Reversal of Paralysis and Reduced Inflammation from Peripheral Administration of β-Amyloid in T H 1 and T H 17 Versions of Experimental Autoimmune Encephalomyelitis
Open accessAbstract
β-Amyloid reduces inflammation and improves symptoms in a mouse model of multiple sclerosis.
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?
Aβ has a physiological role in innate immunity.
“these studies highlight a physiological role for Aβ in innate immunity”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [142]
The Results section reports that administered Aβ affects myeloid cells, including macrophages and dendritic cells, and the Discussion describes an anti-inflammatory effect in EAE mice. But the Introduction says the physiological role of peripheral Aβ is not completely understood; effects of administered Aβ do not establish a physiological role in innate immunity. (LLM, conf=0.83)
Experimental — accuracy not yet measuredAβ maintains both pathological and beneficial properties which are dependent on the type of CNS injury and the inflammatory context, namely lymphoid or brain tissue.
“These results indicate that Aβ maintains both pathological and beneficial properties which are dependent on the type of CNS injury and the inflammatory context, namely lymphoid or brain tissue.”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [142]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
Lesné, S., Koh, M. T., Kotilinek, L., Kayed, R., Glabe, C. G., Yang, A., Gallagher, M., & Ashe, K. H. (2006) · Nature · doi:10.1038/nature04533 · Cited by 2,769 · see citing works
RetractedCluster analysis and display of genome-wide expression patterns
Eisen, M. B., Spellman, P. T., Brown, P. O., & Botstein, D. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.25.14863 · Cited by 12,617 · see citing works
Fetal Cardiac Rhabdomyoma: A Case Report
Suwardewa, T. G. A., Negara, I. S., Kusuma, A. J., Wiradnyana, A., Surya, R., & Tunas, I. (2016) · doi:10.15562/bmj.v5i3.346 · Cited by 12,306 · cited 1×
“Active immunization against Ab formulated in an immunogenic adjuvant in clinical trials caused meningoencephalitis (38), suggesting that an autoimmune T cell response to Ab is triggered in these subjects.”
BackgroundInterleukin-10 and the Interleukin-10 Receptor
Moore, K. W., de Waal Malefyt, R., Coffman, R. L., & O'Garra, A. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.683 · Cited by 6,737 · see citing works
Walsh, D. M., Klyubin, I., Fadeeva, J. V., Cullen, W. K., Anwyl, R., Wolfe, M. S., Rowan, M. J., & Selkoe, D. J. (2002) · Nature · doi:10.1038/416535a · Cited by 4,291 · see citing works
Axonal transection in the lesions of multiple sclerosis
Trapp, B. D., Peterson, J., Ransohoff, R. M., Rudick, R., Mörk, S., & Bö, L. (1998) · New England Journal of Medicine · doi:10.1056/nejm199801293380502 · Cited by 4,029 · see citing works
Shankar, G. M., Li, S., Mehta, T. H., Garcia-Munoz, A., Shepardson, N. E., Smith, I., Brett, F. M., Farrell, M. A., Rowan, M. J., Lemere, C. A., et al. (2008) · Nature Medicine · doi:10.1038/nm1782 · Cited by 3,685 · see citing works
Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse
Schenk, D., Barbour, R., Dunn, W., Gordon, G., Grajeda, H., Guido, T., Hu, K., Huang, J., Johnson-Wood, K., Khan, K., et al. (1999) · Nature · doi:10.1038/22124 · Cited by 3,160 · see citing works
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., et al. (1995) · Nature · doi:10.1038/373523a0 · Cited by 2,516 · cited 1× · see citing works
“Notably, these transgenic mice use the plateletderived growth factor b promoter to overexpress APP, and in these mice, Ab is expressed in many tissues but in particularly high concentrations in the brain (55).”
BackgroundJarrett, J. T., & Lansbury, P. T. (1993) · Cell · doi:10.1016/0092-8674(93)90635-4 · Cited by 2,178 · cited 1× · see citing works
“In the context of AD, Ab42 has a well-characterized role in neurodegeneration and has been implicated in various cytotoxic pathologies including excitotoxicity and oxidative stress on neurons (46).”
BackgroundBard, F., Cannon, C., Barbour, R., Burke, R.-L., Games, D., Grajeda, H., Guido, T., Hu, K., Huang, J., Johnson-Wood, K., et al. (2000) · Nature Medicine · doi:10.1038/78682 · Cited by 2,012 · see citing works
Amyloid β-peptide is produced by cultured cells during normal metabolism
Haass, C., Schlossmacher, M. G., Hung, A. Y., Vigo-Pelfrey, C., Mellon, A., Ostaszewski, B. L., Lieberburg, I., Koo, E. H., Schenk, D., Teplow, D. B., et al. (1992) · Nature · doi:10.1038/359322a0 · Cited by 1,921 · cited 1× · see citing works
“Under normal physiological conditions, Ab40 is present at 10-fold higher concentration levels compared to Ab42 in the central nervous system (CNS) (14).”
BackgroundMultiple sclerosis--the plaque and its pathogenesis.
Frohman, E., Racke, M., & Raine, C. (2006) · New England Journal of Medicine · doi:10.1056/nejmra052130 · Cited by 1,793 · cited 1× · see citing works
“These demyelinated regions called plaques are composed, in part, of lymphocytes and macrophages that have infiltrated the CNS, resulting in axonal damage (19).”
BackgroundBrain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease.
Griffin, W. S., Stanley, L. C., Ling, C., White, L., MacLeod, V, Perrot, L. J., White, C. L., & Araoz, C. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.19.7611 · Cited by 1,777 · cited 1× · see citing works
“Within and around Ab senile plaques, activated microglia (6), astrogliotic astrocytes (7), components of the classical complement pathway (8), and cytokines such as transforming growth factor–b (TGF-b), tumor necrosis factor–a (TNF-a), and interleukin-1b (IL-1b) are all present (9, 10).”
BackgroundCitron, M., Oltersdorf, T., Haass, C., McConlogue, L., Hung, A. Y., Seubert, P., Vigo-Pelfrey, C., Lieberburg, I., & Selkoe, D. J. (1992) · Nature · doi:10.1038/360672a0 · Cited by 1,757 · see citing works
Axonal damage in acute multiple sclerosis lesions
Ferguson, B. (1997) · Brain · doi:10.1093/brain/120.3.393 · Cited by 1,532 · cited 1× · see citing works
“Ab is up-regulated in acute and chronic MS lesions and is a sensitive immunohistochemical marker of axonal damage (20, 21).”
BackgroundInterleukin-17 and Type 17 Helper T Cells
Miossec, P., Korn, T., & Kuchroo, V. K. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0707449 · Cited by 1,409 · cited 2× · see citing works
“Transfer of myelin-specific CD4 T cells can also induce EAE in naïve recipients (32).”
