Gene Symbol: Zbtb20
Description: zinc finger and BTB domain containing 20
Alias: 1300017A20Rik, 7330412A13Rik, A930017C21Rik, D16Wsu73e, DPZF, HOF, J20, ODA-8S, Oda8, Tg(PDGFB-APPSwInd)20Lms, Zfp288, zinc finger and BTB domain-containing protein 20, APP Tg, BTB/POZ domain zinc finger factor HOF, PDGF-APPSwInd, PDGF-hAPP695,751,770V171F, KM670/671NL, POZ/zinc finger transcription factor ODA-8, zinc finger protein 288
Species: mouse
Products:     Zbtb20

Top Publications

  1. Poirier R, Wolfer D, Welzl H, Tracy J, Galsworthy M, Nitsch R, et al. Neuronal neprilysin overexpression is associated with attenuation of Abeta-related spatial memory deficit. Neurobiol Dis. 2006;24:475-83 pubmed
  2. Nielsen J, Blom J, Noraberg J, Jensen N. Zbtb20-induced CA1 pyramidal neuron development and area enlargement in the cerebral midline cortex of mice. Cereb Cortex. 2010;20:1904-14 pubmed publisher
    Expression of the transcriptional repressor Zbtb20 is confined to the hippocampal primordium of the developing dorsal midline cortex in mice...
  3. Roberson E, Scearce Levie K, Palop J, Yan F, Cheng I, Wu T, et al. Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model. Science. 2007;316:750-4 pubmed
    ..Thus, tau reduction can block Abeta- and excitotoxin-induced neuronal dysfunction and may represent an effective strategy for treating Alzheimer's disease and related conditions. ..
  4. Karl T, Bhatia S, Cheng D, Kim W, Garner B. Cognitive phenotyping of amyloid precursor protein transgenic J20 mice. Behav Brain Res. 2012;228:392-7 pubmed publisher
    ..In the current study, we characterised the cognitive abilities of the J20 transgenic mouse line (expressing the Swedish 670/671(KM->NL) and Indiana (717(V->F)hAPP mutations) and non-..
  5. Rosenthal E, Tonchev A, Stoykova A, Chowdhury K. Regulation of archicortical arealization by the transcription factor Zbtb20. Hippocampus. 2012;22:2144-56 pubmed publisher
    ..Previous analyses have outlined an important role of the transcription factor (TF) Zbtb20 for hippocampal CA1 field specification (Nielsen et al. (2007) Development 134:1133-1140; Nielsen et al...
  6. Chin J, Palop J, Puoliväli J, Massaro C, Bien Ly N, Gerstein H, et al. Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease. J Neurosci. 2005;25:9694-703 pubmed
    ..Thus, increased Fyn expression is sufficient to trigger prominent neuronal deficits in the context of even relatively moderate Abeta levels, and inhibition of Fyn activity may help counteract Abeta-induced impairments. ..
  7. Meilandt W, Cisse M, Ho K, Wu T, Esposito L, Scearce Levie K, et al. Neprilysin overexpression inhibits plaque formation but fails to reduce pathogenic Abeta oligomers and associated cognitive deficits in human amyloid precursor protein transgenic mice. J Neurosci. 2009;29:1977-86 pubmed publisher
    ..Reduction of Abeta oligomers will likely be required for anti-Abeta treatments to improve cognitive functions. ..
  8. Xie Z, Zhang H, Tsai W, Zhang Y, Du Y, Zhong J, et al. Zinc finger protein ZBTB20 is a key repressor of alpha-fetoprotein gene transcription in liver. Proc Natl Acad Sci U S A. 2008;105:10859-64 pubmed publisher
    ..We previously identified a zinc finger protein gene ZBTB20. To determine its physiological functions in vivo, we have generated hepatocyte-specific ZBTB20 knockout mice by ..
  9. Cheng I, Palop J, Esposito L, Bien Ly N, Yan F, Mucke L. Aggressive amyloidosis in mice expressing human amyloid peptides with the Arctic mutation. Nat Med. 2004;10:1190-2 pubmed
    ..Amyloid plaques formed faster and were more extensive in Arctic mice than in hAPP mice expressing wild-type Abeta, even though Arctic mice had lower Abeta(1-42/1-40) ratios. Thus, the Arctic mutation is highly amyloidogenic in vivo. ..

More Information


  1. Harris J, Devidze N, Halabisky B, Lo I, Thwin M, Yu G, et al. Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of the amyloid precursor protein. J Neurosci. 2010;30:372-81 pubmed publisher
    ..Here we compared human APP transgenic mice with (B254) and without (J20) the D664A mutation in a battery of tests...
