantly reduced.
Conclusions
Mononuclear cells of newly diagnosed PD subjects display a hyper‐expression of the P2X7R/NLRP3 inflammasome platform that seems to modulate cellular α‐synuclein content and is reduced after PD treatment; an impaired JNK phosphorylation might be the intracellular signalling mediating this effect, undergoing an epigenetic regulation by miR‐7 and miR‐30.
This study, performed in neo‐diagnosed Parkinson's disease patients, shows that a systemic hyper‐expression of the P2X7R/NLRP3 inflammasome platform is able to modulate circulating and lymphomonocyte α‐synuclein. This system is activated in an early phase of the disease, and undergoes a novel epigenetic regulation mediated by miRNAs showing a modulatory function in experimental models of the disease. A putative intracellular signalling responsible for this has also been identified. These results suggest a future use of the systemic evaluation of the P2X7R/NLRP3 complex in an integrated view of an early diagnosis and a correct identification of the main pathophysiological mechanisms of Parkinson's disease.
</abstract><cop>HOBOKEN</cop><pub>Wiley</pub><pmid>33991356</pmid><doi>10.1111/ene.14918</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-7855-8253</orcidid><orcidid>https://orcid.org/0009-0007-5792-4393</orcidid><orcidid>https://orcid.org/0000-0002-1410-4375</orcidid><orcidid>https://orcid.org/0000-0002-4690-1387</orcidid></addata></record> |
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| source | Web of Science - Science Citation Index Expanded - 2021<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; Wiley Online Library All Journals |
| subjects | Blood Brain Brain diseases Clinical Neurology Drug therapy Epigenetics Inflammasomes Inflammation Intracellular Intracellular signalling JNK protein Kinases Leukocytes (mononuclear) Life Sciences & Biomedicine Movement disorders Neurodegenerative diseases Neurosciences Neurosciences & Neurology NLRP3 inflammasome P2X7 receptor Parkinson's disease Parkinson's disease/parkinsonism Pathogenesis Patients Peripheral blood mononuclear cells Phosphorylation Receptors Regulatory mechanisms (biology) Science & Technology Signaling Synuclein Transcription α‐synuclein |
| title | P2X7 receptor/NLRP3 inflammasome complex and α‐synuclein in peripheral blood mononuclear cells: a prospective study in neo‐diagnosed, treatment‐naïve Parkinson’s disease |
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