BackgroundNeuropathology of human Alzheimer disease after immunization with amyloid-β peptide: a case report
Nicoll, J. A. R., Wilkinson, D., Holmes, C., Steart, P., Markham, H., & Weller, R. O. (2003) · Nature Medicine · doi:10.1038/nm840 · Cited by 1,397 · see citing works
Steinman, L. (2007) · Nature Medicine · doi:10.1038/nm1551 · Cited by 1,367 · cited 2× · see citing works
“Either Ab42 or Ab40 was administered three times per week starting 7 or 8 days after recipient mice received MOG35–55autoreactive TH1 or TH17 cells (33) (experimental scheme in fig.”
BackgroundMethodWyss-Coray (2006) · doi:10.1038/nm1484 · Cited by 1,284 · see citing works
Simard, A. R., Soulet, D., Gowing, G., Julien, J.-P., & Rivest, S. (2006) · Neuron · doi:10.1016/j.neuron.2006.01.022 · Cited by 1,265 · cited 1× · see citing works
“Within and around Ab senile plaques, activated microglia (6), astrogliotic astrocytes (7), components of the classical complement pathway (8), and cytokines such as transforming growth factor–b (TGF-b), tumor necrosis factor–a (TNF-a), and interleukin-1b (IL-1b) are all present (9, 10).”
BackgroundZamzami, N., Marchetti, P., Castedo, M., Zanin, C., Vayssière, J. L., Petit, P. X., & Kroemer, G. (1995) · The Journal of experimental medicine · doi:10.1084/jem.181.5.1661 · Cited by 1,166 · see citing works
Amyloid Precursor Protein Trafficking, Processing, and Function
Thinakaran, G., & Koo, E. H. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.r800019200 · Cited by 1,141 · cited 1× · see citing works
“Scien ically altered due to the up-regulation of Ab42 during injury, inflammation, and stress in the brain (15, 16).”
BackgroundThe T lymphocyte in experimental allergic encephalomyelitis.
Zamvil, S., & Steinman, L. (1990) · Annual Review of Immunology · doi:10.1146/annurev.iy.08.040190.003051 · Cited by 1,091 · cited 1× · see citing works
“of experimental autoimmune encephalomyelitis (EAE), often considered an animal model of MS (24).”
BackgroundSelf-citationFerber, I., Brocke, S., Taylor-Edwards, C., Ridgway, W., Dinisco, C., Steinman, L., Dalton, D., & Fathman, C. (1996) · Journal of Immunology · doi:10.4049/jimmunol.156.1.5 · Cited by 1,088 · see citing works
Self-citationRelationship of microglia and astrocytes to amyloid deposits of Alzheimer disease
Itagaki, S., McGeer, P. L., Akiyama, H., Zhu, S., & Selkoe, D. (1989) · Journal of Neuroimmunology · doi:10.1016/0165-5728(89)90115-x · Cited by 940 · cited 1× · see citing works
“Within and around Ab senile plaques, activated microglia (6), astrogliotic astrocytes (7), components of the classical complement pathway (8), and cytokines such as transforming growth factor–b (TGF-b), tumor necrosis factor–a (TNF-a), and interleukin-1b (IL-1b) are all present (9, 10).”
BackgroundComplement activation by beta-amyloid in Alzheimer disease.
Rogers, J., Cooper, N. R., Webster, S., Schultz, J., McGeer, P. L., Styren, S. D., Civin, W. H., Brachova, L., Bradt, B., & Ward, P. (1992) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.89.21.10016 · Cited by 817 · see citing works
Mechanism of Action of Oral Fingolimod (FTY720) in Multiple Sclerosis
Chun, J., & Hartung, H.-P. (2010) · Clinical Neuropharmacology · doi:10.1097/wnf.0b013e3181cbf825 · Cited by 796 · cited 1× · see citing works
“These approved drugs treat relapsingremitting MS by blocking or sequestering lymphocytes outside the CNS, preventing their infiltration from the peripheral circulation into the CNS parenchyma (25, 26).”
BackgroundTwo physically, functionally, and developmentally distinct peritoneal macrophage subsets
Ghosn, E. E. B., Cassado, A. A., Govoni, G. R., Fukuhara, T., Yang, Y., Monack, D. M., Bortoluci, K. R., Almeida, S. R., Herzenberg, L. A., & Herzenberg, L. A. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0915000107 · Cited by 689 · see citing works
Self-citationCharacterization of the Drosophila melanogaster genome at the nuclear lamina
Pickersgill, H., Kalverda, B., de Wit, E., Talhout, W., Fornerod, M., & van Steensel, B. (2006) · Nature Genetics · doi:10.1038/ng1852 · Cited by 656 · see citing works
Active induction of experimental allergic encephalomyelitis
Stromnes, I. M., & Goverman, J. M. (2006) · Nature Protocols · doi:10.1038/nprot.2006.285 · Cited by 572 · cited 2× · see citing works
“EAE induction In the C57BL/6 model, EAE was induced in 8- to 12-week-old female mice by subcutaneous immunization with 100 mg of MOG35–55 in emulsified CFA followed by intraperitoneal injection of 500 ng of Bordetella pertussis toxin (Difco Laboratories) in phosphate-buffered saline (PBS) at the time of and 2 days aft…”
BackgroundMethodMUTANT GENES IN FAMILIAL ALZHEIMER'S DISEASE AND TRANSGENIC MODELS
Price, D. L., & Sisodia, S. S. (1998) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.21.1.479 · Cited by 568 · see citing works
DeMattos, R. B., Bales, K. R., Cummins, D. J., Paul, S. M., & Holtzman, D. M. (2002) · Science · doi:10.1126/science.1067568 · Cited by 563 · see citing works
Spectral compensation for flow cytometry: Visualization artifacts, limitations, and caveats
Roederer, M. (2001) · Cytometry · doi:10.1002/1097-0320(20011101)45:3 · Cited by 561 · see citing works
Axtell, R., de Jong, B. D., Boniface, K., van der Voort, L. F., Bhat, R., Sarno, P. D., Naves, R., Han, M. H., Zhong, F., Castellanos, J. G., et al. (2010) · Nature Medicine · doi:10.1038/nm.2110 · Cited by 556 · see citing works
Self-citationProteomic analysis of active multiple sclerosis lesions reveals therapeutic targets
Han, M. H., Hwang, S.-I., Roy, D. B., Lundgren, D. H., Price, J. V., Ousman, S., Fernald, G., Gerlitz, B., Robinson, W., Baranzini, S., et al. (2008) · Nature · doi:10.1038/nature06559 · Cited by 539 · see citing works
Self-citationCoordination of Early Protective Immunity to Viral Infection by Regulatory T Cells
Lund, J. M., Hsing, L., Pham, T., & Rudensky, A. Y. (2008) · Science · doi:10.1126/science.1155209 · Cited by 514 · cited 1× · see citing works
“Tregs have been implicated in suppressing autoimmunity and maintaining immune homeostasis during inflammation and disease (44).”
