The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.
Activity-Dependent Neuroprotective Protein Snippet NAP Reduces Tau Hyperphosphorylation and Enhances Learning in a Novel Transgenic Mouse Model
Abstract
Activity-dependent neuroprotective protein (ADNP) differentially interacts with chromatin to regulate essential genes. Because complete ADNP deficiency is embryonic lethal, the outcome of partial ADNP deficiency was examined. ADNP(+/-) mice exhibited cognitive deficits, significant increases in phosphorylated tau, tangle-like structures, and neurodegeneration compared with ADNP(+/+) mice. Increased tau hyperphosphorylation is known to cause memory impairments in neurodegenerative diseases associated with tauopathies, including the most prevalent Alzheimer's disease. The current results suggest that ADNP is an essential protein for brain function and plays a role in normal cognitive performance. ADNP-deficient mice offer an ideal paradigm for evaluation of cognitive enhancers. NAP (NAPVSIPQ) is a peptide derived from ADNP that interacts with microtubules and provides potent neuroprotection. NAP treatment partially ameliorated cognitive deficits and reduced tau hyperphosphorylation in the ADNP(+/-) mice. NAP is currently in phase II clinical trials assessing effects on mild cognitive impairment.
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“while ADNP+/- mice show tauopathy, neuronal cell death and abnormalities in social behaviour and cognitive functioning18,34.”
From A SWI/SNF-related autism syndrome caused by de novo mutations in ADNP (2014) · cites this paper as [18]
In the citing paper
“Of the other genes reported as differentially expressed in Adnp-/-23 and Adnp+/-18 mice (down: CCNC, TMPO, PLAGL2; up: ABCF3), only PLAGL2 was found to be differentially regulated in our patients (Supplementary Fig. 3e).”
From A SWI/SNF-related autism syndrome caused by de novo mutations in ADNP (2014) · cites this paper as [18]
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Self-citationThe Roles of Cyclin-dependent Kinase 5 and Glycogen Synthase Kinase 3 in Tau Hyperphosphorylation
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Self-citationActivity-dependent neuroprotective protein: a novel gene essential for brain formation
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BackgroundSelf-citationTau-Centric targets and drugs in clinical development for the treatment of alzheimer's disease
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Self-citationDual Role of Autophagy in Diseases of the Central Nervous System
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NAP protects memory, increases soluble tau and reduces tau hyperphosphorylation in a tauopathy model
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“NAP protected against increased tau hyperphosphorylation that was associated with ADNP-deficiency (Vulih-Shultzman et al., 2007) and in the same model, NAP treatment improved cognitive performance in the Morris water maze (MWM).”
ResultSelf-citationJavitt, D. C., Buchanan, R. W., Keefe, R. S. E., Kern, R. S., McMahon, R. P., Green, M. F., Lieberman, J. A., GOFF, D. C., Csernansky, J. G., McEvoy, J. P., et al. (2011) · Schizophrenia Research · doi:10.1016/j.schres.2011.11.001 · Cited by 118
“…e Columbia University Medical Center, New York, NY, United States f Massachusetts General Hospital/Harvard Medical School, Boston, MA, United States g Washington University, St. Louis, MO, United States ☆ Presented at the 2009meeting of the American Colleg Hollywood, Florida, Dec. 6–10, 2009.”
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Self-citationADNP promotes neural differentiation by modulating Wnt/β-catenin signaling
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InfluentialSelf-citationJouroukhin, Y., Ostritsky, R., Assaf, Y., Pelled, G., Giladi, E., & Gozes, I. (2013) · Neurobiology of Disease · doi:10.1016/j.nbd.2013.04.012 · Cited by 105
Self-citationTau-Based Therapeutics for Alzheimer’s Disease: Active and Passive Immunotherapy
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“In mice, the depletion of Adnp is embryonic lethal, and the heterozygous model is affected by cognitive deficits and neurodegeneration (Vulih-Shultzman et al., 2007).”
Ivashko‐Pachima, Y., Sayas, C. L., Malishkevich, A., & Gozes, I. (2017) · Molecular Psychiatry · doi:10.1038/mp.2016.255 · Cited by 102
Self-citationMandel, S., Spivak-Pohis, I., & Gozes, I. (2008) · Journal of Molecular Neuroscience · doi:10.1007/s12031-007-9013-y · Cited by 91
“2001), a region potentially associated with mental function (Borozdin et al. 2007; Vulih-Shultzman et al. 2007).”
