Inflammation in multiple system atrophy
Open accessAbstract
Misfolding protein aggregation inside or outside cells is the major pathological hallmark of several neurodegenerative diseases. Among proteinopathies are neurodegenerative diseases with atypical Parkinsonism and an accumulation of insoluble fibrillary alpha-synuclein (synucleinopathies) or hyperphosphorylated tau protein fragments (tauopathies). As there are no therapies available to slow or halt the progression of these disea ses, targeting the inflammatory process is a promising approach. The inflammatory biomarkers could also help in the differential diagnosis of Parkinsonian syndromes. Here, we review inflammation’s role in multiple systems atrophy pathogenesis, diagnosis, and treatment.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Excessive or dysregulated inflammation is a major driver of tissue damage and the pathogenesis of numerous diseases, including stroke, Parkinson's disease, atherosclerosis, and cancer.
“Excessive or dysregulated inflammation is a major driver of tissue damage and the pathogenesis of numerous diseases, including stroke, Parkinson’s disease, atherosclerosis, and cancer [9,30,31,32,33].”
From Picroside II as a Potential Anti-Inflammatory Agent (2026) · cites this paper as [33]
The sections “Immune response in MSA brain parenchyma” and “Conclusion and remarks” (page numbers unavailable) link inflammation to cell injury and propose a role in neurodegenerative disease. The paper says it is uncertain whether inflammation is a primary driver of MSA, and the passages do not support extending that claim to stroke, atherosclerosis, or cancer. (LLM, conf=0.87)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 104 · Cited by 45
Research works printed but not linked: 95
- [1]Wenning GK Stankovic I Vignatelli L Fanciulli A Calandra-Buonaura G Seppi K. The movement disorder society criteria for the diagnosis of multiple system atrophy. Mov Disord (2022) 37(6): 1131–48. doi: 10.1002/mds.29005 PMC9321158 35445419 · DOI
- [2]Monzio Compagnoni G Di Fonzo A. Understanding the pathogenesis of multiple system atrophy: state of the art and future perspectives. Acta Neuropathol Commun (2019) 7(1): 113. doi: 10.1186/s40478-019-0730-6 31300049 PMC6624923 · DOI
- [4]Hoffmann A Ettle B Battis K Reiprich S Schlachetzki JCM Masliah E. Oligodendroglial α-synucleinopathy-driven neuroinflammation in multiple system atrophy. Brain Pathol (2019) 29(3): 380–96. doi: 10.1111/bpa.12678 PMC6850330 30444295 · DOI · Paper page
- [5]Bourdenx M Koulakiotis NS Sanoudou D Bezard E Dehay B Tsarbopoulos A. Protein aggregation and neurodegeneration in prototypical neurodegenerative diseases: examples of amyloidopathies, tauopathies and synucleinopathies. Prog Neurobiol (2017) 155: 171–93. doi: 10.1016/j.pneurobio.2015.07.003 26209472 · DOI
- [6]Harms AS Kordower JH Sette A Lindestam Arlehamn CS Sulzer D Mach RH. Inflammation in experimental models of α-synucleinopathies. Mov Disord (2021) 36(1): 37– 49. doi: 10.1002/mds.28264 33009855 PMC8115204 · DOI
- [8]Refolo V Stefanova N. Neuroinflammation and glial phenotypic changes in alpha-synucleinopathies. Front Cell Neurosci (2019) 13: 263. doi: 10.3389/fncel.2019.00263 31263402 PMC6585624 · DOI
