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Microglial Receptor for Advanced Glycation End Product-Dependent Signal Pathway Drives β-Amyloid-Induced Synaptic Depression and Long-Term Depression Impairment in Entorhinal Cortex
Open accessAbstract
Overproduction of β-amyloid (Aβ) is a pathologic feature of Alzheimer's disease, leading to cognitive impairment. Here, we investigated the impact of cell-specific receptor for advanced glycation end products (RAGE) on Aβ-induced entorhinal cortex (EC) synaptic dysfunction. We found both a transient depression of basal synaptic transmission and inhibition of long-term depression (LTD) after the application of Aβ in EC slices. Synaptic depression and LTD impairment induced by Aβ were rescued by functional suppression of RAGE. Remarkably, the rescue was only observed in slices from mice expressing a defective form of RAGE targeted to microglia, but not in slices from mice expressing defective RAGE targeted to neurons. Moreover, we found that the inflammatory cytokine IL-1β (interleukin-1β) and stress-activated kinases [p38 MAPK (p38 mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase)] were significantly altered and involved in RAGE signaling pathways depending on RAGE expression in neuron or microglia. These findings suggest a prominent role of microglial RAGE signaling in Aβ-induced EC synaptic dysfunction.
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“AGEs and the receptor for advanced glycation end-products (RAGE) can play an important role in AD pathogenesis as higher levels of RAGE expression in neuronal, microglial, and endothelial cells in patients with AD compared with age-matched, non- demented controls are found [43,44,45,46].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [44]
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“Binding of Aβ to the microglial SR-J1 (also called RAGE) activates MAPK and NF-κB and contributes to synaptic dysfunction through IL-1β release in 2- to 3-month-old animals139.”
From Microglia in neurodegeneration (2018) · cites this paper as [139]
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“Furthermore, AGEs cross-linked with Aβ can also decrease the ability of microglia to clear plaques113.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [113]
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Inflammation and Alzheimer’s disease
Akiyama, H. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00124-x · Cited by 4,514
Alzheimer's Disease Is a Synaptic Failure
Selkoe, D. J. (2002) · Science · doi:10.1126/science.1074069 · Cited by 4,420
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
Triple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126
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
Diffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
Lambert, M. P., Barlow, A. K., Chromy, B. A., Edwards, C., Freed, R., Liosatos, M., Morgan, T. E., Rozovsky, I., Trommer, B., Viola, K. L., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.11.6448 · Cited by 3,506
SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase
Bennett, B. L., Sasaki, D. T., Murray, B. W., O'Leary, E. C., Sakata, S. T., Xu, W., Leisten, J. C., Motiwala, A., Pierce, S., Satoh, Y., et al. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.251194298 · Cited by 2,558
RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease
Yan, S. D., Chen, X., Fu, J., Chen, M., Zhu, H., Roher, A., Slattery, T., Zhao, L., Nagashima, M., Morser, J., et al. (1996) · Nature · doi:10.1038/382685a0 · Cited by 2,012
Self-citationRAGE Mediates a Novel Proinflammatory Axis
Hofmann, M. A., Drury, S., Fu, C., Qu, W., Taguchi, A., Lu, Y., Avila, C., Kambham, N., Bierhaus, A., Nawroth, P., et al. (1999) · Cell · doi:10.1016/s0092-8674(00)80801-6 · Cited by 1,864
Mucke, L., Masliah, E., Yu, G.-Q., Mallory, M., Rockenstein, E. M., Tatsuno, G., Hu, K., Kholodenko, D., Johnson-Wood, K., & McConlogue, L. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-11-04050.2000 · Cited by 1,856
Regulation of NMDA receptor trafficking by amyloid-β
Snyder, E. M., Nong, Y., Almeida, C. G., Paul, S., Moran, T., Choi, E. Y., Nairn, A. C., Salter, M. W., Lombroso, P. J., Gouras, G. K., et al. (2005) · Nature Neuroscience · doi:10.1038/nn1503 · Cited by 1,561 · cited 7×
“…LTP (Origlia et al., 2008, 2009) depressed synaptic transmission and impaired a second form of long-term synaptic plasticity, namely the LTD, by increasing the synaptic removal of glutamate receptors (Snyder et al., 2005; Tyszkiewicz and Yan, 2005; Hsieh et al., 2006; Parameshwaran et al., 2007).”
