The DOI matches its Crossref record; 72 of the 72 references it cites were found in a registry or an index.
RAGE mediates Aβ accumulation in a mouse model of Alzheimer’s disease via modulation of β- and γ-secretase activity
Open accessAbstract
Receptor for Advanced Glycation End products (RAGE) has been implicated in amyloid β-peptide (Aβ)-induced perturbation relevant to the pathogenesis of Alzheimer's disease (AD). However, whether and how RAGE regulates Aβ metabolism remains largely unknown. Aβ formation arises from aberrant cleavage of amyloid pre-cursor protein (APP) by β- and γ-secretase. To investigate whether RAGE modulates β- and γ-secretase activity potentiating Aβ formation, we generated mAPP mice with genetic deletion of RAGE (mAPP/RO). These mice displayed reduced cerebral amyloid pathology, inhibited aberrant APP-Aβ metabolism by reducing β- and γ-secretases activity, and attenuated impairment of learning and memory compared with mAPP mice. Similarly, RAGE signal transduction deficient mAPP mice (mAPP/DN-RAGE) exhibited the reduction in Aβ40 and Aβ42 production and decreased β-and γ-secretase activity compared with mAPP mice. Furthermore, RAGE-deficient mAPP brain revealed suppression of activation of p38 MAP kinase and glycogen synthase kinase 3β (GSK3β). Finally, RAGE siRNA-mediated gene silencing or DN-RAGE-mediated signaling deficiency in the enriched human APP neuronal cells demonstrated suppression of activation of GSK3β, accompanied with reduction in Aβ levels and decrease in β- and γ-secretases activity. Our findings highlight that RAGE-dependent signaling pathway regulates β- and γ-secretase cleavage of APP to generate Aβ, at least in part through activation of GSK3β and p38 MAP kinase. RAGE is a potential therapeutic target to limit aberrant APP-Aβ metabolism in halting progression of AD.
Overview
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
Verification
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?
The cited source says what the claim attributes to it.
In the citing paper
“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 [43]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
1 retracted
Ma, H., Li, S., Xu, P., Babcock, S. A., Dolence, E. K., Brownlee, M., Li, J., & Ren, J. T. (2008) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2008.00547.x · Cited by 154
RetractedAnalysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method
Livak, K. J., & Schmittgen, T. D. (2001) · Methods · doi:10.1006/meth.2001.1262 · Cited by 180,860
Mutation of the mouse klotho gene leads to a syndrome resembling ageing
Kuro-o, M., Matsumura, Y., Aizawa, H., Kawaguchi, H., Suga, T., Utsugi, T., Ohyama, Y., Kurabayashi, M., Kaname, T., Kume, E., et al. (1997) · Nature · doi:10.1038/36285 · Cited by 3,837
Pathological roles of MAPK signaling pathways in human diseases
Kim, E. K., & Choi, E.-J. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2009.12.009 · Cited by 2,472
Amyloid Precursor Protein Processing and Alzheimer's Disease
O'Brien, R. J., & Wong, P. C. (2011) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-061010-113613 · Cited by 2,061
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-citationMucke, 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
Neeper, M. P., Schmidt, A. M., Brett, J., Yan, S. D., Wang, F., Pan, Y., Elliston, K. O., Stern, D., & SHAW, A. R. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)42138-2 · Cited by 1,545
Molecular cloning and expression of glycogen synthase kinase‐3/factor A.