- [9]Rydbirk R Elfving B Andersen MD Langbøl MA Folke J Winge K. Cytokine profiling in the prefrontal cortex of parkinson's disease and multiple system atrophy patients. Neurobiol Dis (2017) 106: 269–78. doi: 10.1016/j.nbd.2017.07.014 28732710 · DOI
- [10]Sidoroff V Bower P Stefanova N Fanciulli A Stankovic I Poewe W. Disease-modifying therapies for multiple system atrophy: where are we in 2022? J Parkinsons Dis (2022) 12(5): 1369–87. doi: 10.3233/JPD-223183 PMC9398078 35491799 · DOI
- [11]Tseng FS Foo JQX Mai AS Tan EK. The genetic basis of multiple system atrophy. J Transl Med (2023) 21(1): 104. doi: 10.1186/s12967-023-03905-1 36765380 PMC9912584 · DOI
- [12]Chen L Deng H Cui H Fang J Zuo Z Deng J. Inflammatory responses and inflammation-associated diseases in organs. Oncotarget. (2017) 9(6): 7204–18. doi: 10.18632/oncotarget.23208 PMC5805548 29467962 · DOI
- [13]Schwarz J Weis S Kraft E Tatsch K Bandmann O Mehraein P. Signal changes on MRI and increases in reactive microgliosis, astrogliosis, and iron in the putamen of two patients with multiple system atrophy. J Neurol Neurosurg Psychiatry (1996) 60(1): 98– 101. doi: 10.1136/jnnp.60.1.98 8558163 PMC486200 · DOI
- [14]Gerhard A Banati RB Goerres GB Cagnin A Myers R Gunn RN. [11C](R)-PK11195 PET imaging of microglial activation in multiple system atrophy. Neurology. (2003) 61(5): 686–9. doi: 10.1212/01.wnl.0000078192.95645.e6 12963764 · DOI
- [15]Ishizawa K Komori T Sasaki S Arai N Mizutani T Hirose T. Microglial activation parallels system degeneration in multiple system atrophy. J Neuropathol Exp Neurol (2004) 63(1): 43– 52. doi: 10.1093/jnen/63.1.43 14748560 · DOI · Paper page
- [17]Kiely AP Murray CE Foti SC Benson BC Courtney R Strand C. Immunohistochemical and molecular investigations show alteration in the inflammatory profile of multiple system atrophy brain. J Neuropathol Exp Neurol (2018) 77(7): 598– 607. doi: 10.1093/jnen/nly035 29850876 PMC6005028 · DOI
- [19]Williams GP Marmion DJ Schonhoff AM Jurkuvenaite A Won WJ Standaert DG. T Cell infiltration in both human multiple system atrophy and a novel mouse model of the disease. Acta Neuropathol (2020) 139(5): 855–74. doi: 10.1007/s00401-020-02126-w PMC7181566 31993745 · DOI · Paper page
- [20]Inoue Y Ayaki T Ishimoto T Yamakado H Maki T Matsuzawa S. The stimulator of interferon genes (STING) pathway is upregulated in striatal astrocytes of patients with multiple system atrophy. Neurosci Lett (2021) 757: 135972. doi: 10.1016/j.neulet.2021.135972 34033888 · DOI
- [21]Langerveld AJ Mihalko D DeLong C Walburn J Ide CF. Gene expression changes in postmortem tissue from the rostral pons of multiple system atrophy patients. Mov Disord (2007) 22(6): 766–77. doi: 10.1002/mds.21259 17290454 · DOI
- [22]Cao B Chen X Zhang L Wei Q Liu H Feng W. Elevated percentage of CD3+ T-cells and CD4+/CD8+ ratios in multiple system atrophy patients. Front Neurol (2020) 11: 658. doi: 10.3389/fneur.2020.00658 32733370 PMC7358310 · DOI
- [23]Bettencourt C Piras IS Foti SC Talboom J Miki Y Lashley T. Epigenomics and transcriptomics analyses of multiple system atrophy brain tissue supports a role for inflammatory processes in disease pathogenesis. Acta Neuropathol Commun (2020) 8(1): 71. doi: 10.1186/s40478-020-00946-1 32410669 PMC7227350 · DOI