BackgroundInfluentialSelf-citationHacohen-Kleiman, G., Sragovich, S., Karmon, G., Gao, A. Y. L., Grigg, I., Pasmanik‐Chor, M., Le, A., Korenková, V., McKinney, R. A., & Gozes, I. (2018) · Journal of Clinical Investigation · doi:10.1172/jci98199 · Cited by 98
Self-citationTauopathy in the young autistic brain: novel biomarker and therapeutic target
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Self-citationThe Role of Tau in Neurodegenerative Diseases and Its Potential as a Therapeutic Target
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A Subset of Autism-Associated Genes Regulate the Structural Stability of Neurons
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“The current studies provide additional weight to observed effects of NAP on tau-related pathology and MT dysfunction [18,27,57,92,93].”
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Self-citationNAP (davunetide) rescues neuronal dysfunction in a Drosophila model of tauopathy
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“This is consistent with observations that NAP administration to ADNP heterozygous mice, a model of tauopathy, for two weeks resulted in reduced tau phosphorylation in the cortex 6 weeks after the cessation of NAP treatment (Vulih-Shultzman et al., 2007).”
MethodResultSelf-citationErratum: Premature primary tooth eruption in cognitive/motor-delayed ADNP-mutated children
Gozes, I., Dijck, A. V., Hacohen-Kleiman, G., Grigg, I., Karmon, G., Giladi, E., Eger, M., Gabet, Y., Pasmanik-Chor, M., Cappuyns, E., et al. (2017) · Translational Psychiatry · doi:10.1038/tp.2017.128 · Cited by 71
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“…been shown to reduce tau hyperphosphorylation and Aβ accumulation in both in vitro and in vivo AD models, and also benefit cognitive test performance in some of these models (Gozes & Divinski, 2004; Matsuoka et al., 2007; Matsuoka et al., 2008; Shiryaev et al., 2009; Vulih-Shultzman et al., 2007).”
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“In this respect, antipsychotic drug treatment may cause tauopathy (Gong et al., 1996) and partial ADNP knockout resulted in tauopathy paralleled by cognitive and social deficiencies (Vulih-Shultzman et al., 2007), suggesting a possible feedback mechanism in the ADNP/ ADNP2 mRNA levels homeostasis.”
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Self-citationIntroducing ADNP and SIRT1 as new partners regulating microtubules and histone methylation
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“for the ADNP syndrome [11, 12], were previously described [1, 16, 49].”
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Self-citationIvashko‐Pachima, Y., Ganaiem, M., Ben-Horin-Hazak, I., Lobyntseva, A., Bellaiche, N., Fischer, I., Levy, G., Sragovich, S., Karmon, G., Giladi, E., et al. (2022) · Molecular Psychiatry · doi:10.1038/s41380-022-01603-w · Cited by 58
“NAP treatment protected against these adverse features, while inhibiting Tau hyperphosphorylation [21].”
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Self-citationPharmacotherapeutic targets in Alzheimer's disease
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“Studies in transgenic mice suggest that AL-108 interacts with microtubules, reduces -hyperphosphorylation and increases soluble levels leading to an improvement in cognition [76, 77].”
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“ADNP deficiency can be ameliorated in part by compensatory treatment with the ADNP fragment, the drug candidate davuentide (NAP), that stabilizes microtubules and inhibits tau pathology while protecting cognitive [12] as well as motor functions [53], by protecting microtubule-dependent axonal transport [48,53].”
BackgroundMethodInfluentialSelf-citationEpisignatures Stratifying Helsmoortel-Van Der Aa Syndrome Show Modest Correlation with Phenotype
Breen, M. S., Garg, P., Tang, L., Mendonca, D., Levy, T., Barbosa, M., Arnett, A. B., Kurtz‐Nelson, E. C., Agolini, E., Battaglia, A., et al. (2020) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2020.07.003 · Cited by 57
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“Meanwhile, ADNP deficiency has been reported to promote tauopathy in AD patients [23, 26, 27].”