BackgroundProtective and therapeutic role for αB-crystallin in autoimmune demyelination
Ousman, S., Tomooka, B. H., van Noort, J., Wawrousek, E., O'Conner, K., Hafler, D., Sobel, R., Robinson, W., & Steinman, L. (2007) · Nature · doi:10.1038/nature05935 · Cited by 491 · cited 5× · see citing works
“We measured cytokine secretion from cell supernatant by sandwich ELISA (BD Pharmingen) and proliferation by radioactive [3H]thymidine incorporation.”
BackgroundMethodInfluentialSelf-citationOccurrence of T cells in the brain of Alzheimer's disease and other neurological diseases
Togo, T., Akiyama, H., Iseki, E., Kondo, H., Ikeda, K., Kato, M., Oda, T., Tsuchiya, K., & Kosaka, K. (2002) · Journal of Neuroimmunology · doi:10.1016/s0165-5728(01)00496-9 · Cited by 481 · cited 1× · see citing works
“Therefore, we explored the effects of augmenting Ab peptide levels outside the CNS as an immunomodulatory mechanism to regulate EAE disease progression, actually expecting that such manipulations would worsen disease because of the induction of proinflammatory, macrophage-driven immune responses (27, 28) or the activa…”
BackgroundEnhancement of experimental allergic encephalomyelitis in mice by antibodies against IFN-gamma.
Billiau, A., Heremans, H., Vandekerckhove, F., Dijkmans, R., Sobis, H., Meulepas, E., & Carton, H. (1988) · Journal of Immunology · doi:10.4049/jimmunol.140.5.1506 · Cited by 447 · see citing works
Expression of the histocompatibility glycoprotein HLA-DR in neurological disease
McGeer, P. L., Itagaki, S., & McGeer, E. G. (1988) · Acta Neuropathologica · doi:10.1007/bf00689592 · Cited by 420 · cited 1× · see citing works
“Therefore, we explored the effects of augmenting Ab peptide levels outside the CNS as an immunomodulatory mechanism to regulate EAE disease progression, actually expecting that such manipulations would worsen disease because of the induction of proinflammatory, macrophage-driven immune responses (27, 28) or the activa…”
BackgroundInterferon‐γ confers resistance to experimental allergic encephalomyelitis
Krakowski, M., & Owens, T. (1996) · European Journal of Immunology · doi:10.1002/eji.1830260735 · Cited by 414 · see citing works
Origins of CD4+ effector and central memory T cells
Pepper, M., & Jenkins, M. K. (2011) · Nature Immunology · doi:10.1038/ni.2038 · Cited by 401 · cited 1× · see citing works
“We observed an increase in the periphery in a subset of lymphocytes resembling central memory effector T cells (58) (CD4CD62L) that produce higher amounts of IFN-g, whereas IFN-g production was reduced at the site of disease in the spinal cord (fig.”
BackgroundIncreased T cell reactivity to amyloid β protein in older humans and patients with Alzheimer disease
Monsonego, A., Zota, V., Karni, A., Krieger, J. I., Bar-Or, A., Bitan, G., Budson, A. E., Sperling, R., Selkoe, D. J., & Weiner, H. L. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200318104 · Cited by 367 · see citing works
Uryu, K., Chen, X.-H., Martinez, D., Browne, K. D., Johnson, V. E., Graham, D. I., Lee, V. M.-Y., Trojanowski, J. Q., & Smith, D. H. (2007) · Experimental Neurology · doi:10.1016/j.expneurol.2007.06.018 · Cited by 360 · see citing works
Waldor, M., Sriram, S., Hardy, R., Herzenberg, L., Lanier, L., Lim, M., & Steinman, L. (1985) · Science · doi:10.1126/science.3155574 · Cited by 329 · see citing works
Self-citationBlocking adhesion molecules as therapy for multiple sclerosis: natalizumab
Steinman, L. (2005) · Nature reviews. Drug discovery · doi:10.1038/nrd1752 · Cited by 328 · see citing works
Self-citationAssociation of Plasma β-Amyloid Level and Cognitive Reserve With Subsequent Cognitive Decline
Yaffe, K. S. (2011) · JAMA · doi:10.1001/jama.2010.1995 · Cited by 244 · cited 3× · see citing works
“Ab treatment given outside the CNS serves to augment levels of Ab peptides that are present endogenously in the circulation (18).”
BackgroundResultInfluentialCurrent Views on the Roles of Th1 and Th17 Cells in Experimental Autoimmune Encephalomyelitis
Behi, M. E., Rostami, A. M., & Ćirić, B. (2010) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-009-9188-9 · Cited by 220 · cited 1× · see citing works
“Ab42- and Ab40-mediated immunosuppression of CD4 TH cells CD4 T effector cells play a central role in EAE pathology (39, 40) and MS (41).”
BackgroundVoorthuis, J. A. C., Uitdehaag, B., Groot, C., Goede, P., van der Meide, P. H., & Dijkstra, C. (1990) · Clinical and Experimental Immunology · doi:10.1111/j.1365-2249.1990.tb03315.x · Cited by 201 · see citing works
An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide
Pedotti, R., Mitchell, D., Wedemeyer, J., Karpuj, M., Chabas, D., Hattab, E., Tsai, M., Galli, S., & Steinman, L. (2001) · Nature Immunology · doi:10.1038/85266 · Cited by 198 · see citing works
Self-citationImmunology and immunotherapy of Alzheimer's disease
Weiner, H., & Frenkel, D. (2006) · Nature reviews. Immunology · doi:10.1038/nri1881 · Cited by 197
Nerve inflammation halts trial for Alzheimer's drug
Check, E. (2002) · Nature · doi:10.1038/415462a · Cited by 186 · cited 1× · see citing works
“AD patients immunized with Ab develop meningoencephalitis, likely because the Ab used in the vaccine AN-1792 was formulated in an adjuvant to purposely make it immunogenic (59).”
BackgroundFrenkel, D., Maron, R., Burt, D. S., & Weiner, H. L. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23241 · Cited by 186 · cited 3× · see citing works
“However, attempts to induce EAE in aged transgenic mice overexpressing pathological forms of APP in the CNS indicate that increased levels of Ab in the CNS do not impair the induction of EAE with MOG and adjuvant (36).”