Woodgett, J. R. (1990) · The EMBO Journal · doi:10.1002/j.1460-2075.1990.tb07419.x · Cited by 1,362
Understanding RAGE, the receptor for advanced glycation end products
Bierhaus, A., Humpert, P. M., Morcos, M., Wendt, T., Chavakis, T., Arnold, B., Stern, D. M., & Nawroth, P. P. (2005) · Journal of Molecular Medicine · doi:10.1007/s00109-005-0688-7 · Cited by 1,297
The 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
A Phase 3 Trial of Semagacestat for Treatment of Alzheimer's Disease
Doody, R. S., Raman, R., Farlow, M., Iwatsubo, T., Vellas, B., Joffe, S., Kieburtz, K., He, F., Sun, X., Thomas, R. G., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1210951 · Cited by 1,224
Translating cell biology into therapeutic advances in Alzheimer's disease
Selkoe, D. J. (1999) · Nature · doi:10.1038/399a023 · Cited by 1,166
BACE1 is the major β-secretase for generation of Aβ peptides by neurons
Cai, H., Wang, Y., McCarthy, D. B., Wen, H., Borchelt, D., Price, D. L., & Wong, P. C. (2001) · Nature Neuroscience · doi:10.1038/85064 · Cited by 1,087
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-citationLuo, Y., Bolon, B., Kahn, S., Bennett, B. D., Babu-Khan, S., Denis, P., Fan, W., Kha, H., Zhang, J., Gong, Y., et al. (2001) · Nature Neuroscience · doi:10.1038/85059 · Cited by 1,001
Du, H., Guo, L., Fang, F., Chen, D., Sosunov, A. A., McKhann, G. M., Yan, Y., Wang, C., Zhang, H., Molkentin, J. D., et al. (2008) · Nature Medicine · doi:10.1038/nm.1868 · Cited by 950
Functional gamma‐secretase inhibitors reduce beta‐amyloid peptide levels in brain
Dovey, H. F., John, V., Anderson, J. P., Chen, L. Z., Andrieu, P. D. S. I., Fang, L. Y., Freedman, S. B., Folmer, B., Goldbach, E. G., Holsztynska, E. J., et al. (2001) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2001.00012.x · Cited by 870
Schmidt, A. M., Vianna, M., Gerlach, M. L., Brett, J., Ryan, J., Kao, J. J., Esposito, C., Hegarty, H. M., Hurley, W. L., & Clauss, M. A. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)42137-0 · Cited by 833
The secretases: enzymes with therapeutic potential in Alzheimer disease
De Strooper, B., Vassar, R., & Golde, T. (2010) · Nature Reviews Neurology · doi:10.1038/nrneurol.2009.218 · Cited by 799
Mitochondrial Aβ: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease
Caspersen, C., Wang, N., Yao, J., Sosunov, A., Chen, X., Lustbader, J. W., Xu, H. W., Stern, D., McKhann, G., & Du Yan, S. (2005) · The FASEB Journal · doi:10.1096/fj.05-3735fje · Cited by 738
Wong, G. T., Manfra, D. J., Poulet, F. M., Zhang, Q., Josien, H. B., Bara, T. A., Engstrom, L., Pinzon-Ortiz, M. C., Fine, J. S., Lee, H.-J. J., et al. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m311652200 · Cited by 723
Roberds, S. L. (2001) · Human Molecular Genetics · doi:10.1093/hmg/10.12.1317 · Cited by 705
Early deficits in synaptic mitochondria in an Alzheimer's disease mouse model
Du, H., Guo, L., Yan, S., Sosunov, A. A., McKhann, G. M., & ShiDu Yan, S. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1006586107 · Cited by 704
Mitogen inactivation of glycogen synthase kinase-3β in intact cells via serine 9 phosphorylation
Stambolic, V., & Woodgett, J. R. (1994) · Biochemical Journal · doi:10.1042/bj3030701 · Cited by 581
Geling, A., Steiner, H., Willem, M., Bally‐Cuif, L., & Haass, C. (2002) · The EMBO Reports · doi:10.1093/embo-reports/kvf124 · Cited by 497
Proteases and Proteolysis in Alzheimer Disease: A Multifactorial View on the Disease Process
De Strooper, B. (2010) · Physiological Reviews · doi:10.1152/physrev.00023.2009 · Cited by 455
Regulation of Akt and glycogen synthase kinase-3β phosphorylation by sodium valproate and lithium
Sarno, P. D., Li, X., & Jope, R. S. (2002) · Neuropharmacology · doi:10.1016/s0028-3908(02)00215-0 · Cited by 440