InfluentialRAGE mediates amyloid-β peptide transport across the blood-brain barrier and accumulation in brain
Deane, R., Du Yan, S., Submamaryan, R. K., LaRue, B., Jovanovic, S., Hogg, E., Welch, D., Manness, L., Lin, C., Yu, J., et al. (2003) · Nature Medicine · doi:10.1038/nm890 · Cited by 1,426
ABAD Directly Links Aß to Mitochondrial Toxicity in Alzheimer's Disease
Lustbader, J. W., Cirilli, M., Lin, C., Xu, H. W., Takuma, K., Wang, N., Caspersen, C., Chen, X., Pollak, S., Chaney, M., et al. (2004) · Science · doi:10.1126/science.1091230 · Cited by 1,303
Self-citationThe multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses
Schmidt, A. M., Yan, S. D., Yan, S. F., & Stern, D. M. (2001) · Journal of Clinical Investigation · doi:10.1172/jci14002 · Cited by 1,256
Self-citationPlaque-independent disruption of neural circuits in Alzheimer’s disease mouse models
Hsia, A. Y., Masliah, E., McConlogue, L., Yu, G.-Q., Tatsuno, G., Hu, K., Kholodenko, D., Malenka, R. C., Nicoll, R. A., & Mucke, L. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.6.3228 · Cited by 1,123
AMPAR Removal Underlies Aβ-Induced Synaptic Depression and Dendritic Spine Loss
Hsieh, H., Boehm, J., Sato, C., Iwatsubo, T., Tomita, T., Sisodia, S., & Malinow, R. (2006) · Neuron · doi:10.1016/j.neuron.2006.10.035 · Cited by 1,042
The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses
Schmidt, A. M., Yan, S. D., Yan, S. F., et al. (2001) · Journal of Clinical Investigation · doi:10.1172/jci200114002 · Cited by 1,039
Self-citationLi, S., Hong, S., Shepardson, N. E., Walsh, D. M., Shankar, G. M., & Selkoe, D. (2009) · Neuron · doi:10.1016/j.neuron.2009.05.012 · Cited by 972
Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice
Chapman, P. F., White, G. L., Jones, M. W., Cooper-Blacketer, D., Marshall, V. J., Irizarry, M., Younkin, L., Good, M. A., Bliss, T. V. P., Hyman, B. T., et al. (1999) · Nature Neuroscience · doi:10.1038/6374 · Cited by 946
Functional organization of the extrinsic and intrinsic circuitry of the parahippocampal region
Witter, M. P., Groenewegen, H. J., Lopes, F. H. D. S., & Lohman, A. H. M. (1989) · Progress in Neurobiology · doi:10.1016/0301-0082(89)90009-9 · Cited by 918
Staging of Alzheimer-Related Cortical Destruction
Braak, H., Braak, E., & Bohl, J. (2008) · European Neurology · doi:10.1159/000116984 · Cited by 836 · cited 2×
“, 2008), two vulnerable areas in AD (Braak and Braak, 1991) that play a crucial role in learning and memory (Witter et al., 1989; Braak et al., 1993; Suzuki and Amaral, 2004).”
