Cited by 355Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration MechanismsNuclear Receptors and Signaling

The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.

Neuroinflammation and α-Synuclein Dysfunction Potentiate Each Other, Driving Chronic Progression of Neurodegeneration in a Mouse Model of Parkinson’s Disease

Open access

Gao, Hui-Ming, Zhang, Feng, Zhou, Hui, Kam, Wayneho, Wilson, Belinda, Hong, Jau-Shyong·2011·Environmental Health Perspectives

DOI 10.1289/ehp.1003013PMC PMC3114815

Open this paper in CoChat — free account Open PDF

Abstract

Background: Mechanisms whereby gene–environment interactions mediate chronic, progressive neurodegenerative processes in Parkinson’s disease (PD)—the second most common neurodegenerative disease—remain elusive. Objective: We created a two-hit [neuroinflammation and mutant α-synuclein (α-syn) overexpression] animal model to investigate mechanisms through which mutant α-syn and inflammation work in concert to mediate chronic PD neurodegeneration. Methods: We used an intraperitoneal injection of the inflammogen lipopolysaccharide (LPS; 3 × 106 EU/kg) to initiate systemic and brain inflammation in wild-type (WT) mice and transgenic (Tg) mice overexpressing human A53T mutant α-syn. We then evaluated nigral dopaminergic neurodegeneration, α-syn pathology, and neuroinflammation. Results: After LPS injection, both WT and Tg mice initially displayed indistinguishable acute neuroinflammation; however, only Tg mice developed persistent neuroinflammation, chronic progressive degeneration of the nigrostriatal dopamine pathway, accumulation of aggregated, nitrated α-syn, and formation of Lewy body-like inclusions in nigral neurons. Further mechanistic studies indicated that 4-week infusion of two inhibitors of inducible nitric oxide synthase and NADPH oxidase, major free radical–generating enzymes in activated microglia, blocked nigral α-syn pathology and neurodegeneration in LPS-injected Tg mice. Conclusions: Microglia-derived oxidative stress bridged neuroinflammation and α-syn pathogenic alteration in mediating chronic PD progression. Our two-hit animal model involving both a genetic lesion and an environmental trigger reproduced key features of PD and demonstrated synergistic effects of genetic predisposition and environmental exposures in the development of PD. The chronic progressive nature of dopaminergic neurodegeneration, which is absent in most existing PD models, makes this new model invaluable for the study of mechanisms of PD progression.

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

Crossref · 10.1289/ehp.1003013

Cites

46 of 46 references verified0 citation errors · 0 not checkable

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?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

α-Synuclein in Lewy bodies
Spillantini, M. G., Schmidt, M. L., Lee, V. M.-Y., Trojanowski, J. Q., Jakes, R., & Goedert, M. (1997) · Nature · doi:10.1038/42166 · Cited by 8,382 · cited 1×
“The low rate of concordance for PD in mono zygotic and dizygotic twins (Marttila et al. 1988; Tanner 2003) strongly suggests the involvement of environmental factors in PD. Epidemiologic and case–control studies have implicated rural living, well water consumption, and pesticide exposure as…”
Background
Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
Polymeropoulos, M. H., Lavedan, C., Leroy, E., Ide, S. E., Dehejia, A., Dutra, A., Pike, B., Root, H., Rubenstein, J., Boyer, R., et al. (1997) · Science · doi:10.1126/science.276.5321.2045 · Cited by 8,240
α-Synuclein Locus Triplication Causes Parkinson's Disease
Singleton, A. B., Farrer, M., Johnson, J., Singleton, A., Hague, S., Kachergus, J., Hulihan, M., Peuralinna, T., Dutra, A., Nussbaum, R., et al. (2003) · Science · doi:10.1126/science.1090278 · Cited by 4,383 · cited 1×
“Furthermore, α-syn aggregates are the primary component of Lewy bodies in both familial and sporadic PD (Spillantini et al. 1997).”
Background
Microglia-mediated neurotoxicity: uncovering the molecular mechanisms
Block, M. L., Zecca, L., & Hong, J.-S. (2007) · Nature Reviews Neuroscience · doi:10.1038/nrn2038 · Cited by 4,110 · cited 1×
“Emerging evidence has indicated that neuroinflammation contributes to PD (Block et al. 2007; Gao and Hong 2008; Hirsch and Hunot 2009).”
BackgroundSelf-citation
AlaSOPro mutation in the gene encoding α-synuclein in Parkinson's disease
Krüger, R., Kuhn, W., Müller, T., Woitalla, D., Graeber, M., Kösel, S., Przuntek, H., Epplen, J. T., Schols, L., & Riess, O. (1998) · Nature Genetics · doi:10.1038/ng0298-106 · Cited by 3,836 · cited 1×
“…genes have been identified in familial PD. α-Synuclein (α-syn) is closely associated with both familial and sporadic PD. Missense mutations (A53T, A30P, and E46K) and multiplications of the α-syn gene (SNCA) cause autosomal-dominant PD (Farrer 2006; Krüger et al. 1998; Polymeropoulos et al. 1997).”
Background
Reactive microglia are positive for HLA‐DR in the substantia nigra of Parkinson's and Alzheimer's disease brains
McGeer, P. L., Itagaki, S., Boyes, B. E., & McGeer, E. G. (1988) · Neurology · doi:10.1212/wnl.38.8.1285 · Cited by 2,990
Guide for the care and use of laboratory animals
(1997) · Choice Reviews Online · doi:10.5860/choice.34-3310 · Cited by 2,930
Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration
Qin, L., Wu, X., Block, M. L., Liu, Y., Breese, G. R., Hong, J., Knapp, D. J., & Crews, F. T. (2007) · Glia · doi:10.1002/glia.20467 · Cited by 2,144 · cited 1×
“Morphologic changes of microglia (the resident brain immune cells) and accumulation of pro inflammatory factors are associated with degenerating DA neurons in the substantia nigra (SN) of PD patients and various PD animal models (Liberatore et al. 1999; McGeer et al. 1988; Sherer et al. 2003).”
BackgroundSelf-citation
α-synuclein locus duplication as a cause of familial Parkinson's disease
Chartier-Harlin, M.-C., Kachergus, J., Roumier, C., Mouroux, V., Douay, X., Lincoln, S., Levecque, C., Larvor, L., Andrieux, J., Hulihan, M., et al. (2004) · The Lancet · doi:10.1016/s0140-6736(04)17103-1 · Cited by 2,029 · cited 1×
“Disease severity in PD patients with SNCA multiplications positively correlates with gene copy number (Chartier-Harlin et al. 2004; Ibanez et al. 2004; Singleton et al. 2003).”
Background
Neuroinflammation in Parkinson’s disease: A target for neuroprotection?
Hirsch, E. C., & Hunot, S. (2009) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70062-6 · Cited by 1,984 · cited 1×
“Emerging evidence has indicated that neuroinflammation contributes to PD (Block et al. 2007; Gao and Hong 2008; Hirsch and Hunot 2009).”
Background