BackgroundInfluentialDistinct progenitors for B-1 and B-2 cells are present in adult mouse spleen
Ghosn, E., Sadate-Ngatchou, P. I., Yang, Y., Herzenberg, L. A., & Herzenberg, L. (2011) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.1019764108 · Cited by 108 · see citing works
Self-citationPasserini, L., di Nunzio, S., Gregori, S., Gambineri, E., Cecconi, M., Seidel, M., Cazzola, G., Perroni, L., Tommasini, A., Vignola, S., et al. (2011) · European Journal of Immunology · doi:10.1002/eji.201040909 · Cited by 88 · see citing works
Early complement components in Alzheimer's disease brains
Veerhuis, R., Janssen, I., Hack, C. E., & Eikelenboom, P. (1995) · Acta Neuropathologica · doi:10.1007/s004019570001 · Cited by 77 · see citing works
Immunologic mechanisms of multiple sclerosis.
Frohman, E., Eagar, T., Monson, N., Stüve, O., & Karandikar, N. (2008) · Neuroimaging clinics of North America · doi:10.1016/j.nic.2008.06.009 · Cited by 29 · cited 1× · see citing works
“Ab42- and Ab40-mediated immunosuppression of CD4 TH cells CD4 T effector cells play a central role in EAE pathology (39, 40) and MS (41).”
BackgroundA possible role for nitric oxide at the sleep/wake interface.
Cudeiro, J., Rivadulla, C., & Grieve, K. (2000) · Sleep · doi:10.1093/sleep/23.6.1j · Cited by 27 · see citing works
Flagged first, then by citations
5 of the 64 references couldn’t be matched to a known paper.
Research works printed but not linked: 5
- [1]Hardy J Selkoe DJ The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics Science 297 353 7 19 2002 12130773
- [14]Monsonego A Weiner HL Immunotherapeutic approaches to Alzheimer’s disease Science 302 834 10 31 2003 14593170
- [16]Haass C Amyloid beta-peptide is produced by cultured cells during normal metabolism Nature 359 322 9 24 1992 1383826
- [55]Willenborg DO Fordham SA Staykova MA Ramshaw IA Cowden WB IFN-gamma is critical to the control of murine autoimmune encephalomyelitis and regulates both in the periphery and in the target tissue: a possible role for nitric oxide J Immunol 163 5278 11 15 1999 10553050
- [57]Villeda S Luo J Mosher K Zou B Britschgi M The ageing systemic milieu negatively regulates neurogenesis and cognitive function Nature 1 1 2011 PMC3170097 21886162
Cited by
Sorted by citations
Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future
Zhang, Y., Chen, H., Li, R., Sterling, K., & Song, W. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01484-7 · Cited by 988 · see citing works
“One potential explanation for the activated glia cells in AD brain could be the response to Aβ produced largely by neurons.157,158 Aβ shares structural similarities with antimicrobial peptides (AMPs) and viral fusion domains, which stimulates glia cells to secrete a mass of pro-inflammatory cytokines.159 Similar to AM…”
BackgroundThe antimicrobial protection hypothesis of Alzheimer’s disease
Moir, R. D., Lathe, R., & Tanzi, R. E. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.06.3040 · Cited by 456 · see citing works
“Consistent with identity as an AMP, administered synthetic Ab can be proinflammatory in the CNS [53] and anti-inflammatory in the periphery [54].”
BackgroundKent, S. A., Spires-Jones, T. L., & Durrant, C. S. (2020) · Acta Neuropathologica · doi:10.1007/s00401-020-02196-w · Cited by 446 · see citing works
The Physiological Roles of Amyloid-β Peptide Hint at New Ways to Treat Alzheimer's Disease
Brothers, H. M., Gosztyla, M. L., & Robinson, S. R. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00118 · Cited by 314 · see citing works
“It is important to note that protection in this model was associated with a hexameric form of Aß that reduces T-cell activation (Grant et al., 2012).”
BackgroundImmunology of relapse and remission in multiple sclerosis.
Steinman, L. (2014) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032713-120227 · Cited by 307 · see citing works
Self-citationLymphatic drainage system of the brain: A novel target for intervention of neurological diseases
Sun, B., Wang, L.-H., Yang, T., Sun, J., Mao, L., Yang, M., Yuan, H., Colvin, R. A., & Yang, X. (2017) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2017.08.007 · Cited by 255 · see citing works
Preventing Alzheimer’s Disease
Selkoe, D. J. (2012) · Science · doi:10.1126/science.1228541 · Cited by 378 · see citing works
Multiple sclerosis: Prospects and promise
Hauser, S. L., Chan, J. R., & Oksenberg, J. R. (2013) · Annals of Neurology · doi:10.1002/ana.24009 · Cited by 179 · see citing works
Iturria‐Medina, Y., Sotero, R. C., Toussaint, P. J., Evans, A. C., & Initiative, A. T. A. D. N. (2014) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1003956 · Cited by 176 · see citing works
Ferroptosis promotes T-cell activation-induced neurodegeneration in multiple sclerosis
Luoqian, J., Yang, W., Ding, X., Tuo, Q., Xiang, Z., Zheng, Z., Guo, Y., Li, L., Guan, P., Ayton, S., et al. (2022) · Cellular and Molecular Immunology · doi:10.1038/s41423-022-00883-0 · Cited by 189 · see citing works
Drainage of Cells and Soluble Antigen from the CNS to Regional Lymph Nodes
Laman, J. D., & Weller, R. O. (2013) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-013-9470-8 · Cited by 165 · see citing works
“Therapeutic relevance of CNS drainage is underscored by a very recent intriguing study that in Th1and Th17-driven EAE models, disease can be ameliorated by administration of Aβ (Grant et al. 2012).”
BackgroundFerretti, M. T., Merlini, M., Späni, C. B., Gericke, C., Schweizer, N., Enzmann, G. U., Engelhardt, B., Kulic, L., Suter, T. B., & Nitsch, R. M. (2016) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2016.02.009 · Cited by 174 · see citing works
Inflammatory pathways in Alzheimer’s disease mediated by gut microbiota
Qian, X.-H., Song, X.-X., Liu, X.-L., Chen, S.-D., & Tang, H.-D. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101317 · Cited by 153 · see citing works
Expansion of oligodendrocyte progenitor cells following SIRT1 inactivation in the adult brain
Rafalski, V. A., Ho, P. P.-K., Brett, J. O., Ucar, D., Dugas, J. C., Pollina, E. A., Chow, L. M. L., Ibrahim, A., Baker, S. J., Barres, B. A., et al. (2013) · Nature Cell Biology · doi:10.1038/ncb2735 · Cited by 145 · see citing works
Self-citationThe Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease
Kokiko-Cochran, O. N., & Godbout, J. P. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00672 · Cited by 128 · see citing works
“For example, a 2013 study revealed that peripheral administration of Aβ42 and Aβ40 attenuates paralysis and reduces neuroinflammation in multiple mouse models of experimental autoimmune encephalomyelitis (EAE) (142).”