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Self-citationPharmacologists and Alzheimer disease therapy: to boldly go where no scientist has gone before
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“Several preclinical studies demonstrated a neuroprotective role for davunetide due to a significant reduction in both hyperphosphorylated and insoluble tau [158,159].”
BackgroundThe autism-mutated ADNP plays a key role in stress response
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“These findings mark ADNP as one of the most frequent ASD-associated genes known to date.”
BackgroundInfluentialSelf-citationDresner, E., Malishkevich, A., Arviv, C., Leibman Barak, S., Alon, S., Ofir, R., Gothilf, Y., & Gozes, I. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.387027 · Cited by 47
Self-citationTau-directed approaches for the treatment of Alzheimer’s disease: focus on leuco-methylthioninium
Seripa, D., Solfrizzi, V., Imbimbo, B. P., Daniele, A., Santamato, A., Lozupone, M., Zuliani, G., Greco, A., Logroscino, G., & Panza, F. (2016) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2016.1140039 · Cited by 50
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“No obvious phenotypic abnormalities were mentioned [13], be it that in follow-up studies a small reduction in body size of the mutant animals was measured [122].”
BackgroundMethodResultInfluentialSelf-citationDavunetide: Peptide Therapeutic in Neurological Disorders
Magen, I., & Gozes, I. (2014) · Current Medicinal Chemistry · doi:10.2174/0929867321666140217124945 · Cited by 45
“In this respect, ADNP heterozygous mice develop Alzheimer's-like tau pathology, cognitive deficits and neuronal cell death [26] and ADNP expression is modulated in a mouse model of Alzheimer's disease [27].”
BackgroundSelf-citationBose, M., Quipildor, G. F., Ehrlich, M. E., & Salton, S. R. (2022) · Cells · doi:10.3390/cells11223629 · Cited by 47
Ballatore, C., Brunden, K. R., Trojanowski, J. Q., Lee, V. M. Y., Smith, A. B., & Huryn, D. M. (2010) · Current Topics in Medicinal Chemistry · doi:10.2174/156802611794072605 · Cited by 46
“Furthermore, davunetide was found to reduce tau-hyperphosphorylation both in vitro [101] as well as in ADNP+/− mice [103].”
BackgroundMagen, I., Ostritsky, R., Richter, F., Zhu, C., Fleming, S. M., Lemesre, V., Stewart, A. J., Morimoto, B. H., Gozes, I., & Chesselet, M. (2014) · Pharmacology Research & Perspectives · doi:10.1002/prp2.65 · Cited by 43
“The intermittent regimen was chosen for long-term drug administration because it was previously shown to be beneficial in a mouse model of AD and frontotemporal dementia (Matsuoka et al. 2007, 2008; Vulih-Shultzman et al. 2007; Shiryaev et al. 2009; Jouroukhin et al. 2012, 2013).”
BackgroundSelf-citationPescosolido, M. F., Schwede, M., Harrison, A. J., Schmidt, M., Uzun, E. D. G., Chen, W. S., Donahue, J. P., Shur, N. E., Jerskey, B. A., Phornphutkul, C., et al. (2014) · Journal of Medical Genetics · doi:10.1136/jmedgenet-2014-102444 · Cited by 43
Tau and Caspase 3 as Targets for Neuroprotection
Idan-Feldman, A., Ostritsky, R., & Gozes, I. (2012) · International Journal of Alzheimer s Disease · doi:10.1155/2012/493670 · Cited by 42
Self-citationThe Compassionate Side of Neuroscience: Tony Sermone’s Undiagnosed Genetic Journey—ADNP Mutation
Gozes, I., Helsmoortel, C., Vandeweyer, G., der Aa, N. V., Kooy, R. F., & Bedrosian‐Sermone, S. (2015) · Journal of Molecular Neuroscience · doi:10.1007/s12031-015-0586-6 · Cited by 41
“Taking advantage of mouse genetics, we have shown that ADNP is crucial for brain formation (Pinhasov et al. 2003) and learning and memory (Vulih-Shultzman et al. 2007), in a sex-dependent manner (Malishkevich et al. 2015; Kleiman et al. 2015).”