Flagged first, then by citations

Show all 46 references

Sorted by citations

Items 201–300 of 355

Systemic inflammation accelerates neurodegeneration in a rat model of Parkinson’s disease overexpressing human alpha synuclein
Cenere, M. M., Tiberi, M., Paldino, E., D’Addario, S. L., Federici, M., Giacomet, C., Cutuli, D., Matteocci, A., Cossa, F., Zarrilli, B., et al. (2024) · npj Parkinson s Disease · doi:10.1038/s41531-024-00824-w · Cited by 23
Brain Damage - Bridging Between Basic Research and Clinics
González-Quevedo, A. (2012) · InTech eBooks · doi:10.5772/2174 · Cited by 21
“Reframing” dopamine signaling at the intersection of glial networks in the aged Parkinsonian brain as innate Nrf2/Wnt driver: Therapeutical implications
Marchetti, B., Giachino, C., Tirolo, C., & Serapide, M. F. (2022) · Aging Cell · doi:10.1111/acel.13575 · Cited by 22
Rescue from a two hit, high-throughput model of neurodegeneration with N-acetyl cysteine
Unnithan, A. S., Choi, H. J. H., Titler, A. M., Posimo, J. M., & Leak, R. K. (2012) · Neurochemistry International · doi:10.1016/j.neuint.2012.06.001 · Cited by 23
Astrocyte Pannexin 1 Suppresses LPS-Induced Inflammatory Responses to Protect Neuronal SH-SY5Y Cells
Ling, Z.-M., Wang, Q., Yu, M., Peng, X., Gu, Y., Cao, M., & Wei, Z. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.710820 · Cited by 20
O-Cyclic Phytosphingosine-1-Phosphate Protects against Motor Dysfunctions and Glial Cell Mediated Neuroinflammation in the Parkinson’s Disease Mouse Models
Lee, H. J., Choe, K., Park, J. S., Khan, A., Kim, M. W., Park, T. J., & Kim, M. O. (2022) · Antioxidants · doi:10.3390/antiox11112107 · Cited by 20
“Furthermore, motor dysfunction is a prominent clinical feature of PD, and MPTP/α-synuclein-induced PD mouse have shown molecular alterations associated with Parkinson’s disease [38,39].”
Background
Neonatal exposure to lipopolysaccharide enhances accumulation of α-synuclein aggregation and dopamine transporter protein expression in the substantia nigra in responses to rotenone challenge in later life
Tien, L., Kaizaki, A., Pang, Y., Cai, Z., Bhatt, A., & Fan, L. (2013) · Toxicology · doi:10.1016/j.tox.2013.03.014 · Cited by 20
Parkinson’s disease: what the model systems have taught us so far
Ghatak, S., Trudler, D., Dolatabadi, N., & Ambasudhan, R. (2018) · Journal of Genetics · doi:10.1007/s12041-018-0960-6 · Cited by 20
The role of α-synuclein in neurodegeneration — An update
Jellinger, K. A. (2012) · Translational Neuroscience · doi:10.2478/s13380-012-0013-1 · Cited by 19
Kolaviron protects against nigrostriatal degeneration and gut oxidative damage in a stereotaxic rotenone model of Parkinson’s disease
Farombi, E. O., Awogbindin, I. O., Olorunkalu, P. D., Ogbuewu, E., Oyetunde, B. F., Agedah, A. E., & Adeniyi, P. A. (2020) · Psychopharmacology · doi:10.1007/s00213-020-05605-w · Cited by 19
Reactive Oxygen Species in Neurodegenerative Diseases: Implications in Pathogenesis and Treatment Strategies
Oladele, J. O., Oladiji, A. T., Oladele, O. T., & Oyeleke, O. M. (2021) · Biochemistry · doi:10.5772/intechopen.99976 · Cited by 21
Towards New Therapies for Parkinson's Disease
Finkelstein, D. I. (2011) · InTech eBooks · doi:10.5772/954 · Cited by 19
Dual modulation on glial cells by tetrahydroxystilbene glucoside protects against dopamine neuronal loss
Zhou, Y., Wang, G., Li, D., Wang, Y., Wu, Q., Shi, J., & Zhang, F. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1194-5 · Cited by 17
“Thus, inhibition of microglial ROS production, rather than the other pro-inflammatory factors, was the most effective in DA neuron protection [24, 25].”
Self-citation
The second phase of brain trauma can be controlled by nutraceuticals that suppress DAMP-mediated microglial activation
McCarty, M. F., & Lerner, A. (2021) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2021.1907182 · Cited by 17
The Role of The Gut Microbiome in Parkinson’s Disease
Gallop, A., Weagley, J. S., Paracha, S.-U.-R., & Grossberg, G. T. (2021) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/08919887211018268 · Cited by 18
α-Synuclein potentiates interleukin-1β-induced CXCL10 expression in human A172 astrocytoma cells
Tousi, N. S., Buck, D. J., Curtis, J. T., & Davis, R. L. (2011) · Neuroscience Letters · doi:10.1016/j.neulet.2011.12.001 · Cited by 17
Neuroinflammation as a therapeutic target in neurodegenerative diseases
Gordon, R., & Woodruff, T. M. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-805120-7.00003-8 · Cited by 19
NPT520-34 improves neuropathology and motor deficits in a transgenic mouse model of Parkinson’s disease
Khan, A., Johnson, R., Wittmer, C., Maile, M., Tatsukawa, K. J., Wong, J. L., Gill, M. B., Stocking, E. M., Natala, S. R., Paulino, A., et al. (2021) · Brain · doi:10.1093/brain/awab214 · Cited by 17
Lycium ruthenicum Murray anthocyanin-driven neuroprotection modulates the gut microbiome and metabolome of MPTP-treated mice
Cao, H., Tian, Q., Chu, L., Wu, L., Gao, H., & Gao, Q. (2024) · Food & Function · doi:10.1039/d4fo01878h · Cited by 16
Self-citation
Neuronal Calcium Imaging, Excitability, and Plasticity Changes in the Aldh2–/– Mouse Model of Sporadic Alzheimer’s Disease
Ghoweri, A. O., Gagolewicz, P. J., Frazier, H. N., Gant, J. C., Andrew, R. D., Bennett, B. M., & Thibault, O. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200617 · Cited by 16
Intracranial administration of alpha-synuclein fibrils in A30P-synuclein transgenic mice causes robust synucleinopathy and microglial induction