BackgroundInsights into T‐cell dysfunction in Alzheimer's disease
Dai, L., & Shen, Y. (2021) · Aging Cell · doi:10.1111/acel.13511 · Cited by 119 · see citing works
Advances in the immunopathogenesis of multiple sclerosis
Yadav, S. K., Mindur, J. E., Ito, K., & Dhib-Jalbut, S. S. (2015) · Current Opinion in Neurology · doi:10.1097/wco.0000000000000205 · Cited by 166 · see citing works
Neural Plasticity in Multiple Sclerosis: The Functional and Molecular Background
Ksiazek-Winiarek, D. J., Szpakowski, P., & Glabinski, A. R. (2015) · Neural Plasticity · doi:10.1155/2015/307175 · Cited by 83 · see citing works
“These findings have made neuronal plasticity and personalized neurorehabilitation the focus of recent neuroscientific researchwith the identification of new therapeutic targets [22, 23].”
BackgroundBandyopadhyay, S., & Rogers, J. T. (2014) · Biochemical Pharmacology · doi:10.1016/j.bcp.2014.01.032 · Cited by 75 · see citing works
“Aβ40 and Aβ42 suppressed the proliferation capacity and cytokine secretion of activated lymphocytes that penetrated and damaged the CNS during EAE, reducing inflammation in lymphoid tissues and CNS parenchyma indicating that the beneficial and pathological roles of Aβ are dependent on whether the inflammation arises f…”
BackgroundResultThe role of T cells in the pathogenesis of Parkinson’s disease
Chen, Z., Chen, S., & Liu, J. (2018) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2018.08.002 · Cited by 78 · see citing works
“…crucial role in the induction of Th17 responses in the CNS (Contreras et al., 2016; Fitzgerald et al., 2014; Flynn et al., 2013; Garris et al., 2013; Grant et al., 2012; Guo et al., 2014; Kannan et al., 2015; McWilliams et al., 2015; Orsini et al., 2014; Saligrama et al., 2013; Wang et al., 2014b;…”
BackgroundAmyloid Fibrils Composed of Hexameric Peptides Attenuate Neuroinflammation
Kurnellas, M. P., Adams, C. M., Sobel, R., Steinman, L., & Rothbard, J. (2013) · Science Translational Medicine · doi:10.1126/scitranslmed.3005681 · Cited by 68 · see citing works
“The symptoms of EAE were exacerbated in mice lacking the expression of Ab A4 (6), the major prion protein (7), SAP (8), and tau (9) compared to wild-type animals.”
BackgroundResultInfluentialSelf-citationAPP Regulates Microglial Phenotype in a Mouse Model of Alzheimer's Disease
Manocha, G. D., Floden, A. M., Rausch, K., Kulas, J. A., McGregor, B. A., Rojanathammanee, L., Puig, K. L., Puig, K. L., Karki, S., Nichols, M. R., et al. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.4654-15.2016 · Cited by 64 · see citing works
“Indeed, prior work from other groups supports the idea that APP has a critical role in regulating overall immune phenotype (Grant et al., 2012; Kurnellas et al., 2014, 2015; Steinman et al., 2014).”
BackgroundImpact of vitamin D on neurocognitive function in dementia, depression, schizophrenia and ADHD.
Roy, N. M., Al-Harthi, L., Sampat, N. A., Al-Mujaini, R., Mahadevan, S., Adawi, S. A., Essa, M., Subhi, L. A. A., Al-Balushi, B., & Qoronfleh, M. (2021) · Frontiers in Bioscience · doi:10.2741/4908 · Cited by 64
“571 © 1996-2021 simply be ‘innocent bystanders’ when understanding the complex pathology of dementia (42).”
BackgroundThe virtuous cycle of human genetics and mouse models in drug discovery
Nadeau, J. H., & Auwerx, J. H. (2019) · Nature Reviews Drug Discovery · doi:10.1038/s41573-018-0009-9 · Cited by 71 · see citing works
Lucaciu, A., Brunkhorst, R., Pfeilschifter, J. M., Pfeilschifter, W., & Subburayalu, J. (2020) · Cells · doi:10.3390/cells9061515 · Cited by 65 · see citing works
Kurnellas, M. P., Brownell, S., Su, L., Malkovskiy, A., Rajadas, J., Dolganov, G., Chopra, S., Schoolnik, G., Sobel, R., Webster, J., et al. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.371229 · Cited by 62 · see citing works
“However, we have observed similar effects when amyloid peptides are used as treatment for EAE (48) and currently are exploring the molecular basis for these effects.”
BackgroundSelf-citationPhysiological Roles of Monomeric Amyloid-β and Implications for Alzheimer’s Disease Therapeutics
Jeong, H., Shin, H., Hong, S., & Kim, Y. S. (2022) · Experimental Neurobiology · doi:10.5607/en22004 · Cited by 56 · see citing works
“In addition, Aβ was also shown effective against EAE accelerated by proinflammatory T helper cells (TH1 and TH17) as it significantly decreased the severity of the disease and prevented the production of TH1 and TH17 related proinflammatory cytokines such as IL-6, IFN-γ, and IL-17 [139].”
BackgroundKokiko-Cochran, O., Ransohoff, L., Veenstra, M., Lee, S., Saber, M., Sikora, M., Teknipp, R., Xu, G., Bemiller, S., Wilson, G., et al. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2015.3970 · Cited by 49 · see citing works
Does α-Synuclein Have A Dual and Opposing Effect in Preclinical versus Clinical Parkinson’s Disease?
Markopoulou, K., Biernacka, J. M., Armasu, S. M., Anderson, K. J., Ahlskog, J., Chase, B., Chung, S., Cunningham, J., Farrer, M., Frigerio, R., et al. (2014) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2014.02.021 · Cited by 48
Pathoetiology of multiple sclerosis: are we barking up the wrong tree?
Stys, P. K. (2013) · F1000Prime Reports · doi:10.12703/p5-20 · Cited by 46 · see citing works
“Steinman and co-workers showed that administering exogenous Ab to mice significantly reduced the severity of EAE [74], a model that recapitulates the inflammatory reaction to myelin antigens.”
BackgroundInfluentialAlzheimer's disease: the potential therapeutic role of the natural antibiotic amyloid-β peptide.