Self-citationIvashko‐Pachima, Y., Maor-Nof, M., & Gozes, I. (2019) · PLoS ONE · doi:10.1371/journal.pone.0213666 · Cited by 40
Self-citationCritical appraisal of the role of davunetide in the treatment of progressive supranuclear palsy
Gozes, I., Gold, Lorenzl, Stewart, A. J., Morimoto, B. H., & Williams (2012) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s12518 · Cited by 40
“In vivo confirmation comes from several animal models in which davunetide reduces the level of phosphorylated tau in models of AD,(47,48) tauopathy(33,49) and ADNP deficiency.(50) A link between davunetide’s effects on microtubules and cell survival pathways is suggested by studies involving neuroprotection against to…”
Self-citationThe ADNP Syndrome and CP201 (NAP) Potential and Hope
Gozes, I. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.608444 · Cited by 39
“The protective effect of CP201 was demonstrated by affecting animal traits that are equivalent to clinical symptoms in human patients with ADNP syndrome (20, 22).”
BackgroundInfluentialSelf-citationCho, H., Yoo, T., Moon, H., Kang, H., Yang, Y., Kang, M., Yang, E., Lee, D., Hwang, D., Kim, H., et al. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-02129-5 · Cited by 36
“These Adnp mouse phenotypes are rescued by the NAP peptide, which corresponds to eight aa residues of ADNP (NAPVSIPQ; also known as davunetide or CP201) [13, 16, 23] and is known to act through microtubule end-binding proteins [14].”
BackgroundBennison, S. A., Blazejewski, S. M., Liu, X., Hacohen-Kleiman, G., Sragovich, S., Zoidou, S., Touloumi, O., Grigoriadis, N., Gozes, I., & Toyo-oka, K. (2023) · Molecular Psychiatry · doi:10.1038/s41380-022-01939-3 · Cited by 42
“Treatment of cells in culture with NAP has been shown to promote or rescue neurite outgrowth [31, 32], enhance microtubule dynamics and Tau-microtubule association [29, 33, 34], and interact with microtubule end binding protein (EB3) to enhance dendritic spine formation [35, 36].”
BackgroundMethodInfluentialSelf-citationDavunetide (NAP) Protects the Retina Against Early Diabetic Injury by Reducing Apoptotic Death
Scuderi, S., D’Amico, A. G., Castorina, A., Federico, C., Marrazzo, G., Drago, F., Bucolo, C., & D’Agata, V. (2014) · Journal of Molecular Neuroscience · doi:10.1007/s12031-014-0244-4 · Cited by 35
Pharmacological approaches for Alzheimer’s disease: neurotransmitter as drug targets
Prakash, A. K., Kalra, J., Mani, V., Ramasamy, K., & Majeed, A. B. A. (2014) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2015.988709 · Cited by 35
“Neuroprotective effect of ADNF is mimicked by NAP via its interaction with tubulin, increasing assembly of microtubules, resulting in improved neuronal outgrowth [174–176].”
BackgroundEvidence of a Cardiovascular Function for Microtubule-Associated Protein Tau
Betrie, A. H., Ayton, S., Bush, A. I., Angus, J. A., Lei, P., & Wright, C. E. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161093 · Cited by 35
Hacohen-Kleiman, G., Barnea, O. Y., Touloumi, O., Lagoudaki, R., Avraham, K. B., Grigoriadis, N., & Gozes, I. (2019) · Neurochemical Research · doi:10.1007/s11064-019-02723-6 · Cited by 35
Self-citationMolecular causes of sex‐specific deficits in rodent models of neurodevelopmental disorders
Mossa, A., & Manzini, M. C. (2019) · Journal of Neuroscience Research · doi:10.1002/jnr.24577 · Cited by 37
“Two small peptide molecules have been widely studied: NAP, a neuroprotective ADNP-derived snippet peptide (also known as NAPVSIPQ, CP201, or davunetide) (Hacohen-Kleiman et al., 2018; Vulih-Shultzman et al., 2007) and SKIP, a four-amino-acid peptide (Amram et al., 2016).”