Gentzel, R. C., Toolan, D. M., Jinn, S., Schachter, J. B., Ma, L., Kahle, P. J., Smith, S. M., & Marcus, J. (2021) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2021.05.012 · Cited by 15
Detailed insight into the pathophysiology and the behavioral complications associated with the Parkinson's disease and its medications
Wal, P., Dwivedi, J., Wal, A., Vig, H., & Singh, Y. (2022) · Future Journal of Pharmaceutical Sciences · doi:10.1186/s43094-022-00425-5 · Cited by 15
“Table 1 Summarizes the list of genes and their details associated with the PARK loci in Parkinson’s disease [86, 87]”
Background
A Mutual Nexus Between Epilepsy and α-Synuclein: A Puzzle Pathway
Ali, N. H., Al-Kuraishy, H. M., Al-Gareeb, A. I., Alnaaim, S. A., Hetta, H. F., Saad, H. M., & Batiha, G. E. (2024) · Molecular Neurobiology · doi:10.1007/s12035-024-04204-6 · Cited by 17
Transient glutathione depletion in the substantia nigra compacta is associated with neuroinflammation in rats
Díaz-Hung, M.-L., Yglesias-Rivera, A., Hernández-Zimbrón, L. F., Orozco-Suárez, S. A., Ruiz-Fuentes, J. L., Díaz-García, A., León-Martínez, R., Blanco-Lezcano, L., Fuentes, N. P., & Pedré, L. L. (2016) · Neuroscience · doi:10.1016/j.neuroscience.2016.08.023 · Cited by 15
“Inflammation has been described in patients and animal models of PD although it has been difficult to establish it as the primary event of the degenerative process (Lee et al., 2009; Gao et al., 2011; Ramsey and Tansey, 2014; Zhou et al., 2016).”
Background
Caspase-1 clipping causes complications for α-synuclein
Nuber, S., & Selkoe, D. J. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1610993113 · Cited by 15
Adulthood Exposure to Lipopolysaccharide Exacerbates the Neurotoxic and Inflammatory Effects of Rotenone in the Substantia Nigra
Huang, C., Zhu, L., Li, H., Shi, F., Wang, G., Wei, Y.-Z., Liu, J., & Zhang, F. (2017) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2017.00131 · Cited by 15
Self-citation
Pathology of Neurodegenerative Diseases
Kim, Y. S., Kim, Y.-K., Hwang, O., & Dong, J. (2012) · InTech eBooks · doi:10.5772/38028 · Cited by 16
“More recently, it has been shown that transgenic mice expressing mutant ┙- synuclein developed persistent neuroinflammation and chronic progressive degeneration of the nigrostriatal DA pathway when inflammation was triggered by a low level of lipopolysaccharide (Gao et al., 2011).”
Background
Infections in the Etiology of Parkinson’s Disease and Synucleinopathies: A Renewed Perspective, Mechanistic Insights, and Therapeutic Implications
Mercado, G., Käufer, C., Richter, F., & Peelaerts, W. (2024) · Journal of Parkinson s Disease · doi:10.3233/jpd-240195 · Cited by 16
Do Bacterial Outer Membrane Vesicles Contribute to Chronic Inflammation in Parkinson’s Disease?
Koukoulis, T. F., Beauchamp, L. C., Kaparakis‐Liaskos, M., McQuade, R. M., Purnianto, A., Finkelstein, D. I., Barnham, K. J., & Vella, L. J. (2024) · Journal of Parkinson s Disease · doi:10.3233/jpd-230315 · Cited by 14
Potential roles of functional bacterial amyloid proteins, bacterial biosurfactants and other putative gut microbiota products in the etiopathogeny of Parkinson’s Disease
Manole, E., Dumitrescu, L., Niculite, C. M., Popescu, B. O., & Ceafalan, L. C. (2021) · Biocell · doi:10.32604/biocell.2021.013452 · Cited by 14
Aggregated alpha-synuclein transcriptionally activates pro-inflammatory canonical and non-canonical NF-κB signaling pathways in peripheral monocytic cells
Bearoff, F. M., Dhavale, D. D., Kotzbauer, P. T., & Kortagere, S. (2022) · Molecular Immunology · doi:10.1016/j.molimm.2022.12.006 · Cited by 15
Apoptosis signal regulating kinase 1 deletion mitigates α-synuclein pre-formed fibril propagation in mice
Zhang, J., Park, E. S., Park, H.-J., Yan, R., Grudniewska, M., Zhang, X., Oh, S. E., Yang, X., Baum, J., & Mouradian, M. M. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2019.09.012 · Cited by 14
“Additionally, an inflammatory environment is known to enhance α-Syn aggregation, which can further activate microglia and promote a feed-forward cascade that leads to additional α-Syn aggregation and propagation (Gao et al., 2011).”
Background
Positron Emission Tomography with [18F]ROStrace Reveals Progressive Elevations in Oxidative Stress in a Mouse Model of Alpha-Synucleinopathy
Gallagher, E. P., Hou, C., Zhu, Y., Hsieh, C., Lee, H. S., Li, S., Xu, K., Henderson, P., Chroneos, R., Sheldon, M., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25094943 · Cited by 15
Physiology and Pathology of Neuroimmunology: Role of Inflammation in Parkinson’s Disease
Ortíz, G. G., González-Usigli, H., Pacheco-Moisés, F. P., Mireles-Ramírez, M. A., Sánchez-López, A. L., Torres-Sánchez, E. D., González-Renovato, E. D., Flores-Alvarado, L. J., Macías-Islas, M. Á., Rivero-Moragrega, P., et al. (2017) · InTech eBooks · doi:10.5772/intechopen.70377 · Cited by 13
“Recent studies demonstrate that excessive inflammation and overactivation of immune cells could play an important role in the onset and progression of this pathology [45].”
Background
Neuroprotective Effects of Bromelain on the Common Neurodegenerative Diseases: A Systematic Review
Rostamian, S., Raeisi, E., Heidari-Soureshjani, S., & Sherwin, C. M. T. (2023) · Neurochemical Journal · doi:10.1134/s1819712423040256 · Cited by 13
Content of Peripheral Blood T- and B-Cell Subpopulations in Transgenic A53T Mice of Different Age (A Model of Parkinson’s Disease)
