Cerebrolysin modulates pronerve growth factor/nerve growth factor ratio and ameliorates the cholinergic deficit in a transgenic model of Alzheimer’s disease
Abstract
Alzheimer's disease (AD) is characterized by degeneration of neocortex, limbic system, and basal forebrain, accompanied by accumulation of amyloid-β and tangle formation. Cerebrolysin (CBL), a peptide mixture with neurotrophic-like effects, is reported to improve cognition and activities of daily living in patients with AD. Likewise, CBL reduces synaptic and behavioral deficits in transgenic (tg) mice overexpressing the human amyloid precursor protein (hAPP). The neuroprotective effects of CBL may involve multiple mechanisms, including signaling regulation, control of APP metabolism, and expression of neurotrophic factors. We investigate the effects of CBL in the hAPP tg model of AD on levels of neurotrophic factors, including pro-nerve growth factor (NGF), NGF, brain-derived neurotrophic factor (BDNF), neurotropin (NT)-3, NT4, and ciliary neurotrophic factor (CNTF). Immunoblot analysis demonstrated that levels of pro-NGF were increased in saline-treated hAPP tg mice. In contrast, CBL-treated hAPP tg mice showed levels of pro-NGF comparable to control and increased levels of mature NGF. Consistently with these results, immunohistochemical analysis demonstrated increased NGF immunoreactivity in the hippocampus of CBL-treated hAPP tg mice. Protein levels of other neurotrophic factors, including BDNF, NT3, NT4, and CNTF, were unchanged. mRNA levels of NGF and other neurotrophins were also unchanged. Analysis of neurotrophin receptors showed preservation of the levels of TrKA and p75(NTR) immunoreactivity per cell in the nucleus basalis. Cholinergic cells in the nucleus basalis were reduced in the saline-treated hAPP tg mice, and treatment with CBL reduced these cholinergic deficits. These results suggest that the neurotrophic effects of CBL might involve modulation of the pro-NGF/NGF balance and a concomitant protection of cholinergic neurons.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
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?
In 6-month-old mice overexpressing APP with the Swedish and London mutations, an ~60% decrease in the number of ChAT-positive cells in the nbM was revealed.
“In good agreement, 6-month-old mice overexpressing APP with the Swedish and London mutations revealed an ~60% decrease in the number of ChAT-positive cells in the nbM [45]”
From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [45]
Cites
2 retracted
Rockenstein, E. M., Ubhi, K. K., Doppler, E., et al. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-110914 · Cited by 21 · see citing works
Self-citationRetractedDoppler, E., Rockenstein, E. M., Ubhi, K. K., Inglis, C. A., Mante, M., Adame, A., Crews, L. A., Hitzl, M., Moessler, H., & Masliah, E. (2008) · Acta Neuropathologica · doi:10.1007/s00401-008-0407-x · Cited by 16 · see citing works
Self-citationRetractedTerry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397 · see citing works
Self-citationTwo amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology
Sturchler-Pierrat, C., Abramowski, D., Duke, M., Wiederhold, K.-H., Mistl, C., Rothacher, S., Ledermann, B., Bürki, K., Frey, P., Paganetti, P. A., et al. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.24.13287 · Cited by 1,507 · see citing works