BackgroundCellular and animal models of skin alterations in the autism-related ADNP syndrome
Mollinedo, P., Kapitansky, O., González‐Lamuño, D., Zaslavsky, A., Real, P. J., Gozes, I., Gandarillas, A., & Fernández-Luna, J. L. (2019) · Scientific Reports · doi:10.1038/s41598-018-36859-2 · Cited by 34
Self-citationGanaiem, M., Karmon, G., Ivashko‐Pachima, Y., & Gozes, I. (2022) · Cells · doi:10.3390/cells11192994 · Cited by 32
“Conversely, ADNP deficiencies and ADNP gene mutations in transgenic mice led to dramatic alterations in mRNA/protein expression profiles as well as slower microtubule-dependent axonal transport, aberrant dendritic spine formation and tauopathy, which could be partially repaired by NAP treatment [7,8,12,13].”
BackgroundSelf-citationGozes, I., Yeheskel, A., & Pasmanik‐Chor, M. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-142490 · Cited by 33
“In ADNP haploinsufficient mice [5], a set of genes related to autism was deregulated including a solute carrier (SLC) transcript, involved in intracellular signaling cascade, transforming growth factor, involved in angiogenesis and Pax6 [20], involved in neuronal migration and axogenesis, which are either mutated or a…”
BackgroundResultInfluentialSelf-citationCosgrave, A. S., McKay, J. S., Bubb, V. J., Morris, R., Quinn, J. P., & Thippeswamy, T. (2008) · Neurobiology of Disease · doi:10.1016/j.nbd.2008.02.005 · Cited by 33
“Importantly, a recent study by Vulih-Shultzman et al. (2007) demonstrated thatADNP+/−mice have cognitive deficits and increased phosphorylated tau, the hallmark of neurodegenerative diseases.”
BackgroundADNP Is a Therapeutically Inducible Repressor of WNT Signaling in Colorectal Cancer
Blaj, C., Bringmann, A., Schmidt, E. M., Urbischek, M., Lamprecht, S., Fröhlich, T., Arnold, G. J., Krebs, S., Blum, H., Hermeking, H., et al. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-1604 · Cited by 33
“It also assumes protective roles against cognitive defects in neurodegenerative disease (12).”
BackgroundYang, M., Chen, S.-C., Lin, Y., Lee, Y., Huang, M., Chen, K., Wu, H., Lin, P., Gozes, I., & Tyan, Y. (2019) · Journal of Food and Drug Analysis · doi:10.1016/j.jfda.2018.11.009 · Cited by 34
“neuroprotection, central nervous system (CNS) development and immunoregulation for the brain damage [17,18,24,25,28].”
BackgroundSelf-citationNAP protects against cytochrome c release: Inhibition of the initiation of apoptosis
Zemlyak, I., Sapolsky, R. M., & Gozes, I. (2009) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2009.07.013 · Cited by 32
“, 2004); 2] ADNP deficiency in vivo has been associated with the microtubule-associated protein tau hyperphosphorylation and neurofibrillary-tangle like structure formation (Vulih-Shultzman et al., 2007); 3] in neuronal-like cells ADNP deficiency resulted in reduction in microtubule-associated protein 2 staining and l…”
BackgroundInfluentialSelf-citationConvergence of spectrums: neuronal gene network states in autism spectrum disorder
Sullivan, J. M., Rubeis, S. D., & Schaefer, A. (2019) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2019.04.011 · Cited by 32
Ganaiem, M., Gildor, N. D., Shazman, S., Karmon, G., Ivashko‐Pachima, Y., & Gozes, I. (2023) · Cells · doi:10.3390/cells12182251 · Cited by 30
Self-citationIntranasal delivery of a Fas-blocking peptide attenuates Fas-mediated apoptosis in brain ischemia
Ullah, I., Chung, K., Oh, J., Beloor, J., Bae, S., Lee, S. C., Lee, M., Kumar, P., & Lee, S. (2018) · Scientific Reports · doi:10.1038/s41598-018-33296-z · Cited by 31
Experimental Models to Study Autism Spectrum Disorders: hiPSCs, Rodents and Zebrafish
Pensado‐López, A., Veiga-Rúa, S., Carracedo, Á., Allegue, C., & Sanchez, L. E. (2020) · Genes · doi:10.3390/genes11111376 · Cited by 34
Mythili, Y., LaPointe, N. E., Lopus, M., Cox, C., Jordan, M. A., Feinstein, S. C., & Wilson, L. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-1335 · Cited by 30
“Recently NAP has been reported to reduce tau hyper-phosphorylation in animal models of Alzheimer’s disease [4], frontotemporal dementia [3], and ADNP (its parent protein)-deficiency [29].”