Idova, G. V., Лазаревна, А. Е., Gevorgyan, M. M., Tikhonova, M. A., & Zhanaeva, S. Y. (2021) · Bulletin of Experimental Biology and Medicine · doi:10.1007/s10517-021-05075-w · Cited by 12
Sesquiterpenes from the Endophyte Glomerella cingulata
Liu, Y., Li, Y., Liu, Z., Li, L., Qu, J., Ma, S., Chen, R., Dai, J., & Yu, S. (2017) · Journal of Natural Products · doi:10.1021/acs.jnatprod.7b00054 · Cited by 12
The gut-brain axis in the pathogenesis of Parkinson’s disease
Meng, L., Yuan, X., Cao, X., & Zhang, Z. (2019) · Brain Science Advances · doi:10.1177/2096595820902566 · Cited by 12
“α-Syn is known to aggregate in an inflammatory environment, which activates microglia [49].”
Background
Experimental peri-implantitis induces neuroinflammation: An exploratory study in rats
Cafferata, E. A., Ramanauskaitė, A., Cuypers, A., Obreja, K., Dohle, E., Ghanaati, S., & Schwarz, F. (2024) · BMC Oral Health · doi:10.1186/s12903-024-04995-z · Cited by 11
“Moreover, E. coli LPS has shown an enhanced capacity to induce microglial pro-inflammatory cytokine production, in comparison with P. gingivalis LPS, astro-gliosis and α-synuclein dysfunction [86, 90, 91].”
Promising molecular targets for pharmacological therapy of neurodegenerative pathologies
Неганова, М. Е., Aleksandrova, Y. R., Nebogatikov, V. O., Klochkov, S. G., & Ustyugov, A. A. (2020) · Acta Naturae · doi:10.32607/actanaturae.10925 · Cited by 11
Neuroinflammation, immune response and α-synuclein pathology: how animal models are helping us to connect dots
Balzano, T., Esteban-García, N., & Blesa, J. (2022) · Expert Opinion on Drug Discovery · doi:10.1080/17460441.2023.2160440 · Cited by 11
“In contrast, the nigrostriatal pathway in normal saline (NS)-injected TG-mice and all WT mice remained intact [29].”
Background
Initiation and Transmission of α-Synuclein Pathology in Parkinson’s Disease
Mazurskyy, A., & Howitt, J. A. (2019) · Neurochemical Research · doi:10.1007/s11064-019-02896-0 · Cited by 10
Systemic inflammation activates coagulation and immune cell infiltration pathways in brains with propagating α-synuclein fibril aggregates
Laursen, A.-L. S., Olesen, M. V., Folke, J., Brudek, T., Knecht, L. H., Sotty, F., Lambertsen, K. L., Fog, K., Dalgaard, L. T., & Aznar, S. (2024) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2024.103931 · Cited by 9
“However, others reported a sustained neuroinflammation in the α -syn expressing mice five months after a single LPS-injection, an effect which was not observed in wild type mice (Gao et al., 2011).”
Background
Immune Response Modifications in the Genetic Forms of Parkinson’s Disease: What Do We Know?
Magistrelli, L., Contaldi, E., Vignaroli, F., Gallo, S., Colombatto, F., Cantello, R. M., & Comi, C. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23073476 · Cited by 11
“These data were further confirmed by Gao [31] and La Vitola [32] who treated A53T mutated and WT mice with intraperitoneal LPS injection.”
Result
Knockdown of interleukin-1 receptor 1 is not neuroprotective in the 6-hydroxydopamine striatal lesion rat model of Parkinson's disease
Walsh, S., Gavin, A. M., Wyatt, S. L., O'Connor, C., Keeshan, K., Nolan, Y. M., O’Keeffe, G. W., & Sullivan, A. M. (2014) · International Journal of Neuroscience · doi:10.3109/00207454.2014.904304 · Cited by 9
Rumex japonicus Houtt. Protects Dopaminergic Neurons by Regulating Mitochondrial Function and Gut–Brain Axis in In Vitro and In Vivo Models of Parkinson’s Disease
Kim, H.-Y., Bae, C., Kim, J., Lee, Y., Jeon, H., Kim, H., & Kim, S. (2022) · Antioxidants · doi:10.3390/antiox11010141 · Cited by 10
“The increased aggregation and propagation of α-synuclein induces the neurodegeneration of DA neurons in the SN, leading to PD motor dysfunction [34,35].”
Background
RNA- and ATAC-sequencing Reveals a Unique CD83+ Microglial Population Focally Depleted in Parkinson’s DiseasePreprint
Chatila, Z. K., Yadav, A., Mares, J., Flowers, X. E., Yun, T., Rashid, M., Talcoff, R., Pelly, Z., Zhang, Y., Jager, P. L. D., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.05.17.540842 · Cited by 11
Microglial and neuronal fates following inhibition of CSF-1R in synucleinopathy mouse model
Iba, M., Lee, Y., Horan-Portelance, L., Chang, K., Szabo, M. P., Rissman, R. A., You, S., Masliah, E., & Kim, C. (2024) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2024.09.016 · Cited by 9
“…microglial neuroinflammation may be triggered by multiple stimuli in the brain, activation of systemic inflammation also could induce neuroinflammation, thereby inducing abnormal accumulation of α -syn in the brain (Gao et al., 2011; Ifuku et al., 2012; Kahn et al., 2012; Tansey et al., 2022).”
Synuclein and Parkinson’s Disease: An Update
Jellinger, K. A. (2013) · Royal Society of Chemistry eBooks · doi:10.1039/9781849737357-00175 · Cited by 9
Toward a Disease-Modifying Therapy of Alpha-Synucleinopathies: New Molecules and New Approaches Came into the Limelight
Upcott, M., Chaprov, K., & Buchman, V. L. (2021) · Molecules · doi:10.3390/molecules26237351 · Cited by 8
Aminoacyl transfer ribonucleic acid synthetase complex-interacting multifunctional protein 1 induces microglial activation and M1 polarization via the mitogen-activated protein kinase/nuclear factor-kappa B signaling pathway
Oh, Y., Jung, H.-J., Hong, S., Cho, Y., Park, J., Cho, D., & Kim, T. S. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.977205 · Cited by 8