BackgroundRas and Rap control AMPA receptor trafficking during synaptic plasticity
Zhu, J. J., Qin, Y., Zhao, M., Van Aelst, L., & Malinow, R. (2002) · Cell · doi:10.1016/s0092-8674(02)00897-8 · Cited by 769
Early Aβ accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain
Ingelsson, M., Fukumoto, H., Newell, K. L., Growdon, J. H., Hedley–Whyte, E. T., Frosch, M. P., Albert, M. S., Hyman, B. T., & Irizarry, M. C. (2004) · Neurology · doi:10.1212/01.wnl.0000115115.98960.37 · Cited by 666
Wendt, T., Tanji, N., Guo, J., Kislinger, T., Qu, W., Lu, Y., Bucciarelli, L. G., Rong, L., Moser, B., Markowitz, G. S., et al. (2003) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)63909-0 · Cited by 599
Demonstration of amyloid deposits and neurofibrillary changes in whole brain sections
Braak, H., & Braak, E. (1991) · Brain Pathology · doi:10.1111/j.1750-3639.1991.tb00661.x · Cited by 598
Vitolo, O. V., Sant'Angelo, A., Costanzo, V., Battaglia, F., Arancio, O., & Shelanski, M. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.172504199 · Cited by 534
Self-citationWang, H.-W., Pasternak, J. F., Kuo, H., Ristic, H., Lambert, M. P., Chromy, B., Viola, K. L., Klein, W. L., Stine, W. B., Krafft, G. A., et al. (2002) · Brain Research · doi:10.1016/s0006-8993(01)03058-x · Cited by 527
MORISHIMA, Y., Gotoh, Y., Zieg, J., Barrett, T., Takano, H., Flavell, R. A., Davis, R. J., Shirasaki, Y., & Greenberg, M. E. (2001) · Journal of Neuroscience · doi:10.1523/jneurosci.21-19-07551.2001 · Cited by 486
Lue, L.-F., Walker, D. G., Brachova, L., Beach, T. G., Rogers, J., Schmidt, A. M., Stern, D. M., & Yan, S. D. (2001) · Experimental Neurology · doi:10.1006/exnr.2001.7732 · Cited by 439
Self-citationWang, Q., Walsh, D. M., Rowan, M. J., Selkoe, D. J., & Anwyl, R. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.1633-03.2004 · Cited by 437
Yan, S. D., Zhu, H., Fu, J., Yan, S. F., Roher, A. E., Tourtellotte, W. W., Rajavashisth, T. B., Chen, X., Godman, G. C., Stern, D. M., et al. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.10.5296 · Cited by 429
Self-citationActions of TNF‐α on glutamatergic synaptic transmission in the central nervous system
Pickering, M., Cumiskey, D., & O'Connor, J. J. (2005) · Experimental Physiology · doi:10.1113/expphysiol.2005.030734 · Cited by 421
Anderson, W. W., & Collingridge, G. L. (2001) · Journal of Neuroscience Methods · doi:10.1016/s0165-0270(01)00374-0 · Cited by 420
Sasahara, M., Fries, J. W. U., Raines, E. W., Gown, A. M., Westrum, L. E., Frosch, M. P., Bonthron, D. T., Ross, R., & Collins, T. (1991) · Cell · doi:10.1016/0092-8674(91)90223-l · Cited by 411
Yan, S. D., Yan, S. F., Chen, X., Fu, J., Chen, M., Kuppusamy, P., Smith, M. A., Perry, G., Godman, G. C., Nawroth, P., et al. (1995) · Nature Medicine · doi:10.1038/nm0795-693 · Cited by 406
Self-citationProgressive age‐related development of Alzheimer‐like pathology in APP/PS1 mice
Trinchese, F., Liu, S., Battaglia, F., Walter, S., Mathews, P. M., & Arancio, O. (2004) · Annals of Neurology · doi:10.1002/ana.20101 · Cited by 384
Self-citationSecondary structure of amyloid beta peptide correlates with neurotoxic activity in vitro.