- [24]Schafferer S Khurana R Refolo V Venezia S Sturm E Piatti P. Changes in the miRNA-mRNA regulatory network precede motor symptoms in a mouse model of multiple system atrophy: clinical implications. PloS One (2016) 11(3): e0150705. doi: 10.1371/journal.pone.0150705 26962858 PMC4786272 · DOI
- [25]Combarros O Infante J Llorca J Berciano J. Interleukin-1A (-889) genetic polymorphism increases the risk of multiple system atrophy. Mov Disord (2003) 18(11): 1385–6. doi: 10.1002/mds.10540 14639688 · DOI
- [26]Infante J Llorca J Berciano J Combarros O. Interleukin-8, intercellular adhesion molecule-1 and tumour necrosis factor-alpha gene polymorphisms and the risk for multiple system atrophy. J Neurol Sci (2005) 228(1): 11–3. doi: 10.1016/j.jns.2004.09.023 15607204 · DOI
- [27]Zhou X Wang C Chen Z Peng Y Peng H Hou X. Association of TNF-α rs1799964 and IL-1β rs16944 polymorphisms with multiple system atrophy in Chinese han population. Int J Neurosci (2018) 128(8): 761–4. doi: 10.1080/00207454.2017.1418346 29251119 · DOI
- [28]Cao B Chen Y Zhou Q Zhang L Ou R Wei Q. Functional variant rs3135500 in NOD2 increases the risk of multiple system atrophy in a Chinese population. Front Aging Neurosci (2018) 10: 150. doi: 10.3389/fnagi.2018.00150 29881342 PMC5976778 · DOI
- [29]Ogaki K Heckman MG Koga S Martens YA Labbé C Lorenzo-Betancor O. Association study between multiple system atrophy and TREM2 p. R47H Neurol Genet (2018) 4(4): e257. doi: 10.1212/NXG.0000000000000257 30109269 PMC6089688 · DOI
- [30]Furiya Y Hirano M Kurumatani N Nakamuro T Matsumura R Futamura N. Alpha-1-antichymotrypsin gene polymorphism and susceptibility to multiple system atrophy (MSA). Brain Res Mol Brain Res (2005) 138(2): 178–81. doi: 10.1016/j.molbrainres.2005.04.011 15907346 · DOI
- [31]Ubhi K Rockenstein E Kragh C Inglis C Spencer B Michael S. Widespread microRNA dysregulation in multiple system atrophy - disease-related alteration in miR-96. Eur J Neurosci (2014) 39(6): 1026–41. doi: 10.1111/ejn.12444 PMC4052839 24304186 · DOI
- [32]Kim T Valera E Desplats P. Alterations in striatal microRNA-mRNA networks contribute to neuroinflammation in multiple system atrophy. Mol Neurobiol (2019) 56(10): 7003–21. doi: 10.1007/s12035-019-1577-3 PMC7216788 30968343 · DOI
- [33]Vallelunga A Ragusa M Di Mauro S Iannitti T Pilleri M Biundo R. Identification of circulating microRNAs for the differential diagnosis of parkinson's disease and multiple system atrophy. Front Cell Neurosci (2014) 8: 156. doi: 10.3389/fncel.2014.00156 24959119 PMC4051126 · DOI
- [34]Kume K Iwama H Deguchi K Ikeda K Takata T Kokudo Y. Serum microRNA expression profiling in patients with multiple system atrophy. Mol Med Rep (2018) 17(1): 852–60. doi: 10.3892/mmr.2017.7995 PMC5780164 29115515 · DOI
- [35]Uwatoko H Hama Y Iwata IT Shirai S Matsushima M Yabe I. Identification of plasma microRNA expression changes in multiple system atrophy and parkinson's disease. Mol Brain (2019) 12(1): 49. doi: 10.1186/s13041-019-0471-2 31088501 PMC6518614 · DOI
- [36]Marques TM Kuiperij HB Bruinsma IB van Rumund A Aerts MB Esselink RAJ. MicroRNAs in cerebrospinal fluid as potential biomarkers for parkinson's disease and multiple system atrophy. Mol Neurobiol (2017) 54(10): 7736–45. doi: 10.1007/s12035-016-0253-0 PMC5684261 27844283 · DOI · Paper page
- [37]Brudek T Winge K Agander TK Pakkenberg B. Screening of toll-like receptors expression in multiple system atrophy brains. Neurochem Res (2013) 38(6): 1252–9. doi: 10.1007/s11064-013-1020-5 23525968 · DOI · Paper page