“Furthermore, it is important to investigate the effects of AIMP1 on the pathological roles of amyloid-β, α-synuclein, and tau, which are the well-known causative factors of neuroinflammation and neuronal diseases (Gao et al., 2011; Ismail et al., 2020).”
Background
Non-invasive systemic viral delivery of human alpha-synuclein mimics selective and progressive neuropathology of Parkinson’s disease in rodent brains
Bérard, M., Martínez-Drudis, L., Sheta, R., El‐Agnaf, O. M. A., & Oueslati, A. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00683-8 · Cited by 8
Disease mechanisms as subtypes: Inflammation in Parkinson disease and related disorders
Standaert, D. G., Harms, A. S., Childers, G. M., & Webster, J. M. (2023) · Handbook of clinical neurology · doi:10.1016/b978-0-323-85555-6.00011-4 · Cited by 8
Alpha-synuclein pathology enhances peripheral and CNS immune responses to bacterial endotoxins
Hartke, A.-S., Schreiber, C. S., Lau, K., Wiesweg, I., Waltl, I., Kalinke, U., Richter, F., & Käufer, C. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106773 · Cited by 8
“…that alterations in aSyn expression may occur after the neuroinflammatory response has subsided, as reported in previous studies (Deng et al., 2021; Gao et al., 2011; He et al., 2013), we determined whether LPS-induced neuroinflammation altered aSyn expression by quantifying aSyn protein…”
Deficits in basal and evoked striatal dopamine release following alpha‐synuclein preformed fibril injection: An in vivo microdialysis study
Centner, A., Priore, I. D., Chambers, N., Cohen, S. R., Terry, M. L., Coyle, M., Glinski, J., Stoll, A. C., Patterson, J. R., Kemp, C. J., et al. (2024) · European Journal of Neuroscience · doi:10.1111/ejn.16275 · Cited by 7
“Transgenic overexpression models of human wild type or mutated α -syn produce abundant α -syn aggregation (Gao et al., 2011; Gomez-Isla et al., 2003) but do not recapitulate the severe loss of nigral dopaminergic neurons.”
Background
Unravelling the Proteinopathic Engagement of α-Synuclein, Tau, and Amyloid Beta in Parkinson’s Disease: Mitochondrial Collapse as a Pivotal Driver of Neurodegeneration
Sahoo, T. A., Chand, J., Kandy, A. T., Shanish Antony, A., & Subramanian, G. (2025) · Neurochemical Research · doi:10.1007/s11064-025-04399-7 · Cited by 9
“Abnormal calcium levels may increase α-Syn aggregation by failing to maintain calcium-dependent chaperones or enzymes [32, 33].”
Early decrease in intermediate monocytes in peripheral blood is characteristic of multiple system atrophy-cerebellar type
Matsuse, D., Yamasaki, R., Maimaitijiang, G., Yamaguchi, H., Masaki, K., Isobe, N., Matsushita, T., & Kira, J. (2020) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2020.577395 · Cited by 7
Early Parkinson’s Disease-Like Pathology in a Transgenic Mouse Model Involves a Decreased Cst3 mRNA Expression But Not Neuroinflammatory Response in the Brain
Короленко, Т. А., Shintyapina, A. B., Беличенко, В. М., Pupyshev, A. B., Akopyan, A. A., Fedoseeva, L. A., Русских, Г. С., Андреевич, В. В., Tenditnik, M. V., Lin, C., et al. (2020) · Medical University · doi:10.2478/medu-2020-0008 · Cited by 7
Nutraceuticals in neurodegenerative diseases
Banerjee, S., Dutta, S., Ghosh, S., & Sil, P. C. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-820593-8.00017-3 · Cited by 7
Motor deficits and brain pathology in the Parkinson’s disease mouse model hA53Ttg
Breznik, L., Daurer, M., Rabl, R., Loeffler, T., Etxeberria-Rekalde, E., Neddens, J., Flunkert, S., & Prokesch, M. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1462041 · Cited by 6
Enhancing sleep quality in synucleinopathies through physical exercise
Canonichesi, J., Bellingacci, L., Rivelli, F., & Tozzi, A. (2025) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2025.1515922 · Cited by 6
Current and Emerging MR Methods and Outcome in Rodent Models of Parkinson’s Disease: A Review
Petiet, A. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.583678 · Cited by 6
“Interestingly, transgenic mice overexpressing α-synuclein and injected with LPS show increased protein aggregation, chronic nigral DA neuronal loss, and nigral inflammation compared to wild-type mice, suggesting a potentiation role of inflammation on α-synuclein dysfunction (Gao et al., 2011).”
Background
The Synergistic Effect Study of Lipopolysaccharide (LPS) and A53T-α-Synuclein: Intranasal LPS Exposure on the A53T-α-Synuclein Transgenic Mouse Model of Parkinson’s Disease
He, Q., Zhang, S., Wang, J., Ma, T., Ma, D., Wu, L., Zhou, M., Zhao, L., Chen, Y., Liu, J., et al. (2024) · Molecular Neurobiology · doi:10.1007/s12035-024-04020-y · Cited by 6
“However, dis-appointedly, most of the α-synuclein transgenic mice did not successfully replicate the degeneration of DAergic neurons [9, 13, 14].”
The acute effects of antimicrobials and lipopolysaccharide on the cellular mechanisms associated with neurodegeneration in pubertal male and female CD1 mice
Esposito, P., Gandelman, M., Rodriguez, C., Liang, J., & Ismail, N. (2022) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2022.100543 · Cited by 7
Dysfunction of the noradrenergic system drives inflammation, α-synucleinopathy, and neuronal loss in mouse colon
Song, S., Tu, D., Meng, C., Liu, J., Wilson, B. C., Wang, Q., Shih, Y. I., Gao, H., & Hong, J. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1083513 · Cited by 7
Self-citation
The effect of hemantane on the level of pro-inflammatory cytokines in the nigrocaudate complex of the brain of mice with experimental parkinsonism