Kumar, D., Eimer, W. A., Tanzi, R., & Moir, R. (2016) · Neurodegenerative Disease Management · doi:10.2217/nmt-2016-0035 · Cited by 41 · see citing works
CSF β-amyloid as a putative biomarker of disease progression in multiple sclerosis
Pietroboni, A., di Cola, F. S., Scarioni, M., Fenoglio, C., Spanó, B., Arighi, A., Cioffi, S. M. G., Oldoni, E., Riz, M. D. D., Basilico, P., et al. (2017) · Multiple Sclerosis · doi:10.1177/1352458516674566 · Cited by 38 · see citing works
β-Amyloid precursor protein (APP) and the human diseases
Nguyen, K. V. (2019) · AIMS neuroscience · doi:10.3934/neuroscience.2019.4.273 · Cited by 53 · see citing works
Amyloid precursor protein modulates macrophage phenotype and diet-dependent weight gain
Puig, K. L., Brose, S. A., Zhou, X.-D., Sens, M., Combs, G., Jensen, M., Golovko, M., & Combs, C. (2017) · Scientific Reports · doi:10.1038/srep43725 · Cited by 35 · see citing works
Immunotherapy in Alzheimer’s Disease: Do We Have All the Pieces of the Puzzle?
Sarazin, M., Dorothée, G., de Souza, L. C., & Aucouturier, P. (2013) · Biological Psychiatry · doi:10.1016/j.biopsych.2013.04.011 · Cited by 35 · see citing works
Apolipoprotein E mediation of neuro-inflammation in a murine model of multiple sclerosis
Shin, S., Walz, K. A., Archambault, A. S., Sim, J., Bollman, B. P., Koenigsknecht-Talboo, J., Cross, A. H., Holtzman, D. M., & Wu, G. F. (2014) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2014.03.010 · Cited by 32 · see citing works
Kokiko-Cochran, O. N., Saber, M., Puntambekar, S., Bemiller, S. M., Katsumoto, A., Lee, Y.-S., Bhaskar, K., Ransohoff, R. M., & Lamb, B. T. (2018) · Journal of Neurotrauma · doi:10.1089/neu.2017.5203 · Cited by 32 · see citing works
Inhibition of amyloid precursor protein secretases reduces recovery after spinal cord injury
Pajoohesh-Ganji, A., Burns, M. P., Pal-Ghosh, S., Tadvalkar, G., Hokenbury, N. G., Stepp, M. A., & Faden, A. I. (2014) · Brain Research · doi:10.1016/j.brainres.2014.02.049 · Cited by 29 · see citing works
“Using a mouse model of MS — experimental autoimmune encephalomyelitis (EAE) — investigators demonstrated that Aβ pep tide injections decreased paralysis and brain inflammation by suppressing activated lymphocytes (Grant et al., 2012).”
BackgroundResultInfluentialCSF β-amyloid predicts prognosis in patients with multiple sclerosis
Pietroboni, A., Caprioli, M., Carandini, T., Scarioni, M., Ghezzi, L., Arighi, A., Cioffi, S. M. G., Cinnante, C., Fenoglio, C., Oldoni, E., et al. (2018) · Multiple Sclerosis · doi:10.1177/1352458518791709 · Cited by 29 · see citing works
Crystallins and neuroinflammation: The glial side of the story
Dulle, J. E., & Fort, P. E. (2015) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2015.05.023 · Cited by 27 · see citing works
Role of Amyloid from a Multiple Sclerosis Perspective: A Literature Review
Chandra, A. (2015) · Neuroimmunomodulation · doi:10.1159/000375309 · Cited by 29 · see citing works
Role of amyloid-β CSF levels in cognitive deficit in MS
Gentile, A., Mori, F., Bernardini, S., & Centonze, D. (2015) · Clinica Chimica Acta · doi:10.1016/j.cca.2015.01.035 · Cited by 32 · see citing works
“Several studies in the experimental autoimmune encephalomyelitis (EAE), animal model of MS, address a role for Αβ in MS immune response: interestingly, on one hand immunization of mice with Αβ1-42 peptide induces EAE-like symptoms and pathology [126]; on the other hand, peripheral injection of Αβ1-42 or amyloid fibril…”
BackgroundHadar, A., Milanesi, E., Squassina, A., Niola, P., Chillotti, C., Pasmanik-Chor, M., Yaron, O., Pavel Martasek, E., Rehavi, M., Weissglas‐Volkov, D., et al. (2016) · Translational Psychiatry · doi:10.1038/tp.2016.179 · Cited by 31 · see citing works
Decreased plasma C‐reactive protein levels in APOE ε4 allele carriers
Martiskainen, H., Takalo, M., Solomon, A., Stančáková, A., Marttinen, M., Natunen, T., Haapasalo, A., Herukka, S., Kuusisto, J., Soininen, H. S., et al. (2018) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.639 · Cited by 25 · see citing works
No quiet surrender: molecular guardians in multiple sclerosis brain.
Steinman, L. (2015) · Journal of Clinical Investigation · doi:10.1172/jci74255 · Cited by 23 · see citing works
“Could amyloid molecules have a different role in MS (30, 31)?”
BackgroundResultInfluentialSelf-citation[Modern conception of the pathogenesis of neurodegenerative diseases and therapeutic strategy].
Litvinenko, I., Krasakov, I., Bisaga, G., Skulyabin, D., & Poltavsky, I. D. (2017) · Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova · doi:10.17116/jnevro2017117623-10 · Cited by 21 · see citing works
Xie, W., Fang, J., Shan, Z., Guo, J., Liao, Y., Zou, Z., Wang, J., Wen, S., Yang, L., Zhang, Y., et al. (2022) · Science Advances · doi:10.1126/sciadv.abo4250 · Cited by 19 · see citing works
“The reversal of inflammatory infiltration in EAE lesion has been found to be associated with improved disease prognosis ( 37 ).”
Krementsov, D. N., Wall, E. H., Martin, R. A., Subramanian, M., Noubade, R., del Río, R., Mawe, G. M., Bond, J. P., Poynter, M. E., Blankenhorn, E. P., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0062743 · Cited by 20 · see citing works
“In this regard, both pertussis toxin (PTX) [36] and complete Freund’s adjuvant (CFA) [37] lead to increased BBB permeability and systemic exposure to lipopolysaccharide (LPS) directly disrupts endothelial cell barrier functions [38] including BBB transport of amyloid proteins [39,40], which have recently been shown to…”
BackgroundKurnellas, M., Schartner, J. M., Fathman, C. G., Jagger, A. L., Steinman, L., & Rothbard, J. B. (2014) · The Journal of Experimental Medicine · doi:10.1084/jem.20140107 · Cited by 15 · see citing works
“This has been reported for knockouts of amyloid precursor protein (Grant et al., 2012), major prion protein (Gourdain et al.”