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
BACE1 inhibitor drugs in clinical trials for Alzheimer’s disease
Vassar, R. J. (2014) · Alzheimer s Research & Therapy · doi:10.1186/s13195-014-0089-7 · Cited by 421
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
p38 Kinase Is Activated in the Alzheimer's Disease Brain
Hensley, K., Floyd, R. A., Zheng, N., Nael, R., Robinson, K. A., Nguyen, X., Pye, Q. N., Stewart, C. A., Geddes, J., Markesbery, W. R., et al. (1999) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1999.0722053.x · Cited by 373
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
Deficiency in neuronal TGF-β signaling promotes neurodegeneration and Alzheimer’s pathology
Tesseur, I., Zou, K., Esposito, L., Bard, F., Berber, E., Can, J. V., Lin, A. H., Crews, L., Tremblay, P., Mathews, P., et al. (2006) · Journal of Clinical Investigation · doi:10.1172/jci27341 · Cited by 355
Fang, 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
A γ‐secretase inhibitor decreases amyloid‐β production in the central nervous system
Bateman, R. J., Siemers, E. R., Mawuenyega, K. G., Wen, G., Browning, K. R., Sigurdson, W. C., Yarasheski, K. E., Friedrich, S. W., DeMattos, R. B., May, P. C., et al. (2009) · Annals of Neurology · doi:10.1002/ana.21623 · Cited by 322
Central 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-citationPINK1 signalling rescues amyloid pathology and mitochondrial dysfunction in Alzheimer’s disease
Du, F., Yu, Q., Yan, S., Hu, G., Lue, L., Walker, D., Wu, L., Yan, S. F., Tieu, K., & Yan, S. S. (2017) · Brain · doi:10.1093/brain/awx258 · Cited by 308
Glycogen Synthase Kinase-3β Facilitates Staurosporine- and Heat Shock-induced Apoptosis
Bijur, G. N., Sarno, P. D., & Jope, R. S. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.11.7583 · Cited by 301
Vassar, R. J., & Citron, M. (2000) · Neuron · doi:10.1016/s0896-6273(00)00051-9 · Cited by 299
Yuan, S., Ryder, J. W., Li, B., Wu, X., Fox, N. W., Solenberg, P., Brune, K. A., Paul, S. M., Zhou, Y., Liu, F., et al. (2004) · Biochemistry · doi:10.1021/bi035627j · Cited by 298
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-citationLessons from a failed γ-secretase Alzheimer trial
De Strooper, B. (2014) · Cell · doi:10.1016/j.cell.2014.10.016 · Cited by 277
Sasaki, N., Toki, S., Chowei, H., Saito, T., Nakano, N., Hayashi, Y., Takeuchi, M., & Makita, Z. (2001) · Brain Research · doi:10.1016/s0006-8993(00)03075-4 · Cited by 253
Developmental expression and localization of glycogen synthase kinase-3β in rat brain
Leroy, K., & Brion, J. (1999) · Journal of Chemical Neuroanatomy · doi:10.1016/s0891-0618(99)00012-5 · Cited by 242
Du, H., Guo, L., Zhang, W., Rydzewska, M., & Yan, S.-D. (2009) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.03.003 · Cited by 234
Munoz, L., Ranaivo, H. R., Roy, S. M., Hu, W., Craft, J. M., McNamara, L. K., Chico, L. W., Van Eldik, L. J., & Watterson, D. M. (2007) · Journal of Neuroinflammation · doi:10.1186/1742-2094-4-21 · Cited by 224
Pyo, H., Jou, I., Jung, S., Hong, S., & Joe, E.-H. (1998) · Neuroreport · doi:10.1097/00001756-199803300-00020 · Cited by 217
Comery, T. A., Martone, R. L., Aschmies, S., Atchison, K. P., Diamantidis, G., Gong, X., Zhou, H., Kreft, A. F., Pangalos, M. N., Sonnenberg‐Reines, J., et al. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.2693-05.2005 · Cited by 214
Origlia, 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
Hippocampal RAGE immunoreactivity in early and advanced Alzheimer’s disease
Miller, M. C., Tavares, R., Johanson, C. E., Hovanesian, V., Donahue, J. E., Gonzalez, L., Silverberg, G. D., & Stopa, E. G. (2008) · Brain Research · doi:10.1016/j.brainres.2008.06.124 · Cited by 194
RAGE and Alzheimer's Disease: A Progression Factor for Amyloid-β-Induced Cellular Perturbation?