  2. Gaikwad S, Larionov S, Wang Y, Dannenberg H, Matozaki T, Monsonego A, et al. Signal regulatory protein-beta1: a microglial modulator of phagocytosis in Alzheimer's disease. Am J Pathol. 2009;175:2528-39 pubmed publisher
    ..found that SIRPbeta1 was up-regulated and acted as a phagocytic receptor on microglia in amyloid precursor protein J20 (APP/J20) transgenic mice and in Alzheimer's disease (AD) patients...
  3. Monsonego A, Imitola J, Petrovic S, Zota V, Nemirovsky A, Baron R, et al. Abeta-induced meningoencephalitis is IFN-gamma-dependent and is associated with T cell-dependent clearance of Abeta in a mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A. 2006;103:5048-53 pubmed
  4. Ongali B, Nicolakakis N, Lecrux C, Aboulkassim T, Rosa Neto P, Papadopoulos P, et al. Transgenic mice overexpressing APP and transforming growth factor-beta1 feature cognitive and vascular hallmarks of Alzheimer's disease. Am J Pathol. 2010;177:3071-80 pubmed publisher
  5. Cheng I, Scearce Levie K, Legleiter J, Palop J, Gerstein H, Bien Ly N, et al. Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. J Biol Chem. 2007;282:23818-28 pubmed
    ..Thus, Abeta*56 is a likelier determinant of functional deficits in hAPP mice than fibrillar Abeta deposits. Therapeutic interventions that reduce Abeta fibrils at the cost of augmenting nonfibrillar Abeta assemblies could be harmful. ..
  6. Mitchelmore C, Kjaerulff K, Pedersen H, Nielsen J, Rasmussen T, Fisker M, et al. Characterization of two novel nuclear BTB/POZ domain zinc finger isoforms. Association with differentiation of hippocampal neurons, cerebellar granule cells, and macroglia. J Biol Chem. 2002;277:7598-609 pubmed
    ..report here the isolation and characterization of two novel nuclear BTB/POZ domain zinc finger isoforms, designated HOF(L) and HOF(S), that are specifically expressed in early hippocampal neurons, cerebellar granule cells, and ..
  7. Palop J, Chin J, Roberson E, Wang J, Thwin M, Bien Ly N, et al. Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. Neuron. 2007;55:697-711 pubmed
    ..Aberrant increases in network excitability and compensatory inhibitory mechanisms in the hippocampus may contribute to Abeta-induced neurological deficits in hAPP mice and, possibly, also in humans with AD. ..
  8. Cisse M, Halabisky B, Harris J, Devidze N, Dubal D, Sun B, et al. Reversing EphB2 depletion rescues cognitive functions in Alzheimer model. Nature. 2011;469:47-52 pubmed publisher
    ..Thus, depletion of EphB2 is critical in amyloid-?-induced neuronal dysfunction. Increasing EphB2 levels or function could be beneficial in Alzheimer's disease. ..
  9. Zhang Y, Xie Z, Zhou L, Li L, Zhang H, Zhou G, et al. The zinc finger protein ZBTB20 regulates transcription of fructose-1,6-bisphosphatase 1 and ? cell function in mice. Gastroenterology. 2012;142:1571-1580.e6 pubmed publisher
    ..The zinc finger protein ZBTB20 regulates glucose homeostasis, so we investigated its effects on expression of FBP-1...
  10. Meilandt W, Yu G, Chin J, Roberson E, Palop J, Wu T, et al. Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease. J Neurosci. 2008;28:5007-17 pubmed publisher
    ..We conclude that enkephalin elevations may contribute to cognitive impairments in hAPP mice and possibly in humans with AD. The therapeutic potential of reducing enkephalin production or signaling merits further exploration. ..
  11. Sutherland A, Zhang H, Zhang Y, Michaud M, Xie Z, Patti M, et al. Zinc finger protein Zbtb20 is essential for postnatal survival and glucose homeostasis. Mol Cell Biol. 2009;29:2804-15 pubmed publisher
    b>Zbtb20 is a member of the POK family of proteins, which function primarily as transcriptional repressors via interactions mediated by their conserved C(2)H(2) Krüppel type zinc finger and BTB/POZ domains...
  12. Sun B, Halabisky B, Zhou Y, Palop J, Yu G, Mucke L, et al. Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's Disease. Cell Stem Cell. 2009;5:624-33 pubmed publisher
    ..Abeta-induced increases in GABAergic neurotransmission or an imbalance between GABAergic and glutamatergic neurotransmission may contribute to impaired neurogenesis in AD. ..
  13. Deipolyi A, Fang S, Palop J, Yu G, Wang X, Mucke L. Altered navigational strategy use and visuospatial deficits in hAPP transgenic mice. Neurobiol Aging. 2008;29:253-66 pubmed
    ..Interventions promoting flexibility in selecting learning strategies might help circumvent otherwise debilitating navigational deficits caused by AD-related hippocampal dysfunction. ..