Воронина, Н. А., Кучеряну, В. Г., Vetrilé, L. A., Goloborshcheva, V., Капица, И. Г., Воронина, Т. А., & Morozov, S. (2021) · Nauchno-prakticheskii zhurnal «Patogenez» · doi:10.25557/2310-0435.2021.02.45-49 · Cited by 6
Oxidative Stress in Parkinson’s Disease: Role in Neurodegeneration and Targets for Therapeutics
Banerjee, R., Kaidery, N. A., & Thomas, B. (2015) · ACS symposium series · doi:10.1021/bk-2015-1200.ch005 · Cited by 7
Enhanced IRE1α Phosphorylation/Oligomerization-Triggered XBP1 Splicing Contributes to Parkin-Mediated Prevention of SH-SY5Y Cell Death under Nitrosative Stress
Chiu, T., Huang, H., Chang, H., Wu, H.-R., & Wang, M.-J. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24032017 · Cited by 5
“Previous studies reported that direct nigral or intraperitoneal administration of LPS results in a dramatic loss of DA neurons in human A53T mutant α-syn transgenic mice compared to WT mice [24,25].”
Background
Neuroinflammation as a Potential Mechanism Underlying Parkinsons Disease
Cebrián, C., & Sulzer, D. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-803783-6.00008-0 · Cited by 7
Roles of Microglia in Inflammation-Mediated Neurodegeneration: Models, Mechanisms, and Therapeutic Interventions for Parkinson's Disease
Gao, H., Tu, D., Gao, Y., Liu, Q., Yang, R., Liu, Y., Guan, T., & Hong, J. (2017) · Advances in neurotoxicology · doi:10.1016/bs.ant.2017.07.005 · Cited by 6
Self-citation
Interplay of alpha-synuclein pathology and gut microbiome in Parkinson’s disease
Srivastava, A., Kataria, A., Yadav, D. K., Han, I., & Choi, E. H. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-91313-3.00003-9 · Cited by 4
Repositioning the existing drugs for neuroinflammation: a fusion of computational approach and biological validation to counter the Parkinson’s disease progression
Tiwari, H., Kumar, A., Barik, M. R., Kaur, H., Mahajan, S., Shukla, M. K., Gupta, M., Yadav, G., & Nargotra, A. (2023) · Molecular Diversity · doi:10.1007/s11030-023-10708-5 · Cited by 4
Recent advances in natural products targeting α-synuclein aggregation or clearance in Parkinson's disease
Gupta, J., & Sashidhara, K. V. (2023) · European Journal of Medicinal Chemistry Reports · doi:10.1016/j.ejmcr.2023.100114 · Cited by 4
Neuropharmacological Interventions of Plant Origin for Parkinson's Disease: A Comprehensive Appraisal
Muzaffer, U., Gull, B., Ahmed, Z., & Ahmad, M. (2025) · Current Neuropharmacology · doi:10.2174/1570159x23666250523112027 · Cited by 4
“Though most PD cases transpire sporadically, genetic factors yield substantial sway over disease susceptibility [28, 29].”
Spatial single-cell multiomics reveals peripheral immune dysfunction in Parkinson’s and inflammatory bowel disease
Bolen, M. L., Buendia, M., Shi, J., Staley, H. A., Kachergus, J. M., Efron, P. A., Park, G., Nagpal, R., Alvarez, S. D., Xue, Q., et al. (2026) · npj Parkinson s Disease · doi:10.1038/s41531-025-01199-2 · Cited by 6
A Forgotten Principle in Immunocytochemistry: Optimal Dilution
Dudás, B., Lane, M. V., Mupparaju, N., Kim, H. M., & Merchenthaler, I. J. (2022) · Journal of Histochemistry & Cytochemistry · doi:10.1369/00221554221146213 · Cited by 4
Cellular models, genomic technologies and clinical practice: a synthesis of knowledge for the study of the mechanisms, diagnostics and treatment of Parkinson's disease
Kovalenko, V., Александровна, Х. Е., Рзаев, Д. А., & Medvedev, S. P. (2017) · Genes and Cells · doi:10.23868/201707012 · Cited by 4
Microglial immune memory in Parkinson’s and Huntington’s diseases: epigenetics, triggers, and therapies
Chowdhury, R., Hendlinger, A., Rieß, O., & Schulze-Hentrich, J. M. (2025) · Epigenomics · doi:10.1080/17501911.2025.2518909 · Cited by 3
Mediators linking gut microbiota and sporadic Creutzfeldt–Jakob disease: a Mendelian randomization study
Shao, J., Su, T., Wang, J., Yin, X., Lang, Y., Fu, Y., & Cui, L. (2025) · AMB Express · doi:10.1186/s13568-025-01932-3 · Cited by 3
“In a mouse model of Parkinson's disease, endotoxin induces α-synuclein production/ aggregation and leads to loss of dopaminergic neurons in the substantia nigra (Gao et al. 2011).”
Parkinson's‐Linked LRRK2 and GBA1 Mutations Modulate the Peripheral Immune Response to Pseudomonas aeruginosa
Mark, J. R., Staley, H. A., Titus, A. M., Agin‐Liebes, J., Garrido, A., Hughes, L. P., Dzamko, N. L., Wallings, R. L., & Tansey, M. G. (2025) · Movement Disorders · doi:10.1002/mds.70123 · Cited by 3
Inflammasome-Mediated Inflammation in Neurodegenerative Diseases
Park, J. Y., Kang, Y. W., & Cho, W. G. (2019) · The Open Neurology Journal · doi:10.2174/1874205x01913010055 · Cited by 3
Unravelling the Parkinson’s puzzle, from medications and surgery to stem cells and genes: a comprehensive review of current and future management strategies
Chandrababu, K., Radhakrishnan, V., Anjana, A. S., Rajan, R. S., Sivan, U., Krishnan, S., & Chakrapani, P. S. B. (2023) · Experimental Brain Research · doi:10.1007/s00221-023-06735-1 · Cited by 3
“It is reported that inhibition of NADPH oxidase and iNOS reduce pathologic alterations of α-synuclein which causes chronic neurodegeneration in PD (Gao et al. 2011)”
Neuroinflammation and Parkinson’s Disease
Ros‐Bernal, F., Yuste, J. E., Tarragón, E., Ortiz, V., Gómez, A., Ros, C. M., Fernández‐Villalba, E., & Herrero, M. T. (2014) · Springer eBooks · doi:10.1007/978-1-4614-5836-4_6 · Cited by 3
Parkinson's disease
Segura‐Aguilar, J. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-822120-4.00001-0 · Cited by 4
LRRK2-G2019S Synergizes with Ageing and Low-Grade Inflammation to Promote Gut and Peripheral Immune Cell Activation that Precede Nigrostriatal DegenerationPreprint