Simmons, L. K., May, P. C., Tomaselli, K. J., Rydel, R. E., Fuson, K. S., Brigham, E. F., Wright, S., Lieberburg, I. M., Becker, G. W., & Brems, D. N. (1994) · Molecular Pharmacology · doi:10.1016/s0026-895x(25)10007-2 · Cited by 371
Central role of RAGE-dependent neointimal expansion in arterial restenosis
Sakaguchi, T., Yan, S. F., Yan, S. D., Belov, D., Rong, L., Sousa, M. M., Andrassy, M., Marso, S. P., Duda, S., Arnold, B., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci17115 · Cited by 371
Self-citationFang, F., Lue, L.-F., Yan, S., Xu, H., Luddy, J. S., Chen, D., Walker, D. G., Stern, D. M., Yan, S., Schmidt, A. M., et al. (2010) · The FASEB Journal · doi:10.1096/fj.09-139634 · Cited by 335
Self-citationRAGE potentiates Aβ‐induced perturbation of neuronal function in transgenic mice
Arancio, O., Zhang, H. P., Chen, X., Lin, C., Trinchese, F., Puzzo, D., Liu, S., Hegde, A. N., Yan, S. F., Stern, A., et al. (2004) · The EMBO Journal · doi:10.1038/sj.emboj.7600415 · Cited by 333
Self-citationCentral role of RAGE-dependent neointimal expansion in arterial restenosis
Sakaguchi, T., Yan, S. F., Yan, S. D., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200317115 · Cited by 313
Self-citationLali, F. V., Hunt, A. E., Turner, S. J., & Foxwell, B. M. J. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.10.7395 · Cited by 304
Walsh, D. M., Townsend, M., Podlisny, M. B., Shankar, G. M., Fadeeva, J. V., El‐Agnaf, O. M. A., Hartley, D. M., & Selkoe, D. J. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.4391-04.2005 · Cited by 295
RAGE-mediated signaling contributes to intraneuronal transport of amyloid-β and neuronal dysfunction
Takuma, K., Fang, F., Zhang, W., Yan, S., Fukuzaki, E., Du, H., Sosunov, A., McKhann, G., Funatsu, Y., Nakamichi, N., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0905686106 · Cited by 290
Self-citationS100B/RAGE-dependent activation of microglia via NF-κB and AP-1
Bianchi, R., Giambanco, I., & Donato, R. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.05.017 · Cited by 280
ABAD enhances Aβ‐induced cell stress via mitochondrial dysfunction
Takuma, K., Yao, J., Huang, J., Xu, H., Chen, X., Luddy, J. S., Trillat, A., Stern, D. M., Arancio, O., & Yan, S. S. (2005) · The FASEB Journal · doi:10.1096/fj.04-2582fje · Cited by 254
Self-citationAMPA receptor downscaling at the onset of Alzheimer's disease pathology in double knockin mice
Chang, E. H., Savage, M. J., Flood, D. G., Thomas, J. M., Levy, R. B., Mahadomrongkul, V., Shirao, T., Aoki, C., & Huerta, P. T. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0507313103 · Cited by 225
beta-Amyloid-induced neuronal apoptosis requires c-Jun N-terminal kinase activation
Troy, C. M., Rabacchi, S. A., Xu, Z., Maroney, A. C., Connors, T. J., Shelanski, M. L., & Greene, L. A. (2001) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2001.t01-1-00218.x · Cited by 223
Dual MAP kinase pathways mediate opposing forms of long-term plasticity at CA3–CA1 synapses
Bolshakov, V. Y., Carboni, L., Cobb, M. H., Siegelbaum, S. A., & Belardetti, F. (2000) · Nature Neuroscience · doi:10.1038/80624 · Cited by 217
RAGE: A Potential Target for Aβ-Mediated Cellular Perturbation in Alzheimers Disease
Yan, S. F., Chen, X., Walker, D. G., Schmidt, A. M., Arancio, O., & Lue, L. (2007) · Current Molecular Medicine · doi:10.2174/156652407783220741 · Cited by 207
Self-citationOriglia, N., Righi, M., Capsoni, S., Cattaneo, A., Fang, F., Stern, D. M., Chen, J. X., Schmidt, A. M., Arancio, O., Yan, S. D., et al. (2008) · Journal of Neuroscience · doi:10.1523/jneurosci.0204-08.2008 · Cited by 206
Self-citationKim, J., Anwyl, R., Suh, Y., Djamgoz, M. B. A., & Rowan, M. J. (2001) · Journal of Neuroscience · doi:10.1523/jneurosci.21-04-01327.2001 · Cited by 186