- [38]De Luca CMG Consonni A Cazzaniga FA Bistaffa E Bufano G Quitarrini G. The alpha-synuclein RT-QuIC products generated by the olfactory mucosa of patients with parkinson's disease and multiple system atrophy induce inflammatory responses in SH-SY5Y cells. Cells. (2021) 11(1): 87. doi: 10.3390/cells11010087 35011649 PMC8750063 · DOI
- [39]Dutta D Jana M Majumder M Mondal S Roy A Pahan K. Selective targeting of the TLR2/MyD88/NF-κB pathway reduces α-synuclein spreading in vitro and in vivo. Nat Commun (2021) 12(1): 5382. doi: 10.1038/s41467-021-25767-1 34508096 PMC8433339 · DOI · Paper page
- [41]Kaufman E Hall S Surova Y Widner H Hansson O Lindqvist D. Proinflammatory cytokines are elevated in serum of patients with multiple system atrophy. PloS One (2013) 8(4): e62354. doi: 10.1371/journal.pone.0062354 23626805 PMC3633844 · DOI
- [42]Kim R Kim HJ Kim A Jang M Kim A Kim Y. Does peripheral inflammation contribute to multiple system atrophy? Parkinsonism Relat Disord (2019) 64: 340–1. doi: 10.1016/j.parkreldis.2019.03.020 30940429 · DOI
- [43]Csencsits-Smith K Suescun J Li K Luo S Bick DL Schiess M. Serum lymphocyte-associated cytokine concentrations change more rapidly over time in multiple system atrophy compared to Parkinson disease. Neuroimmunomodulation. (2016) 23(5-6): 301–8. doi: 10.1159/000460297 PMC5491391 28395279 · DOI
- [44]Compta Y Dias SP Giraldo DM Pérez-Soriano A Muñoz E Saura J. Cerebrospinal fluid cytokines in multiple system atrophy: a cross-sectional Catalan MSA registry study. Parkinsonism Relat Disord (2019) 65: 3– 12. doi: 10.1016/j.parkreldis.2019.05.040 31178335 · DOI
- [45]Starhof C Winge K Heegaard NHH Skogstrand K Friis S Hejl A. Cerebrospinal fluid pro-inflammatory cytokines differentiate parkinsonian syndromes. J Neuroinflammation (2018) 15(1): 305. doi: 10.1186/s12974-018-1339-6 30390673 PMC6215346 · DOI
- [46]Hall S Janelidze S Surova Y Widner H Zetterberg H Hansson O. Cerebrospinal fluid concentrations of inflammatory markers in parkinson's disease and atypical parkinsonian disorders. Sci Rep (2018) 8(1): 13276. doi: 10.1038/s41598-018-31517-z 30185816 PMC6125576 · DOI
- [47]Ayton S Hall S Janelidze S Kalinowski P Palmqvist S Belaidi AA. The neuroinflammatory acute phase response in parkinsonian-related disorders. Mov Disord (2022) 37(5): 993– 1003. doi: 10.1002/mds.28958 35137973 · DOI
- [48]Folke J Rydbirk R Løkkegaard A Hejl AM Winge K Starhof C. Cerebrospinal fluid and plasma distribution of anti-α-synuclein IgMs and IgGs in multiple system atrophy and parkinson's disease. Parkinsonism Relat Disord (2021) 87: 98– 104. doi: 10.1016/j.parkreldis.2021.05.001 34020303 · DOI
- [49]Jiang L Zhong Z Huang J Bian H Huang W. Monocytohigh-density lipoprotein ratio has a high predictive value for the diagnosis of multiple system atrophy and the differentiation from parkinson's disease. Front Aging Neurosci (2022) 14: 1035437. doi: 10.3389/fnagi.2022.1035437 36313023 PMC9607904 · DOI
- [50]Wan L Zhou X Wang C Chen Z Peng H Hou X. Alterations of the gut microbiota in multiple system atrophy patients. Front Neurosci (2019) 13: 1102. doi: 10.3389/fnins.2019.01102 31680836 PMC6813281 · DOI