Yan, S. D., Bierhaus, A., Nawroth, P. P., & Stern, D. M. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1030 · Cited by 184
BACE1 Deficiency Causes Altered Neuronal Activity and Neurodegeneration
Hu, X., Zhou, X., He, W., Yang, J., Xiong, W., Wong, P., Wilson, C. G., & Yan, R. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.1334-10.2010 · Cited by 162
β-secretase inhibitor; a promising novel therapeutic drug in Alzheimer’s disease
Menting, K. W., & Claassen, J. A. H. R. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00165 · Cited by 144
γ‐Secretase/presenilin inhibitors for Alzheimer's disease phenocopy Notch mutations in Drosophila
Micchelli, C. A., Esler, W. P., Kimberly, W. T., Jack, C. E., Berezovska, O., Kornilova, A. Y., Hyman, B. T., Perrimon, N., & Wolfe, M. S. (2002) · The FASEB Journal · doi:10.1096/fj.02-0394fje · Cited by 142
Nunan, J., Shearman, M. S., Checler, F., Cappai, R., Evin, G. M., Beyreuther, K., Masters, C. L., & Small, D. H. (2001) · European Journal of Biochemistry · doi:10.1046/j.0014-2956.2001.02465.x · Cited by 127
Amyloid-beta-induced neurotoxicity is reduced by inhibition of glycogen synthase kinase-3
Koh, S., Noh, M., & Kim, S. H. (2007) · Brain Research · doi:10.1016/j.brainres.2007.10.064 · Cited by 126
RAGE is a key cellular target for A -induced perturbation in Alzheimer s disease
Yan, S. S. (2011) · Frontiers in Bioscience-Scholar · doi:10.2741/265 · Cited by 108
The p38 MAP kinase signaling pathway in Alzheimer's disease
Johnson, G. (2003) · Experimental Neurology · doi:10.1016/s0014-4886(03)00268-1 · Cited by 106
Lee, K., Koh, S., Noh, M., Park, K. W., Lee, Y. J., & Kim, S. H. (2006) · Brain Research · doi:10.1016/j.brainres.2006.10.055 · Cited by 88
Du, F., Wang, Y., Zhang, Z., Du, H., Yan, S., Sun, Q., Zhong, C., Wu, L., Vangavaragu, J. R., Yan, S., et al. (2015) · Human Molecular Genetics · doi:10.1093/hmg/ddv241 · Cited by 86
Criscuolo, C., Fontebasso, V., Middei, S., Stazi, M., Ammassari‐Teule, M., Yan, S. S., & Origlia, N. (2017) · Scientific Reports · doi:10.1038/srep42370 · Cited by 83
Chang, Y., Tesco, G., Jeong, W. J., Lindsley, L., Eckman, E. A., Eckman, C. B., Tanzi, R. E., & Guénette, S. Y. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m309561200 · Cited by 78
Methylglyoxal Induces Tau Hyperphosphorylation via Promoting AGEs Formation
Li, X., Xie, J., Jiang, X., Lv, B.-L., Cheng, X., Du, L., Zhang, J. Y., Wang, J., & Zhou, X. (2012) · NeuroMolecular Medicine · doi:10.1007/s12017-012-8191-0 · Cited by 72
Origlia, N., Criscuolo, C., Arancio, O., Yan, S., & Domenici, L. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.0141-14.2014 · Cited by 57
Advances in the identification of γ-secretase inhibitors for the treatment of Alzheimer's disease
D’Onofrio, G., Panza, F., Frisardi, V., Solfrizzi, V., Imbimbo, B. P., Paroni, G., Cascavilla, L., Seripa, D., & Pilotto, A. (2011) · Expert Opinion on Drug Discovery · doi:10.1517/17460441.2012.645534 · Cited by 52
Du, F., Zhang, Z., Li, H., Yu, Q., Douglas, J. T., Bratasz, A., Kuppusamy, P., & Yan, S. S. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150917 · Cited by 48