Giachino, C., Tirolo, C., Caniglia, S., Serapide, M. F., L’Episcopo, F., Bertoli, F., Giuliano, C., Mearelli, M., Jakobi, M., Schneiderhan‐Marra, N., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.09.01.505977 · Cited by 4
Carbon quantum dots exacerbate Parkinson's disease-like pathology through microglia-mediated neuroinflammatory responses with toxicological implications
Yang, J., Chen, S., Xing, P., Hu, D., Liu, K., Ye, Z., Xia, J., He, J., Qian, Y., & Wu, T. (2026) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2026.112005 · Cited by 2
The cGAS-STING-Glymphatic-gut Axis in Parkinson's disease: A proposed self-amplifying triad of Neuroinflammation and therapeutic opportunity
Abdelaziz, A. M. (2026) · International Immunopharmacology · doi:10.1016/j.intimp.2026.116628 · Cited by 2
Neuronal vulnerability in Parkinson’s disease: insights from murine α-synuclein pathology models
Asadpoordezaki, Z., & Prehn, J. H. M. (2026) · Neuroscience · doi:10.1016/j.neuroscience.2026.04.007 · Cited by 2
Molecular Pathogenesis of Memory Impairment in Parkinson's Disease: An Exploration of Underlying Mechanisms
Pourfridoni, M., Hakemi, Z., Mashayekhi‐Sardoo, H., & Baghcheghi, Y. (2026) · Health Science Reports · doi:10.1002/hsr2.72024 · Cited by 2
“The spread of alpha‐synuclein pathology throughout the brain occurs in a prion‐like manner, where misfolded proteins induce neighboring neurons to misfold as well [95–97].”
Dysregulation of the Extracellular Matrix in the Synaptic Pathology of Parkinson’s Disease: Molecular Mechanisms and Novel Therapeutic Approaches
Rubio, C., Pérez-Rubio, R., Pérez-Villavicencio, J., Serrano‐García, N., Lee, Á., Granados-Rojas, L., Tena‐Suck, M. L., & Rubio‐Osornio, M. (2026) · Life · doi:10.3390/life16061007 · Cited by 2
Neuroprotection of Kolaviron by Regulation of Nuclear Factor Erythroid 2-related Factor 2 in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Mice Model of Parkinson Disease
Awogbindin, I. O., Onasanwo, S. A., Ezekiel, O. G., Akindoyeni, I. A., Mustapha, Y., & Farombi, O. E. (2021) · American Journal of Biopharmacy and Pharmaceutical Sciences · doi:10.25259/ajbps_8_2021 · Cited by 2
Neuroinflammation and Immune Dysfunction in the Mechanisms of Development of Parkinson’s Disease
Idova, G. V., Лазаревна, А. Е., & Zhanaeva, S. Y. (2023) · Neuroscience and Behavioral Physiology · doi:10.1007/s11055-023-01549-8 · Cited by 2
“…rheumatism, Crohn’s disease, and ulcerative colitis [Hirsch subject of a signi ﬁ cant number of reports [McGeer et al., 1988; Nagatsu et al., 2000; Gao et al., 2011; Grozdanov et al., 2014; Kustrimovic et al., 2018; Idova et al., 2021] and reviews [Ugrumov, 2020; Harms et al., 2021; Hirsch and…”
Causal relationships between genetically predicted particulate air pollutants and neurodegenerative diseases: A two-sample Mendelian randomization study
Liu, X., Zhang, X., Chang, T., Zhao, Z., Zhang, Y., Yang, X., & Lü, M. (2024) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2024.116960 · Cited by 2
Alpha-Synuclein and the Immune Response in Parkinson’s Disease
Roodveldt, C., Labrador‐Garrido, A., Izquierdo, G., & Pozo, D. (2011) · InTech eBooks · doi:10.5772/17417 · Cited by 3
“In the second study, the authors evaluated dopaminergic neurodegeneration, Syn pathology and neuroinflammation in Wt and transgenic A53T Syn-overexpressing mice (Gao et al., 2011).”
Influential
Therapeutic Viewpoint on Rat Models of Locomotion Abnormalities and Neurobiological Indicators in Parkinson's Disease
Chaudhary, R., & Singh, R. (2023) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527322666230518111323 · Cited by 2
Role of the Gut Microbiome and Bacterial Amyloids in the Development of Synucleinopathies
Trubitsina, N. P., Matiiv, A. B., Rogoza, T. M., Zudilova, A. A., Bezgina, M. D., Zhouravleva, G. A., & Bondarev, S. A. (2024) · Biochemistry (Moscow) · doi:10.1134/s0006297924030118 · Cited by 2
“This is in agreement with the earlier data indicating that the inflammatory processes induced by injection of LPS stimulate aggregation of αSyn in transgenic mice producing human αSyn with A53T replacement [169].”
Non-Surgical Periodontal Therapy’s Influence on Alpha-Synuclein and Inflammatory Marker Levels: A Pilot Study
Lyra, P., Botelho, J., Rota, S., Popławska-Domaszewicz, K., Machado, V., Guerreiro, D., Proença, L., Barroso, H., Mendes, J. J., & Chaudhuri, К. R. (2024) · Journal of Clinical Medicine · doi:10.3390/jcm13123586 · Cited by 2
“Mice exposed to lipopolysaccharide (LPS) exhibited α -Syn adopting a fibrillar form in the brain tissue, with cognitive deficits and enhanced dopaminergic neuronal loss, suggesting LPS-induced neuroinflammation and the periodontitis-related genetic background interact synergically [24,25].”
Background
Neuroinflammation in Neurological Dysfunction and Degeneration
Chen, S., Oyarzabal, E. A., Santos, J. H., Wang, Q., Jiang, L., & Hong, J. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-800228-5.00018-2 · Cited by 2
Self-citation
Comunicación bidireccional de la microbiota intestinal en el desarrollo del sistema nervioso central y en la enfermedad de Parkinson
Gómez-Chavarı́n, M., & Morales-Gómez, M. R. (2017) · Archivos de Neurociencias · doi:10.31157/an.v22i2.153 · Cited by 2
Immunotherapy for Neurodegenerative Movement Disorders
Mosley, R. L., Saleh, M., & Olson, K. E. (2024) · Springer eBooks · doi:10.1007/978-3-031-68237-7_52 · Cited by 1