- [51]Engen PA Dodiya HB Naqib A Forsyth CB Green SJ Voigt RM. The potential role of gut-derived inflammation in multiple system atrophy. J Parkinsons Dis (2017) 7(2): 331–46. doi: 10.3233/JPD-160991 28234259 · DOI
- [52]Hor JW Lim SY Khor ES Chong KK Song SL Ibrahim NM. Fecal calprotectin in parkinson's disease and multiple system atrophy. J Mov Disord (2022) 15(2): 106–14. doi: 10.14802/jmd.21085 PMC9171316 34937162 · DOI
- [53]Tan AH Chong CW Song SL Teh CSJ Yap IKS Loke MF. Altered gut microbiome and metabolome in patients with multiple system atrophy. Mov Disord (2018) 33(1): 174–6. doi: 10.1002/mds.27203 29083071 · DOI
- [54]Santaella A Kuiperij HB van Rumund A Esselink RAJ van Gool AJ Bloem BR. Inflammation biomarker discovery in parkinson's disease and atypical parkinsonisms. BMC Neurol (2020) 20(1): 26. doi: 10.1186/s12883-020-1608-8 31952511 PMC6967088 · DOI
- [55]Vallelunga A Iannitti T Dati G Capece S Maugeri M Tocci E. Serum miR-30c-5p is a potential biomarker for multiple system atrophy. Mol Biol Rep (2019) 46(2): 1661–6. doi: 10.1007/s11033-019-04614-z 30810945 · DOI
- [56]Shin JH Kim HJ Lee CY Chang HJ Woo KA Jeon B. Laboratory prognostic factors for the long-term survival of multiple system atrophy. NPJ Parkinsons Dis (2022) 8(1): 141. doi: 10.1038/s41531-022-00413-9 36302764 PMC9613998 · DOI
- [57]Battis K Florio JB Mante M Lana A Naumann I Gauer C. CSF1R-mediated myeloid cell depletion prolongs lifespan but aggravates distinct motor symptoms in a model of multiple system atrophy. J Neurosci (2022) 42(40): 7673–88. doi: 10.1523/JNEUROSCI.0417-22.2022 PMC9546481 36333098 · DOI
- [58]Vidal-Martinez G Segura-Ulate I Yang B Diaz-Pacheco V Barragan JA De-Leon Esquivel J. FTY720-mitoxy reduces synucleinopathy and neuroinflammation, restores behavior and mitochondria function, and increases GDNF expression in multiple system atrophy mouse models. Exp Neurol (2020) 325: 113120. doi: 10.1016/j.expneurol.2019.113120 31751571 PMC8021391 · DOI
- [59]Stefanova N Georgievska B Eriksson H Poewe W Wenning GK. Myeloperoxidase inhibition ameliorates multiple system atrophy-like degeneration in a transgenic mouse model. Neurotox Res (2012) 21(4): 393– 404. doi: 10.1007/s12640-011-9294-3 22161470 · DOI · Paper page
- [60]Kaindlstorfer C Sommer P Georgievska B Mather RJ Kugler AR Poewe W. Failure of neuroprotection despite microglial suppression by delayed-start myeloperoxidase inhibition in a model of advanced multiple system atrophy: clinical implications. Neurotox Res (2015) 28(3): 185–94. doi: 10.1007/s12640-015-9547-7 PMC4556742 26194617 · DOI
- [61]Stefanova N Reindl M Neumann M Kahle PJ Poewe W Wenning GK. Microglial activation mediates neurodegeneration related to oligodendroglial alpha-synucleinopathy: implications for multiple system atrophy. Mov Disord (2007) 22(15): 2196–203. doi: 10.1002/mds.21671 17853477 · DOI
- [62]Starhof C Hejl AM Korbo L Winge K Friis S. Risk of multiple system atrophy and the use of anti-inflammatory drugs: a Danish register-based case-control study. Neuroepidemiology. (2020) 54(1): 58– 63. doi: 10.1159/000503003 31661696 · DOI
- [63]Zhang F Zhou H Wilson BC Shi JS Hong JS Gao HM. Fluoxetine protects neurons against microglial activation-mediated neurotoxicity. Parkinsonism Relat Disord (2012) 18 Suppl 1(0 1): S213–7. doi: 10.1016/S1353-8020(11)70066-9 PMC3608679 22166439 · DOI · Paper page