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
Molecular Rationale for the Pharmacological Treatment of Alzheimer??s Disease
Zimmermann, M., Gardoni, F., & Luca, M. D. (2005) · Drugs & Aging · doi:10.2165/00002512-200522001-00003 · Cited by 41
Genetic deficiency of neuronal RAGE protects against AGE-induced synaptic injury
Zhang, H., Wang, Y., Yan, S., Wu, L., Wu, L., Yan, S. S. D., & Yan, S. S. D. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.248 · Cited by 40
Jack, C. E., Berezovska, O., Wolfe, M. S., & Hyman, B. T. (2001) · Molecular Brain Research · doi:10.1016/s0169-328x(01)00010-9 · Cited by 26
Cited by
Sorted by citations
Hypertension, Neurovascular Dysfunction, and Cognitive Impairment
Santisteban, M. M., Iadecola, C., & Carnevale, D. (2022) · Hypertension · doi:10.1161/hypertensionaha.122.18085 · Cited by 317
Paudel, Y. N., Angelopoulou, E., Piperi, C., Othman, I., Aamir, K., & Shaikh, M. F. (2020) · Cells · doi:10.3390/cells9020383 · Cited by 257
Pathophysiology of RAGE in inflammatory diseases
Dong, H., Zhang, Y., Huang, Y., & Deng, H. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.931473 · Cited by 268
Involvement of p38 MAPK in Synaptic Function and Dysfunction
Falcicchia, C., Tozzi, F., Arancio, O., Watterson, D. M., & Origlia, N. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21165624 · Cited by 251
Amyloidosis in Alzheimer’s Disease: Pathogeny, Etiology, and Related Therapeutic Directions
Ma, C., Hong, F., & Yang, S. (2022) · Molecules · doi:10.3390/molecules27041210 · Cited by 243
Metadata
- Authors
- Fang, F., Yu, Q., Arancio, O., Chen, D., Gore, S. S., Yan, S. S., & Yan, S. F.
- Affiliations
- University of Kansas (US)
- Columbia University (US)
- Corresponding author
- Yan, Shirley ShiDu
- Yan, Shi Fang
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2018-01-10
- Volume
- 27
- Issue
- 6
- Pages
- 1002-1014
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- PMC
- PMC6075512
- OpenAlex
- W2782715813
- Cited by
- 103
- References
- 72
- Citations by year
- 2026: 16 · 2025: 12 · 2024: 11 · 2023: 12 · 2022: 17 · 2021: 17 · 2020: 13 · 2019: 2 · 2018: 3
- FWCI
- 6.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Human Molecular Genetics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Health (R37AG037319, R01AG044793, R01AG053041, R01NS089116)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- receptor for advanced glycation end products, Alzheimer's disease, amyloid-beta deposition, beta-secretase, gamma-secretase, amyloid precursor protein, GSK3β, p38 MAPK, APP processing, learning and memory impairment, therapeutic target
- MeSH terms
- Receptor for Advanced Glycation End Products, Glycogen Synthase Kinase 3 beta, Alzheimer Disease, Animals, Brain, Disease Models, Animal, Humans, Memory, Mice, Transgenic, Neurons, Signal Transduction, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, p38 Mitogen-Activated Protein Kinases, Mice, Amyloid Precursor Protein Secretases
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