A phase 1 clinical trial of nerve growth factor gene therapy for Alzheimer disease
Tuszynski, M. H., Thal, L., Pay, M., Salmon, D. P., U, H. S., Bakay, R., Patel, P., Blesch, A., Vahlsing, H. L., Ho, G., et al. (2005) · Nature Medicine · doi:10.1038/nm1239 · Cited by 1,050 · see citing works
Nagahara, A. H., Merrill, D. A., Coppola, G., Tsukada, S., Schroeder, B. E., Shaked, G. M., Wang, L., Blesch, A., Kim, A., Conner, J. M., et al. (2009) · Nature Medicine · doi:10.1038/nm.1912 · Cited by 1,034 · see citing works
Self-citationNeural stem cells improve cognition via BDNF in a transgenic model of Alzheimer disease
Blurton-Jones, M. M., Kitazawa, M., Martínez‐Coria, H., Castello, N. A., Müller, F.-J., Loring, J. F., Yamasaki, T. R., Poon, W. W., Green, K. N., & LaFerla, F. M. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0901402106 · Cited by 858 · see citing works
Hisano, S., Hoshi, K., Ikeda, Y., Maruyama, D., Kanemoto, M., Ichijo, H., Kojima, I., Takeda, J., & Nogami, H. (2000) · Molecular Brain Research · doi:10.1016/s0169-328x(00)00194-7 · Cited by 806 · see citing works
Seidah, N. G., & Chrétien, M. (1999) · Brain Research · doi:10.1016/s0006-8993(99)01909-5 · Cited by 760 · see citing works
Altered expression of synaptic proteins occurs early during progression of Alzheimer's disease
Masliah, E., Mallory, M., Alford, M., DeTeresa, R., Hansen, L. A., McKeel, D. W., & Morris, J. C. (2001) · Neurology · doi:10.1212/wnl.56.1.127 · Cited by 720 · see citing works
Self-citationPeng, S., Wuu, J., Mufson, E. J., & Fahnestock, M. (2005) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2005.03135.x · Cited by 691 · see citing works
Self-citationFahnestock, M., Michalski, B., Xu, B., & Coughlin, M. (2001) · Molecular and cellular neurosciences · doi:10.1006/mcne.2001.1016 · Cited by 482 · see citing works
Self-citationQuantitative assessment of cortical synaptic density in Alzheimer's disease
Scheff, S. W., DeKosky, S. T., & Price, D. A. (1990) · Neurobiology of Aging · doi:10.1016/0197-4580(90)90059-9 · Cited by 446 · see citing works
Structural Correlates of Cognition in Dementia: Quantification and Assessment of Synapse Change
DeKosky, S. T., Scheff, S. W., & Styren, S. D. (1996) · Neurodegeneration · doi:10.1006/neur.1996.0056 · Cited by 405 · see citing works
Interactions between β-amyloid and central cholinergic neurons: implications for Alzheimer’s disease
Kar, S., Slowikowski, S. P. M., Westaway, D. A., & Mount, H. T. J. (2004) · Journal of Psychiatry and Neuroscience · doi:10.1139/jpn.0442 · Cited by 363 · see citing works
Neurotrophic factors in Alzheimer’s disease: role of axonal transport
Schindowski, K., Bélarbi, K., & Buée, L. (2008) · Genes Brain & Behavior · doi:10.1111/j.1601-183x.2007.00378.x · Cited by 335 · see citing works
Secreted proNGF is a pathophysiological death-inducing ligand after adult CNS injury
Harrington, A. W., Leiner, B., Blechschmitt, C., Arevalo, J. C., Lee, R., Mörl, K., Meyer, M., Hempstead, B. L., Yoon, S. O., & Giehl, K. M. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0305755101 · Cited by 269 · see citing works
Scott, S. A., Mufson, E. J., Weingartner, J. A., Skau, K., & Crutcher, K. A. (1995) · Journal of Neuroscience · doi:10.1523/jneurosci.15-09-06213.1995 · Cited by 264 · see citing works
Rockenstein, E. M., McConlogue, L., Tan, H. T., Power, M., Masliah, E., & Mucke, L. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.47.28257 · Cited by 259 · see citing works