- [64]Grossauer A Sidoroff V Heim B Seppi K. Symptomatic care in multiple system atrophy: state of the art. Cerebellum. (2022) 22(3): 433– 446. doi: 10.1007/s12311-022-01411-6 35581488 PMC10125958 · DOI
- [65]Przewodowska D Marzec W Madetko N. Novel therapies for parkinsonian syndromes-recent progress and future perspectives. Front Mol Neurosci (2021) 14: 720220. doi: 10.3389/fnmol.2021.720220 34512258 PMC8427499 · DOI
- [66]Dodel R Spottke A Gerhard A Reuss A Reinecker S Schimke N. Minocycline 1-year therapy in multiple-system-atrophy: effect on clinical symptoms and [(11)C] (R)-PK11195 PET (MEMSA-trial). Mov Disord (2010) 25(1): 97– 107. doi: 10.1002/mds.22732 20014118 · DOI
- [67]Pezzoli G Tesei S Canesi M Sacilotto G Vittorio M Mizuno Y. The effect of repeated administrations of granulocyte colony stimulating factor for blood stem cells mobilization in patients with progressive supranuclear palsy, corticobasal degeneration and multiple system atrophy. Clin Neurol Neurosurg (2010) 112(1): 65–7. doi: 10.1016/j.clineuro.2009.08.023 19765889 · DOI
- [68]Novak P Williams A Ravin P Zurkiya O Abduljalil A Novak V. Treatment of multiple system atrophy using intravenous immunoglobulin. BMC Neurol (2012) 12: 131. doi: 10.1186/1471-2377-12-131 23116538 PMC3551813 · DOI
- [69]Heras-Garvin A Stefanova N. MSA: from basic mechanisms to experimental therapeutics. Parkinsonism Relat Disord (2020) 73: 94– 104. doi: 10.1016/j.parkreldis.2020.01.010 32005598 · DOI
- [70]Stanley ER Chitu V. CSF-1 receptor signaling in myeloid cells. Cold Spring Harb Perspect Biol (2014) 6(6): a021857. doi: 10.1101/cshperspect.a021857 24890514 PMC4031967 · DOI · Paper page
- [71]Valera E Spencer B Fields JA Trinh I Adame A Mante M. Combination of alpha-synuclein immunotherapy with anti-inflammatory treatment in a transgenic mouse model of multiple system atrophy. Acta Neuropathol Commun (2017) 5(1): 2. doi: 10.1186/s40478-016-0409-1 28057080 PMC5217191 · DOI
- [72]Papadopoulos V Baraldi M Guilarte TR Knudsen TB Lacapère JJ Lindemann P. Translocator protein (18 kDa): new nomenclature for the peripheral-type benzodiazepine receptor based on its structure and molecular function. Trends Pharmacol Sci (2006) 27: 402–9. doi: 10.1016/j.tips.2006.06.005 16822554 · DOI
- [73]Casellas P Galiegue S Basile AS. Peripheral benzodiazepine receptors and mitochondrial function. Neurochem Int (2002) 40: 475–86. doi: 10.1016/s0197-0186(01)00118-8 11850104 · DOI
- [74]Perry VH Nicoll JA. Holmes C microglia in neurodegenerative disease. Nat Rev Neurol (2010) 6: 193– 201. doi: 10.1038/nrneurol.2010.17 20234358 · DOI · Paper page
- [75]Singh P Adhikari A Singh D Gond Ch Tiwari AK. The 18-kDa translocator protein PET tracers as a diagnostic marker for neuroinflammation: development and current standing. ACS Omega (2022) 18: 14412–29. doi: 10.1021/acsomega.2c00588 PMC9089361 35557664 · DOI
- [76]Grimm A Lejri I Hallé F Schmitt M Götz J Bihel F. Mitochondria modulatory effects of new TSPO ligands in a cellular model of tauopathies. Neuroendocrinol. (2020) 32(1): e12796. doi: 10.1111/jne.12796 PMC7003898 31536662 · DOI
- [77]Taliani S Pugliesi I Da Settimo F. Structural requirements to obtain highly potent and selective 18 kDa translocator protein (TSPO) ligands. Curr Top Med Chem (2011) 11(7): 860–86. doi: 10.2174/156802611795165142 21291396 · DOI