Kelly, A. M., Vereker, E., Nolan, Y. M., Brady, M., Barry, C. E., Loscher, C. E., Mills, K. H. G., & Lynch, M. A. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m301938200 · Cited by 182
Chen, Q.-S., Wei, W., Shimahara, T., & Xie, C.-W. (2002) · Neurobiology of Learning and Memory · doi:10.1006/nlme.2001.4034 · Cited by 176
JNK activation is associated with intracellular β-amyloid accumulation
Shoji, M., Iwakami, N., Takeuchi, S., Waragai, M., Suzuki, M., Kanazawa, I., Lippa, C. F., Ono, S., & Okazawa, H. (2000) · Molecular Brain Research · doi:10.1016/s0169-328x(00)00245-x · Cited by 167
Pei, J.-J., Braak, E., Braak, H., Grundke-Iqbal, I., Iqbal, K., Winblad, B., & Cowburn, R. F. (2001) · Journal of Alzheimer's Disease · doi:10.3233/jad-2001-3107 · Cited by 165
Abeta 17-42 in Alzheimer's disease activates JNK and caspase-8 leading to neuronal apoptosis
Wei, W. (2002) · Brain · doi:10.1093/brain/awf205 · Cited by 155
Zhao, D., Watson, J. B., & Xie, C.-W. (2004) · Journal of Neurophysiology · doi:10.1152/jn.00485.2004 · Cited by 152
Coogan, A. N., O'Neill, L. A. J., & O'Connor, J. J. (1999) · Neuroscience · doi:10.1016/s0306-4522(99)00100-1 · Cited by 129
Preventing Activation of Receptor for Advanced Glycation Endproducts in Alzheimers Disease
Lue, L.-F., Yan, S. D., Stern, D. F., & Walker, D. G. (2005) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1568007054038210 · Cited by 126
Self-citationHuang, C., Lee, C., & Hsu, K. (2004) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2003.02307.x · Cited by 120
Minogue, A. M., Schmid, A. W., Fogarty, M. P., Moore, A. C., Campbell, V. A., Herron, C. E., & Lynch, M. A. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m302530200 · Cited by 117
Rush, A. M., Wu, J., Rowan, M. J., & Anwyl, R. (2002) · Journal of Neuroscience · doi:10.1523/jneurosci.22-14-06121.2002 · Cited by 116
Functional Neuroanatomy of the Medial Temporal Lobe Memory System
SUZUKI, W., & AMARAL, D. (2004) · Cortex · doi:10.1016/s0010-9452(08)70958-4 · Cited by 111
Chang, J. S., Wendt, T., Qu, W., Kong, L., Zou, Y. S., Schmidt, A. M., & Yan, S. (2008) · Circulation Research · doi:10.1161/circresaha.107.165308 · Cited by 110
Self-citationCurran, B. P., Murray, H. J., & O'Connor, J. J. (2003) · Neuroscience · doi:10.1016/s0306-4522(02)00941-7 · Cited by 107
NMDA receptor regulation by amyloid-β does not account for its inhibition of LTP in rat hippocampus
Raymond, C. R., Ireland, D. R., & Abraham, W. C. (2003) · Brain Research · doi:10.1016/s0006-8993(03)02269-8 · Cited by 94
Shemer, I., Holmgren, C. D., Min, R., Fülöp, L., Zilberter, M. Y., Sousa, K. M., Farkas, T., Härtig, W., Penke, B., Burnashev, N., et al. (2006) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2006.04733.x · Cited by 86
Li, Q., Maynard, C. J., Cappai, R., McLean, C., Cherny, R. A., Lynch, T., Culvenor, J. G., Trevaskis, J., Tanner, J. E., Bailey, K. A., et al. (1999) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1999.0722479.x · Cited by 73
Amyloid β‐peptide Aβ1–42 but not Aβ1–40 attenuates synaptic AMPA receptor function
Parameshwaran, K., Sims‐Robinson, C., Kanju, P. M., Vaithianathan, T., Shonesy, B. C., Dhanasekaran, M., Bahr, B. A., & Suppiramaniam, V. D. (2007) · Synapse · doi:10.1002/syn.20386 · Cited by 71
Li, X., Li, C., Yu, S., Chen, J., Sabapathy, K., & Ruan, D. (2007) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2006.05300.x · Cited by 70
Surface Plasmon Resonance and Nuclear Magnetic Resonance Studies of ABAD−Aβ Interaction
Yan, Y., Liu, Y., Sorci, M., Belfort, G., Lustbader, J. W., Yan, S. S., & Wang, C. (2007) · Biochemistry · doi:10.1021/bi061314n · Cited by 67