BackgroundSelf-citationShi, M., Chu, F., Tian, X., Aerqin, Q., Zhu, F., & Zhu, J. (2021) · The Neuroscientist · doi:10.1177/1073858420987224 · Cited by 14 · see citing works
Janus faces of amyloid proteins in neuroinflammation
Steinman, L., Rothbard, J. B., & Kurnellas, M. P. (2014) · Journal of Clinical Immunology · doi:10.1007/s10875-014-0034-3 · Cited by 14 · see citing works
Self-citationAxonal and Myelin Neuroprotection by the Peptoid BN201 in Brain Inflammation
Villoslada, P., Vila, G., Colafrancesco, V., Moreno, B., Fernández-Díez, B., Vázquez, R., Pertsovskaya, I., Zubizarreta, I., Pulido-Valdeolivas, I., Messeguer, J., et al. (2019) · Neurotherapeutics · doi:10.1007/s13311-019-00717-4 · Cited by 14 · see citing works
Self-citationThe Serum Amyloid β Level in Multiple Sclerosis: A Case- Control Study
Etemadifar, M., Ghadimi, M., Ghadimi, K., & Alsahebfosoul, F. (2017) · Caspian Journal of Neurological Sciences · doi:10.29252/nirp.cjns.3.11.214 · Cited by 13 · see citing works
“On the other hand, former studies suggested a protective role for the increased serum Aβ in the rat models of MS (15).”
BackgroundAmyloids in Site-Specific Autoimmune Reactions and Inflammatory Responses
Huang, Y., Hong, X., Shen, J. X., Geng, L.-J., Pan, Y.-H., Ling, W., & Zhao, H. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02980 · Cited by 16 · see citing works
Mørkholt, A. S., Kastaniegaard, K., Trabjerg, M., Gopalasingam, G., Niganze, W., Larsen, A., Stensballe, A., Nielsen, S., & Nieland, J. (2018) · Scientific Reports · doi:10.1038/s41598-018-25391-y · Cited by 11
Polepole, P., Bartenslager, A. C., Liu, Y., Petro, T. M., Fernando, S. C., & Zhang, L. (2020) · Journal of Medical Virology · doi:10.1002/jmv.26188 · Cited by 10 · see citing works
Nordberg, A., Kadir, A., Andreasen, N., Almkvist, O., Wall, A., Blennow, K., Långström, B., & Zetterberg, H. (2015) · Journal of Alzheimer's Disease · doi:10.3233/jad-132474 · Cited by 10 · see citing works
Emerging and Evolving Topics in Multiple Sclerosis Pathogenesis and Treatments
Flamme, A. C. L., & Orian, J. M. (2015) · Current topics in behavioral neurosciences · doi:10.1007/978-3-319-25543-9 · Cited by 7 · see citing works
Distinct responses of human peripheral blood cells to different misfolded protein oligomers
Leal‐Lasarte, M., Mannini, B., Chiti, F., Vendruscolo, M., Dobson, C. M., Roodveldt, C., & Pozo, D. (2021) · Immunology · doi:10.1111/imm.13377 · Cited by 8 · see citing works
“Interestingly, a significant reduction in human CD4+ T cells had been reported in the context of PD pathology [70– 72] whereas no significant changes have been found in the percentage of viable CD4+ T cells nor increases in proliferative responses after in vitro treatment with Aβ peptides [45,73].”
BackgroundTrudler, D., Levy-barazany, H., Nash, Y., Samuel, L., Sharon, R., & Frenkel, D. (2020) · Journal of Neurochemistry · doi:10.1111/jnc.14871 · Cited by 8
HIV-1 Tat protein attenuates the clinical course of experimental autoimmune encephalomyelitis (EAE)
Karampoor, S., Zahednasab, H., Bokharaei‐Salim, F., Mirzaei, R., Mojallal-Tabatabaei, Z., Esghaei, M., & Keyvani, H. (2019) · International Immunopharmacology · doi:10.1016/j.intimp.2019.105943 · Cited by 9 · see citing works
The role of APP in Alzheimer’s disease
Pung, L., Wang, X.-J., Li, M., & Xue, L. (2013) · Advances in Alzheimer s Disease · doi:10.4236/aad.2013.22008 · Cited by 8 · see citing works
“Finally, peripheral injection of Aβ peptides in an experimental autoimmune encephalomyelitis (EAE) animal model suppressed inflammation in lymphoid tissues, which further led to reduced brain inflammation and delayed occurrence of motor paralysis, suggest a neuroprotective effect of Aβ peptides in autoimmune diseases…”
Steinman, L., Axtell, R., Barbieri, D., Bhat, R., Brownell, S., de Jong, B. D., Dunn, S., Grant, J. L., Han, M. H., Ho, P., et al. (2013) · Multiple Sclerosis · doi:10.1177/1352458512470730 · Cited by 8 · see citing works
Self-citationKurnellas, M. P., Rothbard, J., & Steinman, L. (2015) · Current topics in behavioral neurosciences · doi:10.1007/7854_2015_377 · Cited by 7 · see citing works
Self-citationHuang, Z. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221042 · Cited by 12 · see citing works
Mahapatra, S., Ying, L.-H., Ho, P., Kurnellas, M. P., Rothbard, J., Steinman, L., & Cornfield, D. (2018) · PLoS ONE · doi:10.1371/journal.pone.0199206 · Cited by 6 · see citing works
Self-citationA protective mutation against Alzheimer disease?
Proft, J., & Weiss, N. (2012) · Communicative & Integrative Biology · doi:10.4161/cib.21799 · Cited by 6 · see citing works
“Hence, it was recently shown a protective effect of Ab in an experimental autoimmune encephalomyelistis (EAE) model of multiple sclerosis.(24) Considering that the A673T mutant reduces the production of Ab, it might be interesting to evaluate if a correlation exist between the presence of the mutation and an eventual…”
BackgroundKraus, A., Race, B., Phillips, K., Winkler, C. W., Saturday, G., Kurnellas, M. P., Rothbard, J., Groveman, B., Steinman, L., & Caughey, B. (2016) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2016.06.010 · Cited by 5 · see citing works
“Multiple lines of evidence demonstrate that amyloidfibrils canmodulate autoimmune processes and decrease the severity of paralysis in the murine model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE) (Grant et al., 2012; Kurnellas et al., 2013; Kurnellas et al., 2014).”