- [78]Wadsworth H Jones PA Chau WF Durrant C Fouladi N Passmore J. [¹⁸F]GE-180: a novel fluorine-18 labelled PET tracer for imaging translocator protein 18 kDa (TSPO). Bioorg Med Chem Lett (2012) 22(3): 1308–13. doi: 10.1016/j.bmcl.2011.12.084 22244939 · DOI
- [79]Boutin H Murray K Pradillo J Maroy R Smigova A Gerhard A. 18F-GE-180: a novel TSPO radiotracer compared to 11C-R-PK11195 in a preclinical model of stroke. Eur J Nucl Med Mol Imaging (2015) 42(3): 503–11. doi: 10.1007/s00259-014-2939-8 25351507 · DOI
- [80]Chau WF Black AM Clarke A Durrant C Gausemel I Khan I. Exploration of the impact of stereochemistry on the identification of the novel translocator protein PET imaging agent [(18)F]GE-180. Nucl Med Biol (2015) 42(9): 711–9. doi: 10.1016/j.nucmedbio.2015.05.004 26072270 · DOI
- [81]Fan Z Calsolaro V Atkinson RA Femminella GD Waldman A Buckley C. Flutriciclamide (18F-GE180) PET: first-in-Human PET study of novel third-generation In vivo marker of human translocator protein. J Nucl Med (2016) 57(11): 1753–9. doi: 10.2967/jnumed.115.169078 27261523 · DOI
- [82]Sokias R Werry EL Alison Cheng HW Lloyd JH Sohler G Danon JJ. Tricyclic heterocycles display diverse sensitivity to the A147T TSPO polymorphism. Eur J Med Chem (2020) 207: 112725. doi: 10.1016/j.ejmech.2020.112725 32920427 · DOI
- [84]Shin J Kim HJ Jeon B. Immunotherapy targeting neurodegenerative proteinopathies: α-synucleinopathies and tauopathies. J Mov Disord (2020) 13(1): 11–9. doi: 10.14802/jmd.19057 PMC6987523 31847513 · DOI
- [85]van Olst L Verhaege D Franssen M Kamermans A Roucourt B Carmans S. Microglial activation arises after aggregation of phosphorylated-tau in a neuron-specific P301S tauopathy mouse model. Neurobiol Aging (2020) 89: 89– 98. doi: 10.1016/j.neurobiolaging.2020.01.003 32008854 · DOI
- [87]Ochoa E Ramirez P Gonzalez E De Mange J Ray WJ Bieniek KF. Pathogenic tau-induced transposable element-derived dsRNA drives neuroinflammation. Sci Adv (2023) 9(1): eabq5423. doi: 10.1126/sciadv.abq5423 36608133 PMC9821943 · DOI · Paper page
- [88]Rexach JE Polioudakis D Yin A Swarup V Chang TS Nguyen T. Tau pathology drives dementia risk-associated gene networks toward chronic inflammatory states and immunosuppression. Cell Rep (2020) 33(7): 108398. doi: 10.1016/j.celrep.2020.108398 33207193 PMC7842189 · DOI · Paper page
- [89]Alausa A Ogundepo S Olaleke B Adeyemi R Olatinwo M Ismail A. Chinese Nutraceuticals and physical activity; their role in neurodegenerative tauopathies. Chin Med (2021) 16(1): 1. doi: 10.1186/s13020-020-00418-7 33407732 PMC7789572 · DOI
- [90]Bäckström D Granåsen G Mo SJ Riklund K Trupp M Zetterberg H. Prediction and early biomarkers of cognitive decline in Parkinson disease and atypical parkinsonism: a population-based study. Brain Commun (2022) 4(2): fcac040. doi: 10.1093/braincomms/fcac040 35350553 PMC8947320 · DOI
- [91]Dunalska A Pikul J Schok K Wiejak KA Alster P. The significance of vascular pathogenesis in the examination of corticobasal syndrome. Front Aging Neurosci (2021) 13: 668614. doi: 10.3389/fnagi.2021.668614 34017244 PMC8129188 · DOI
- [93]Alster P Madetko N Friedman A. Neutrophil-to-lymphocyte ratio (NLR) at boundaries of progressive supranuclear palsy syndrome (PSPS) and corticobasal syndrome (CBS). Neurol Neurochir Pol (2021) 55(1): 97– 101. doi: 10.5603/PJNNS.a2020.0097 33315235 · DOI