  14. Nielsen J, Nielsen F, Ismail R, Noraberg J, Jensen N. Hippocampus-like corticoneurogenesis induced by two isoforms of the BTB-zinc finger gene Zbtb20 in mice. Development. 2007;134:1133-40 pubmed
    ..The BTB (broad complex, tramtrack, bric-a-brac)-zinc finger gene Zbtb20 (also known as HOF, Znf288, Zfp288) encodes two protein isoforms, designated Zbtb20(S) and Zbtb20(L), which are ..
  15. Palop J, Jones B, Kekonius L, Chin J, Yu G, Raber J, et al. Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits. Proc Natl Acad Sci U S A. 2003;100:9572-7 pubmed
  16. Mucke L, Masliah E, Yu G, Mallory M, Rockenstein E, Tatsuno G, et al. High-level neuronal expression of abeta 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation. J Neurosci. 2000;20:4050-8 pubmed
    ..Our results support the emerging view that plaque-independent Abeta toxicity plays an important role in the development of synaptic deficits in AD and related conditions. ..
  17. Tong X, Nicolakakis N, Kocharyan A, Hamel E. Vascular remodeling versus amyloid beta-induced oxidative stress in the cerebrovascular dysfunctions associated with Alzheimer's disease. J Neurosci. 2005;25:11165-74 pubmed
    ..We conclude that brain vessel remodeling and associated alterations in levels of vasoactive signaling molecules are key contributors to AD cerebrovascular dysfunctions. ..
  18. Saura C, Chen G, Malkani S, Choi S, Takahashi R, Zhang D, et al. Conditional inactivation of presenilin 1 prevents amyloid accumulation and temporarily rescues contextual and spatial working memory impairments in amyloid precursor protein transgenic mice. J Neurosci. 2005;25:6755-64 pubmed
    ..We found that conditional inactivation of PS1 in APP transgenic mice (PS1 cKO;APP Tg) effectively prevented the accumulation of Abeta peptides and formation of amyloid plaques and inflammatory ..
  19. Kitaguchi H, Tomimoto H, Ihara M, Shibata M, Uemura K, Kalaria R, et al. Chronic cerebral hypoperfusion accelerates amyloid beta deposition in APPSwInd transgenic mice. Brain Res. 2009;1294:202-10 pubmed publisher
    ..Taken together, chronic cerebral hypoperfusion increased Abeta fibrils and induced Abeta deposition in the intracellular compartment and, therefore, may accelerate the pathological changes of Alzheimer's disease. ..
  20. Buckwalter M, Coleman B, Buttini M, Barbour R, Schenk D, Games D, et al. Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1. J Neurosci. 2006;26:11437-41 pubmed
    ..Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization. ..
  21. Talantova M, Sanz Blasco S, Zhang X, Xia P, Akhtar M, Okamoto S, et al. A? induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss. Proc Natl Acad Sci U S A. 2013;110:E2518-27 pubmed publisher
    ..Importantly, the improved NMDAR antagonist NitroMemantine, which selectively inhibits extrasynaptic over physiological synaptic NMDAR activity, protects synapses from A?-induced damage both in vitro and in vivo. ..
  22. Ongali B, Nicolakakis N, Tong X, Aboulkassim T, Papadopoulos P, Rosa Neto P, et al. Angiotensin II type 1 receptor blocker losartan prevents and rescues cerebrovascular, neuropathological and cognitive deficits in an Alzheimer's disease model. Neurobiol Dis. 2014;68:126-36 pubmed publisher
    ..We conclude that losartan exerts potent preventive and restorative effects on AD hallmarks, possibly by mitigating AT1-initiated oxidative stress and normalizing memory-related AT4 receptors. ..
  23. Takahashi K, Kong Q, Lin Y, Stouffer N, Schulte D, Lai L, et al. Restored glial glutamate transporter EAAT2 function as a potential therapeutic approach for Alzheimer's disease. J Exp Med. 2015;212:319-32 pubmed publisher
    ..Importantly, the observed benefits were sustained one month after compound treatment cessation, suggesting that EAAT2 is a potential disease modifier with therapeutic potential for AD. ..
  24. Savas J, Wang Y, DeNardo L, Martinez Bartolome S, McClatchy D, Hark T, et al. Amyloid Accumulation Drives Proteome-wide Alterations in Mouse Models of Alzheimer's Disease-like Pathology. Cell Rep. 2017;21:2614-2627 pubmed publisher
    ..Expression of TARP?-2 in hAPP transgenic mice restored AMPA currents. This proteomic database represents a resource for the identification of protein alterations responsible for AD. ..
  25. Leissring M, Farris W, Chang A, Walsh D, Wu X, Sun X, et al. Enhanced proteolysis of beta-amyloid in APP transgenic mice prevents plaque formation, secondary pathology, and premature death. Neuron. 2003;40:1087-93 pubmed
    ..Our findings demonstrate that chronic upregulation of Abeta-degrading proteases represents an efficacious therapeutic approach to combating Alzheimer-type pathology in vivo. ..