Self-citationIncreased proNGF Levels in Subjects with Mild Cognitive Impairment and Mild Alzheimer Disease
Peng, S., Wuu, J., Mufson, E. J., & Fahnestock, M. L. (2004) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/63.6.641 · Cited by 236 · see citing works
Self-citationRockenstein, E. M., Mallory, M. E., Mante, M., Sisk, A., & Masliaha, E. (2001) · Journal of Neuroscience Research · doi:10.1002/jnr.1247 · Cited by 224 · see citing works
Self-citationCrews, L., Adame, A., Patrick, C., DeLaney, A., Pham, E., Rockenstein, E., Hansen, L., & Masliah, E. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.1305-10.2010 · Cited by 222 · see citing works
Self-citationWong, T. P., Debeir, T., Duff, K., & Cuello, A. C. (1999) · The Journal of Neuroscience · doi:10.1523/jneurosci.19-07-02706.1999 · Cited by 196 · see citing works
Zhang, C., Chopp, M., Cui, Y., Wang, L., Zhang, R., Zhang, L., Lü, M., Szalad, A., Doppler, E., Hitzl, M., et al. (2010) · Journal of Neuroscience Research · doi:10.1002/jnr.22495 · Cited by 194 · see citing works
Self-citation(1995) · PubMed · Cited by 167 · see citing works
Pedraza, C. E., Podlesniy, P., Vidal, N., Arévalo, J. C., Lee, R., Hempstead, B. L., Ferrer, I., Iglesias, M., & Espinet, C. (2005) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)62275-4 · Cited by 164 · see citing works
Cholinergic Changes in the APP23 Transgenic Mouse Model of Cerebral Amyloidosis
Boncristiano, S., Calhoun, M. E., Kelly, P. H., Pfeifer, M., Bondolfi, L., Stalder, M., Phinney, A. L., Abramowski, D., Sturchler-Pierrat, C., Enz, A., et al. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-08-03234.2002 · Cited by 160 · see citing works
Synaptic remodeling during aging and in Alzheimer's disease
Masliah, E., Crews, L., & Hansen, L. (2006) · Journal of Alzheimer's Disease · doi:10.3233/jad-2006-9s311 · Cited by 132 · see citing works
Self-citationTrophic factors counteract elevated FGF-2-induced inhibition of adult neurogenesis
Chen, H., Tung, Y. C., Li, B., Iqbal, K., & Grundke, I. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.05.036 · Cited by 121 · see citing works
Cholinergic Involvement in Alzheimer’s Disease. A Link with NGF Maturation and Degradation
Cuello, A. C., Bruno, M. A., Allard, S., León, W., & Iulita, M. F. (2009) · Journal of Molecular Neuroscience · doi:10.1007/s12031-009-9238-z · Cited by 119 · see citing works
On the Molecular Basis Linking Nerve Growth Factor (NGF) to Alzheimer’s Disease
Capsoni, S., & Cattaneo, A. (2006) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-006-9112-2 · Cited by 109 · see citing works
Rüther, E., Ritter, R., Apecechea, M., et al. (1994) · Pharmacopsychiatry · doi:10.1055/s-2007-1014271 · Cited by 106 · see citing works
Cutting back on pro-protein convertases: the latest approaches to pharmacological inhibition
Fugère, M., & Day, R. W. (2005) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2005.04.006 · Cited by 101 · see citing works
Effects of Cerebrolysin™ on neurogenesis in an APP transgenic model of Alzheimer’s disease
Rockenstein, E. M., Mante, M., Adame, A., Crews, L. A., Moessler, H., & Masliah, E. (2006) · Acta Neuropathologica · doi:10.1007/s00401-006-0166-5 · Cited by 99 · see citing works