Self-citationSimm, A., Caßelmann, C. A., Schubert, A., Hofmann, S., Reimann, A., & Silber, R. (2004) · Experimental Gerontology · doi:10.1016/j.exger.2003.12.006 · Cited by 66
Fogarty, M. P., Downer, E. J., & Campbell, V. A. (2003) · Biochemical Journal · doi:10.1042/bj20021660 · Cited by 66
β‐Amyloid Induces Oxidative DNA Damage and Cell Death through Activation of c‐Jun N Terminal Kinase
Jang, J.-H., & Surh, Y. (2002) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2002.tb04639.x · Cited by 54
Origlia, N., Capsoni, S., Cattaneo, A., Fang, F., Arancio, O., Yan, S. D., & Domenici, L. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1045 · Cited by 53
Self-citationPesavento, E., Capsoni, S., Domenici, L., & Cattaneo, A. (2002) · European Journal of Neuroscience · doi:10.1046/j.1460-9568.2002.01937.x · Cited by 52
Self-citationTyszkiewicz, J. P., & Yan, Z. (2005) · Journal of Neurophysiology · doi:10.1152/jn.00939.2004 · Cited by 51
Patterns of synaptic activity in forward and feedback pathways within rat visual cortex
Domenici, L., Harding, G. W., & Burkhalter, A. (1995) · Journal of Neurophysiology · doi:10.1152/jn.1995.74.6.2649 · Cited by 50
Self-citationInterleukin‐1β abrogates long‐term depression of hippocampal CA1 synaptic transmission
Ikegaya, Y., Delcroix, I., Iwakura, Y., Matsuki, N., & Nishiyama, N. (2002) · Synapse · doi:10.1002/syn.10154 · Cited by 49
Anisomycin activates p38 MAP kinase to induce LTD in mouse primary visual cortex
Xiong, W., Kojić, L., Zhang, L., Prasad, S. S., Douglas, R., Wang, Y., & Cynader, M. S. (2006) · Brain Research · doi:10.1016/j.brainres.2006.02.015 · Cited by 44
P38 Activation Mediates Amyloid-β Cytotoxicity
Zhu, X., Mei, M. G., Lee, H., Wang, Y., Han, J., Perry, G. L., & Smith, M. A. (2005) · Neurochemical Research · doi:10.1007/s11064-005-6872-x · Cited by 42
NMDA Receptor-Dependent Long-Term Synaptic Depression in the Entorhinal Cortex In Vitro
Kourrich, S., & Chapman, C. A. (2003) · Journal of Neurophysiology · doi:10.1152/jn.00714.2002 · Cited by 33
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Metadata
- Authors
- Origlia, N., Bonadonna, C., Rosellini, A., Leznik, E., Arancio, O., Yan, S. S., & Domenici, L.
- Affiliations
- Neuroscience Institute (IT)
- Columbia University (US)
- University of L'Aquila (IT)
- Corresponding author
- Domenici, Luciano
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-08-25
- Volume
- 30
- Issue
- 34
- Pages
- 11414-11425
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3842472
- OpenAlex
- W2015426193
- Cited by
- 111
- References
- 82
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 6 · 2023: 9 · 2022: 11 · 2021: 10 · 2020: 4 · 2019: 7 · 2018: 4 · 2017: 10 · 2016: 5 · 2015: 6 · 2014: 13 · 2013: 7 · 2012: 8
- FWCI
- 3.81
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- KU ScholarWorks (University of Kansas) (submittedVersion, other-oa)
- Archivio Istituzionale della Ricerca - Università degli Studi dell Aquila (submittedVersion)
- Funders
- American Health Assistance Foundation
- Regione Toscana
- National Institutes of Health
- National Institute on Aging (P01AG017490, P01 AG 17490)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- receptor for advanced glycation end products, RAGE, amyloid-beta, Alzheimer's disease, entorhinal cortex, synaptic depression, long-term depression, microglia, synaptic dysfunction, IL-1β, p38 MAPK, JNK, neuroinflammation
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Mice, Inbred C57BL, Mice, Transgenic, Neural Inhibition, Receptors, Immunologic, Signal Transduction, Amyloid beta-Peptides, Glycation End Products, Advanced, Microglia, Mice, Knockout, Entorhinal Cortex, Long-Term Synaptic Depression, Mice
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