BackgroundSelf-citationSims, C. S., Vaughan, C., Theologis, H., Boal, A. L., & Osilla, K. (2015) · Rand health quarterly · doi:10.7249/rhq-05-02-17 · Cited by 5 · see citing works
Proft, J., & Weiss, N. (2012) · Communicative & Integrative Biology · doi:10.4161/cib.22571 · Cited by 5 · see citing works
Diversity of amyloid beta peptide actions
Mardanyan, S. S., Sharoyan, S. G., & Antonyan, A. A. (2024) · Reviews in the Neurosciences · doi:10.1515/revneuro-2023-0100 · Cited by 5 · see citing works
Shi, C., Cha, J., Gong, J.-Y., Wang, S., Zeng, P. H., Lian, J.-J., Zhang, B., Hua, Q., Lv, J., Du, C., et al. (2022) · Cells · doi:10.3390/cells11061004 · Cited by 4 · see citing works
beta-Amyloid: Enemy or Remedy?
Hohlfeld, R., & Wekerle, H. (2012) · Science Translational Medicine · doi:10.1126/scitranslmed.3004586 · Cited by 4 · see citing works
Pansieri, J., Pisa, M., Yee, S., Gutnikova, A., Ridgeon, E., Hickman, R., Spencer, J., Esiri, M., & DeLuca, G. (2024) · bioRxiv · doi:10.1002/ana.27231 · Cited by 3 · see citing works
Current Concepts in the Pathogenesis of Neurodegenerative Diseases and Treatment Strategies
Litvinenko, I., Krasakov, I., Bisaga, G., Skulyabin, D., & Poltavsky, I. D. (2019) · Neuroscience and Behavioral Physiology · doi:10.1007/s11055-019-00746-8 · Cited by 3 · see citing works
RGS2 and SIRT1 Link Renin Angiotensin Aldosterone System to Alzheimer’s Disease
Hadar, A., Gozes, I., & Gurwitz, D. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-803690-7.00012-0 · Cited by 28 · see citing works
APP as an innate injury-response molecule
Olmsted, Z. T., & Sofroniew, M. V. (2026) · Neurobiology of Disease · doi:10.1016/j.nbd.2026.107361 · Cited by 2 · see citing works
Nutrient‐sensing amyloid metastasis
Lima, L. M. T. R., & Sisnande, T. (2022) · BioFactors · doi:10.1002/biof.1825 · Cited by 5 · see citing works
A Journey in Science: The Privilege of Exploring the Brain and the Immune System
Steinman, L. (2016) · Molecular Medicine · doi:10.2119/molmed.2015.00263 · Cited by 2
Self-citationSteinman, L. (2014) · Revue neurologique (Paris) · doi:10.1016/j.neurol.2014.07.011 · Cited by 2 · see citing works
Self-citationTranslational molecular imaging and drug development in multiple sclerosis
Tay, D., Ahmed, H., Dawoud, A., Salam, M., Gobbi, L., Grether, U., Edelmann, M. R., Wittwer, M., Collin, L., Atz, K., et al. (2026) · Theranostics · doi:10.7150/thno.119559 · Cited by 1
“Indeed, various reports corroborated that the amyloid precursor protein (APP) accumulates in damaged axons [85-87] [88].”
Pyka‐Fościak, G., Jasek-Gajda, E., Wójcik, B., LIS, G. J., & Litwin, J. A. (2024) · Biomedicines · doi:10.3390/biomedicines12122770 · Cited by 4 · see citing works
Antipsychotics, versatility in action
Mahapatra, S., & Marques, T. R. (2021) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2108946118 · Cited by 1 · see citing works
Robinson, S. R., Brothers, H., & Gosztyla, M. L. (2018) · Neural Regeneration Research · doi:10.4103/1673-5374.241456 · Cited by 1 · see citing works
“Further, in four different mouse models of multiple sclerosis, intraperitoneal injections of hexameric Aβ40 or Aβ42 led to improvements in motor function, remyelination of lesions and reduced inflammation (Grant et al., 2012).”
BackgroundNeurological disorders: Two sides to β-amyloid
Jones, R. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3336 · Cited by 1
Khatami, S. H., Karima, S., Kondori, B. J., Sepandi, M., & Jangravi, Z. (2025) · Biotechnology and Applied Biochemistry · doi:10.1002/bab.2790
“A study conducted by Grant et al. [40] revealed that the injection of beta-amyloid into EAE mice markedly reversed paralysis and reduced the number of Th1-and Th17-positive T cells in the peripheral blood of EAE mice.”
Kwon, H. J., Santhosh, D., & Huang, Z. (2024) · bioRxiv · doi:10.1101/2024.06.13.598890
“In contrast, when employed under conditions that favor the monomer conformation, A β inhibits T cell activation ( Grant et al., 2012 ).”
Kwon, H. J., Santhosh, D., & Huang, Z. (2023) · bioRxiv · doi:10.1101/2023.07.24.550398
“Others have found that Aβ monomers inhibit T cell activation in the periphery (Grant et al., 2012).”
BackgroundInfluentialDavis, T. H. (2016) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.1600083113
Kim, H. Y., Kim, H., Jo, S., Lee, C. J., Choi, S. Y., Kim, D. J., & Kim, Y. (2015) · Nature Communications · doi:10.1038/ncomms9997
- Authors
- Grant, J. L., Ghosn, E. E. B., Axtell, R. C., Herges, K., Kuipers, H. F., Woodling, N. S., Andreasson, K., Herzenberg, L. A., Herzenberg, L. A., & Steinman, L.
- Affiliations
- Stanford University (US)
- Stanford Medicine (US)
- Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA.
- Corresponding author
- Steinman, Lawrence
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2012-08
- Volume
- 4
- Issue
- 145
- Pages
- 145ra105-145ra105
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC3677069
- OpenAlex
- W2143535578
- Cited by
- 92
- References
- 64
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 5 · 2023: 3 · 2022: 6 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 9 · 2017: 6 · 2016: 8 · 2015: 12 · 2014: 9 · 2013: 9 · 2012: 7
- FWCI
- 8.52
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1f31ai094869-01)
- U.S. Public Health Service (R0155997)
- National Institute on Aging (R01AG030209, R21AG033914)
- National Institute of Allergy and Infectious Diseases (R01AI076434, 1F31AI094869-01, F31 AI094869, R56AI076434, AI 076434)
- National Institute of Neurological Disorders and Stroke (R01NS055997)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- amyloid-beta 42, Aβ40, experimental autoimmune encephalomyelitis, multiple sclerosis, Th1 cells, Th17 cells, motor paralysis, neuroinflammation, adoptive transfer, amyloid precursor protein, peripheral administration, anti-inflammatory activity, inflammatory cytokines, chemokines, lymphocyte activation
- MeSH terms
- Animals, Cell Differentiation, Cell Survival, Cells, Cultured, Encephalomyelitis, Autoimmune, Experimental, Female, Flow Cytometry, Inflammation, Mice, Inbred C57BL, Paralysis, Amyloid beta-Peptides, Th1 Cells, Mice, Th17 Cells
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