Self-citationAlvarez, X. A., Cacabelos, R., Laredo, M., et al. (2006) · European Journal of Neurology · doi:10.1111/j.1468-1331.2006.01222.x · Cited by 98 · see citing works
Nerve Growth Factor Gene Therapy in Alzheimer Disease
Tuszynski, M. H. (2007) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0b013e318068d6d2 · Cited by 95 · see citing works
Longo, F. M., Yang, T., Knowles, J. K., Xie, Y., Moore, L. J., & Massa, S. M. (2007) · Current Alzheimer Research · doi:10.2174/156720507783018316 · Cited by 92 · see citing works
Relationship between plaques, tangles, and dystrophic processes in Alzheimer's disease
Trojanowski, J. Q., Shin, R., Schmidt, M. L., & Lee, V. M.-Y. (1995) · Neurobiology of Aging · doi:10.1016/0197-4580(94)00176-2 · Cited by 89 · see citing works
Rockenstein, E. M., Torrance, M., Mante, M., Adame, A., Paulino, A., Rose, J. B., Crews, L. A., Moessler, H., & Masliah, E. (2006) · Journal of Neuroscience Research · doi:10.1002/jnr.20818 · Cited by 88 · see citing works
Self-citationBlanchard, J., Wanka, L., Tung, Y.-C., Cárdenas-Aguayo, M. D. C., LaFerla, F. M., Iqbal, K., & Grundke-Iqbal, I. (2010) · Acta Neuropathologica · doi:10.1007/s00401-010-0734-6 · Cited by 85 · see citing works
Spencer, B. J., Marr, R. A., Rockenstein, E. M., Crews, L. A., Adame, A., Potkar, R., Patrick, C., Gage, F. H., Verma, I. M., & Masliah, E. (2008) · BMC Neuroscience · doi:10.1186/1471-2202-9-109 · Cited by 84 · see citing works
Self-citationRockenstein, E. M., Adame, A., Mante, M., Moessler, H., Windisch, M., & Masliah, E. (2003) · Journal of Neural Transmission · doi:10.1007/s00702-003-0025-7 · Cited by 83 · see citing works
Self-citationAkai, F., Hiruma, S., Sato, T., et al. (1992) · PubMed · Cited by 82 · see citing works
Modulation of aberrant CDK5 signaling rescues impaired neurogenesis in models of Alzheimer's disease
Crews, L. A., Patrick, C., Adame, A., Rockenstein, E. M., & Masliah, E. (2011) · Cell Death and Disease · doi:10.1038/cddis.2011.2 · Cited by 81 · see citing works
Self-citationPlosker, G. L., & Gauthier, S. G. (2009) · Drugs & Aging · doi:10.2165/11203320-000000000-00000 · Cited by 81 · see citing works
Rockenstein, E. M., Crews, L. A., & Masliah, E. (2007) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2007.08.013 · Cited by 79 · see citing works
Self-citationPodlesniy, P., Kichev, A., Pedraza, C. E., Saurat, J., Encinas, M., Pérez, B. F., Ferrer, I., & Espinet, C. (2006) · American Journal Of Pathology · doi:10.2353/ajpath.2006.050787 · Cited by 78 · see citing works
Chohan, M. O., Li, B., Blanchard, J., Tung, Y. C., Heaney, A. T., Rabe, A., Iqbal, K., & Grundke, I. (2009) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.08.008 · Cited by 72 · see citing works
Alvarez, X. A., Cacabelos, R., Sampedro, C., et al. (2010) · European Journal of Neurology · doi:10.1111/j.1468-1331.2010.03092.x · Cited by 69 · see citing works
Alvarez, X. A., Cacabelos, R., Sampedro, C., Couceiro, V., Aleixandre, M., Vargas, M., Linares, C., Granizo, E., García-Fantini, M., Baurecht, W., et al. (2011) · Current Alzheimer Research · doi:10.2174/156720511796391863 · Cited by 67 · see citing works
Self-citationCuello, A. C., & Bruno, M. A. (2007) · Neurochemical Research · doi:10.1007/s11064-006-9270-0 · Cited by 66 · see citing works
Turner, L. F., & Valoušková, V. (1996) · Neuroscience Letters · doi:10.1016/0304-3940(95)12240-0 · Cited by 63 · see citing works