Authors: Gao, H.-M., Zhang, F., Zhou, H., Kam, W., Wilson, B., & Hong, J.-S.
Affiliations: National Institutes of Health (US)
Corresponding author: Gao, Hui-Ming
ORCID: Gao, Hui-Ming
Zhang, Feng
Zhou, Hui
Kam, Wayneho
Hong, Jau-Shyong
Venue: Environmental Health Perspectives
Publisher: American Chemical Society (ACS)
Published: 2011-01-18
Volume: 119
Issue: 6
Pages: 807-814
ISSN: 0091-6765 (ISSN-L)
1552-9924
DOI: 10.1289/ehp.1003013
PMC: PMC3114815
OpenAlex: W1971599063
Cited by: 355
References: 46
Citations by year: 2026: 16 · 2025: 13 · 2024: 36 · 2023: 23 · 2022: 28 · 2021: 37 · 2020: 39 · 2019: 17 · 2018: 28 · 2017: 20 · 2016: 18 · 2015: 16 · 2014: 19 · 2013: 18 · 2012: 19
FWCI: 13.00
Type: journal article
Language: en
Open access: gold
doi.org
Licence: public-domain
creativecommons.org/licenses/by/4.0/ (vor, 2537 d)
Locations: Environmental Health Perspectives (publishedVersion, public-domain)
PubMed Central (publishedVersion, public-domain)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute of Environmental Health Sciences
Topics: Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
Keywords: Parkinson's disease, neuroinflammation, alpha-synuclein, lipopolysaccharide, two-hit model, gene-environment interaction, microglia, oxidative stress, inducible nitric oxide synthase, NADPH oxidase, dopaminergic neuron loss, nigrostriatal pathway, Lewy bodies, chronic neurodegeneration
MeSH terms: Amidines, Animals, Benzylamines, Disease Models, Animal, Injections, Intraperitoneal, Lipopolysaccharides, Nerve Degeneration, Onium Compounds, Parkinson Disease, Substantia Nigra, Lewy Bodies, Oxidative Stress, NADPH Oxidases, Neurodegenerative Diseases, Animals, Genetically Modified, Mice, alpha-Synuclein, Nitric Oxide Synthase Type II

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

Neuroinflammation and α-Synuclein Dysfunction Potentiate Each Other, Driving Chronic Progression of Neurodegeneration in a Mouse Model of Parkinson’s Disease

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Self-check

Citations

Cites

Cited by

Related

Metadata

Record

About these checks