Brown, B. P., Kang, S., Gawelek, K., Zacharias, R. A., Anderson, S. R., Turner, C. P., & Morris, J. K. (2015) · Neuroscience · doi:10.1016/j.neuroscience.2014.12.076 · Cited by 29
Sokołowska, P., Passemard, S., Mok, A., Schwendimann, L., Gozes, I., & Gressèns, P. (2010) · Neuroscience · doi:10.1016/j.neuroscience.2010.10.074 · Cited by 29
Self-citationNAP Alpha-Aminoisobutyric Acid (IsoNAP)
Gozes, I., Schirer, Y., Idan-Feldman, A., David, M. P., & Furman-Assaf, S. (2013) · Journal of Molecular Neuroscience · doi:10.1007/s12031-013-0103-8 · Cited by 28
“The procedure used to generate ADNP heterozygous mice was previously described (Vulih-Shultzman et al. 2007).”
BackgroundMethodResultInfluentialSelf-citationReciprocal control of translation and transcription in autism spectrum disorder
Longo, F., & Klann, E. (2021) · EMBO Reports · doi:10.15252/embr.202052110 · Cited by 29
“Haploinsufficient ADNP ( Adnp + /- ) mice mimic human HVDAS in terms of altered gene expression patterns and synapse density, as well as compromised developmental, motor, and cognitive ability (Vulih-Shultzman et al, 2007; Amram et al, 2016).”
A convergent mechanism of high risk factors ADNP and POGZ in neurodevelopmental disorders
Conrow‐Graham, M., Williams, J. B., Martin, J. A., Zhong, P., Cao, Q., Rein, B. A., & Yan, Z. (2022) · Brain · doi:10.1093/brain/awac152 · Cited by 29
Greggio, S., de Paula, S., de Oliveira, I. M., Trindade, C., Rosa, R. M., Henriques, J. A. P., & DaCosta, J. C. (2011) · Neurobiology of Disease · doi:10.1016/j.nbd.2011.06.018 · Cited by 28
“, 2006) and ADNPdeficient mice (Vulih-Shultzman et al., 2007), fetal alcohol syndrome (Brenneman et al.”
BackgroundGardiner, J. C. (2012) · Plant Signaling & Behavior · doi:10.4161/psb.21325 · Cited by 29
“NAP treatment partially ameliorates cognitive deficit and Tau hyperphosphorylation in ADNP(+/-) mice.(14) MAP2 targets PKA to microtubules.”
BackgroundGozes, I., Iram, T., Maryanovsky, E., Arviv, C., Rozenberg, L., Schirer, Y., Giladi, E., & Furman-Assaf, S. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-131664 · Cited by 27
“in part against ADNP deficiency [33, 85], and it is of”
Self-citation
Metadata
- Authors
- Vulih-Shultzman, I., Pinhasov, A., Mandel, S., Grigoriadis, N., Touloumi, O., Pittel, Z., & Gozes, I.
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 2007-11
- Volume
- 323
- Issue
- 2
- Pages
- 438-449
- ISSN
- 0022-3565 (ISSN-L)
- OpenAlex
- W2136172091
- Cited by
- 219
- References
- 40
- Citations by year
- 2026: 10 · 2025: 12 · 2024: 12 · 2023: 9 · 2022: 14 · 2021: 9 · 2020: 19 · 2019: 18 · 2018: 7 · 2017: 11 · 2016: 15 · 2015: 13 · 2014: 14 · 2013: 11 · 2012: 13
- FWCI
- 5.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- ADNP, NAP peptide, tau hyperphosphorylation, cognitive impairment, learning, neurodegeneration, tauopathy, Alzheimer's disease, mild cognitive impairment, neuroprotection, microtubule binding
- MeSH terms
- Animals, Astrocytes, Cognition Disorders, Female, Learning, Male, Mice, Inbred ICR, Mice, Transgenic, Nerve Tissue Proteins, Oligopeptides, Phosphorylation, tau Proteins, Homeodomain Proteins, Mice
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