Cerebrolysin enhances functional recovery following focal cerebral infarction in rats
Ren, J., Sietsma, D. K., Qiu, S., et al. (2007) · Restorative Neurology and Neuroscience · doi:10.3233/rnn-2007-00349 · Cited by 58 · see citing works
Rüther, E., Ritter, R., Apecechea, M., Freytag, S., Gmeinbauer, R., & Windisch, M. (2000) · Journal of Neural Transmission · doi:10.1007/s007020070061 · Cited by 56 · see citing works
Neurotrophic effects of Cerebrolysin® in animal models of excitotoxicity
Veinbergs, I., Mante, M., Mallory, M. E., & Masliah, E. (2000) · Springer eBooks · doi:10.1007/978-3-7091-6781-6_29 · Cited by 53 · see citing works
Self-citationAβ1–42 promotes cholinergic sprouting in patients with AD and Lewy body variant of AD
Masliah, E., Alford, M. F., Adame, A., Rockenstein, E. M., Galasko, D., Salmon, D. P., Hansen, L. A., & Thal, L. J. (2003) · Neurology · doi:10.1212/01.wnl.0000073987.79060.4b · Cited by 53 · see citing works
Self-citationLi, B., Wanka, L., Blanchard, J., Liu, F., Chohan, M. O., Iqbal, K., & Grundke, I. (2010) · FEBS Letters · doi:10.1016/j.febslet.2010.06.025 · Cited by 49 · see citing works
Effects of Cerebrolysin on amyloid-beta deposition in a transgenic model of Alzheimer's disease.
Rockenstein, E. M., Mallory, M. E., Mante, M., Alford, M. F., Windisch, M., Moessler, H., & Masliah, E. (2002) · PubMed · Cited by 48 · see citing works
Self-citationA Longitudinal Study of Behavioral Deficits in an AβPP Transgenic Mouse Model of Alzheimer's Disease
Havas, D., Hutter‐Paier, B., Ubhi, K. K., Rockenstein, E. M., Crailsheim, K., Masliah, E., & Windisch, M. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-101866 · Cited by 45 · see citing works
Self-citationRockenstein, E. M., Adame, A., Mante, M., Larrea, G., Crews, L. A., Windisch, M., Moessler, H., & Masliah, E. (2004) · Journal of Neural Transmission · doi:10.1007/s00702-004-0181-4 · Cited by 43 · see citing works
Self-citationBlanchard, J., Chohan, M. O., Li, B., Liu, F., Iqbal, K., & Grundke, I. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-1000069 · Cited by 41 · see citing works
Genetically altered transgenic models of Alzheimer’s disease
Masliah, E., & Rockenstein, E. M. (2000) · Springer eBooks · doi:10.1007/978-3-7091-6781-6_20 · Cited by 37 · see citing works
Self-citationProteolytic processing of proNGF is necessary for mature NGF regulated secretion from neurons
Lim, K., Tyler, C. M., Seung Taik, L. I. M., Giuliano, R. E., & Federoff, H. J. (2007) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2007.07.039 · Cited by 29 · see citing works
Kichev, A., Ilieva, E. V., Piñol‐Ripoll, G., Podlesniy, P., Ferrer, I., Portero‐Otín, M., Pamplona, R., & Espinet, C. (2009) · American Journal Of Pathology · doi:10.2353/ajpath.2009.090018 · Cited by 29 · see citing works
Changes at the focus of experimental ischemic stroke treated with neuroprotective agents
Onishchenko, L. S., Gaikova, O. N., & Yanishevskii, S. N. (2007) · Neuroscience and Behavioral Physiology · doi:10.1007/s11055-008-0007-1 · Cited by 28 · see citing works
Tomidokoro, Y., Harigaya, Y., Matsubara, E., Ikeda, M., Kawarabayashi, T., Okamoto, K., & Shoji, M. (2000) · Neuroscience Letters · doi:10.1016/s0304-3940(00)01443-9 · Cited by 27 · see citing works
Analysis of Cerebrospinal Fluid of Alzheimer Patients
Marksteiner, J., Pirchl, M., Ullrich, C., OBERBAUER, H., Blasko, I., Lederer, W., Hinterhuber, H., & Humpel, C. (2008) · Pharmacology · doi:10.1159/000156487 · Cited by 26 · see citing works