- [94]Inci I Kusbeci OY Eskut N. The neutrophil-to-lymphocyte ratio as a marker of peripheral inflammation in progressive supranuclear palsy: a retrospective study. Neurol Sci (2020) 41(5): 1233–7. doi: 10.1007/s10072-019-04208-4 31901125 · DOI
- [95]Madetko-Alster N Alster P Bartošová T Klempíř J Migda B Przewodowska D. Could hyperlipidemia be a risk factor for corticobasal syndrome? - a pilot study. Neurol Neurochir Pol (2022) 57(2): 117– 182. doi: 10.5603/PJNNS.a2022.0078 36519660 · DOI
- [97]Rissardo JP Caprara AL F. Parkinsonism-plus syndrome secondary to neurosyphilis: case report and literature review. Neurol India (2022) 70(4): 1635–8. doi: 10.4103/0028-3886.355119 36076672 · DOI
- [98]Benito-León J Alvarez-Linera J Louis ED. Neurosyphilis masquerading as corticobasal degeneration. Mov Disord (2004) 19: 1367–70. doi: 10.1002/mds.20221 15389980 · DOI
- [99]Murialdo A Marchese R Abbruzzese G Tabaton M Michelozzi G Schiavoni S. Neurosyphilis presenting as progressive supranuclear palsy. Mov Disord (2000) 15: 730–1. doi: 10.1002/1531-8257(200007)15:4<730::aid-mds1020>3.0.co;2-o 10928586 · DOI · Paper page
- [100]Jang W Kim JS Ahn JY Kim HT. Reversible progressive supranuclear palsy-like phenotype as an initial manifestation of HIV infection. Neurol Sci (2012) 33(5): 1169–71. doi: 10.1007/s10072-011-0875-y 22160793 · DOI
- [101]Jabbari E Zetterberg H Morris HR. Tracking and predicting disease progression in progressive supranuclear palsy: CSF and blood biomarkers. J Neurol Neurosurg Psychiatry (2017) 88(10): 883–8. doi: 10.1136/jnnp-2017-315857 28600442 · DOI
- [102]Tian H Wang J Feng R Zhang R Liu H Qin C. Efficacy of faecal microbiota transplantation in patients with progressive supranuclear palsy-richardson's syndrome: a phase 2, single centre, randomised clinical trial. EClinicalMedicine. (2023) 58: 101888. doi: 10.1016/j.eclinm.2023.101888 36969340 PMC10034412 · DOI
- [103]Marras C Cunningham CR Hou J Proudfoot J Standaert DG Juncos J. Anti-inflammatory drug use and progressive supranuclear palsy. Parkinsonism Relat Disord (2018) 48: 89– 92. doi: 10.1016/j.parkreldis.2017.11.346 29307562 · DOI
- [104]Litvan I Agid Y Calne D Campbell G Dubois B Duvoisin RC. Clinical research criteria for the diagnosis of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome): report of the NINDS-SPSP international workshop. Neurology. (1996) 47(1): 1– 9. doi: 10.1212/wnl.47.1.1 8710059 · DOI · Paper page
- Authors
- Leńska-Mieciek, M., Madetko-Alster, N., Alster, P., Królicki, L., Fiszer, U., & Koziorowski, D.
- Affiliations
- Medical University of Warsaw (PL)
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2023-06-22
- Volume
- 14
- Pages
- 1214677-1214677
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC10327640
- OpenAlex
- W4381929894
- Cited by
- 45
- References
- 104
- Citations by year
- 2026: 14 · 2025: 18 · 2024: 13
- FWCI
- 1.83
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- multiple system atrophy, neuroinflammation, alpha-synuclein, synucleinopathies, tauopathy, protein misfolding, protein aggregation, neurodegenerative diseases, inflammatory markers, differential diagnosis of parkinsonism, atypical parkinsonism
- MeSH terms
- Synucleinopathies, Humans, Inflammation, Multiple System Atrophy, Parkinsonian Disorders, Tauopathies
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review