Wronski, R., Kronawetter, S., Hutter‐Paier, B., et al. (2000) · Springer eBooks · doi:10.1007/978-3-7091-6781-6_28 · Cited by 21 · see citing works
Rockenstein, E. M., Ubhi, K. K., Pham, E., Michael, S. A., Doppler, E., Novak, P. H., Inglis, C. A., Mante, M., Adame, A., Alvarez, X. A., et al. (2011) · Journal of Neuroscience Research · doi:10.1002/jnr.22712 · Cited by 21 · see citing works
Self-citationSpotlight on Cerebrolysin in Dementia†
Plosker, G. L., & Gauthier, S. G. (2010) · CNS Drugs · doi:10.2165/11204820-000000000-00000 · Cited by 18 · see citing works
Francis-Turner, L., Valoušková, V., & Mokrý, J. (1996) · Journal of neural transmission. Supplementum · doi:10.1007/978-3-7091-6892-9_22 · Cited by 11 · see citing works
Серкина, Е. В., Громова, О. А., Torshin, I. Y., et al. (2008) · PubMed · Cited by 6 · see citing works
[Clastogenic, aneugenic, pro- and antioxidant properties of some neurotropic preparations].
Dd, G., Vv, S., Mf, I., et al. (2006) · PubMed · Cited by 2 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models
Wirths, O., & Zampar, S. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21218144 · Cited by 75 · see citing works
“In good agreement, 6-month-old mice overexpressing APP with the Swedish and London mutations revealed an ~60% decrease in the number of ChAT-positive cells in the nbM [45] and reduced ChAT-positive neuron numbers were also reported in the medial septum of 3xTg [58] and 5xFAD mice [136].”
Background
- Authors
- Ubhi, K., Rockenstein, E., Vazquez‐Roque, R., Mante, M., Inglis, C., Patrick, C., Adame, A., Fahnestock, M., Doppler, E., Novak, P., Moessler, H., & Masliah, E.
- Affiliations
- University of California San Diego (US)
- McMaster University (CA)
- EVER Neuro Pharma (Austria) (AT)
- Corresponding author
- Masliah, Eliezer
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2012-11-14
- Volume
- 91
- Issue
- 2
- Pages
- 167-177
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- OpenAlex
- W2026758192
- Cited by
- 65
- References
- 73
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 1 · 2023: 4 · 2022: 3 · 2021: 2 · 2020: 5 · 2019: 11 · 2018: 2 · 2017: 7 · 2016: 6 · 2015: 12 · 2014: 4 · 2013: 4
- FWCI
- 4.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroscience Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of California, San Diego
- National Institute on Aging (P01AG010435, AG05131, R37AG018440, P50AG005131, P01AG031097, P01AG022074)
- National Institute of Neurological Disorders and Stroke (P30NS076411)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
- Keywords
- Cerebrolysin, Alzheimer's disease, nerve growth factor, neurotrophic factors, amyloid precursor protein transgenic mice, cholinergic deficit, nucleus basalis of Meynert, TrkA, p75 neurotrophin receptor, hippocampus, neuroprotection, brain-derived neurotrophic factor, neurotrophin-3, neurotrophin-4, ciliary neurotrophic factor
- MeSH terms
- Alzheimer Disease, Amino Acids, Animals, Brain, Choline O-Acetyltransferase, Disease Models, Animal, Gene Expression Regulation, Humans, Mice, Transgenic, Mutation, Nerve Growth Factors, RNA, Messenger, Amyloid beta-Protein Precursor, Receptors, Nerve Growth Factor, Cholinergic Agents, Neuroprotective Agents, Receptor, trkA, Mice
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