  26. Lin M, Cheng X, Tammineni P, Xie Y, Zhou B, Cai Q, et al. Releasing Syntaphilin Removes Stressed Mitochondria from Axons Independent of Mitophagy under Pathophysiological Conditions. Neuron. 2017;94:595-610.e6 pubmed publisher
    ..Our study provides new mechanistic insights into the maintenance of axonal mitochondrial quality through SNPH-mediated coordination of mitochondrial stress and motility before activation of Parkin-mediated mitophagy. VIDEO ABSTRACT. ..
  27. Feng T, Tammineni P, Agrawal C, Jeong Y, Cai Q. Autophagy-mediated Regulation of BACE1 Protein Trafficking and Degradation. J Biol Chem. 2017;292:1679-1690 pubmed publisher
    ..Therefore, our study provides new insights into autophagy-mediated regulation of BACE1 turnover and APP processing, thus building a foundation for future development of potential Alzheimer's disease therapeutic strategies. ..
  28. Xia D, Watanabe H, Wu B, Lee S, Li Y, Tsvetkov E, et al. Presenilin-1 knockin mice reveal loss-of-function mechanism for familial Alzheimer's disease. Neuron. 2015;85:967-81 pubmed publisher
    ..Collectively, our findings reveal that FAD mutations can cause complete loss of Presenilin-1 function in vivo, suggesting that clinical PSEN mutations produce FAD through a loss-of-function mechanism. ..
  29. Larson M, Sherman M, Greimel S, Kuskowski M, Schneider J, Bennett D, et al. Soluble ?-synuclein is a novel modulator of Alzheimer's disease pathophysiology. J Neurosci. 2012;32:10253-66 pubmed publisher
    ..Altogether, our data reveal an unexpected role for soluble, intraneuronal ?Syn in AD pathophysiology. ..
  30. Sehgal N, Gupta A, Valli R, Joshi S, Mills J, Hamel E, et al. Withania somnifera reverses Alzheimer's disease pathology by enhancing low-density lipoprotein receptor-related protein in liver. Proc Natl Acad Sci U S A. 2012;109:3510-5 pubmed publisher
    ..It was similarly effective in reversing behavioral deficits and plaque load in APPSwInd mice (line J20)...
  31. Serneels L, Van Biervliet J, Craessaerts K, Dejaegere T, Horré K, Van Houtvin T, et al. gamma-Secretase heterogeneity in the Aph1 subunit: relevance for Alzheimer's disease. Science. 2009;324:639-42 pubmed publisher
    ..The Aph1B complex contributes to total gamma-secretase activity in the human brain, and thus specific targeting of Aph1B-containing gamma-secretase complexes may help generate less toxic therapies for Alzheimer's disease. ..
  32. Yin J, Maalouf M, Han P, Zhao M, Gao M, Dharshaun T, et al. Ketones block amyloid entry and improve cognition in an Alzheimer's model. Neurobiol Aging. 2016;39:25-37 pubmed publisher
    ..These observations provide us insights to understand and to establish a novel therapeutic use of ketones in AD prevention. ..
  33. Wang Y, Bhattacharya D. Adjuvant-specific regulation of long-term antibody responses by ZBTB20. J Exp Med. 2014;211:841-56 pubmed publisher
    ..alum-adjuvanted immunization, antigen-specific bone marrow plasma cells deficient in the transcription factor ZBTB20 failed to accumulate over time, leading to a progressive loss of antibody production relative to wild-type ..
  34. Liu X, Zhang P, Bao Y, Han Y, Wang Y, Zhang Q, et al. Zinc finger protein ZBTB20 promotes Toll-like receptor-triggered innate immune responses by repressing I?B? gene transcription. Proc Natl Acad Sci U S A. 2013;110:11097-102 pubmed publisher
    ..Zinc finger and BTB domain-containing 20 (ZBTB20), a member of BTB/POZ family, functions in neurogenesis and represses ?-fetoprotein gene transcription in liver...
  35. Pozueta J, Lefort R, Ribe E, Troy C, Arancio O, Shelanski M. Caspase-2 is required for dendritic spine and behavioural alterations in J20 APP transgenic mice. Nat Commun. 2013;4:1939 pubmed publisher
    ..show that caspase-2 is required for the cognitive decline seen in human amyloid precursor protein transgenic mice (J20)...
  36. Choi S, Gerencser A, Ng R, Flynn J, Melov S, Danielson S, et al. No consistent bioenergetic defects in presynaptic nerve terminals isolated from mouse models of Alzheimer's disease. J Neurosci. 2012;32:16775-84 pubmed publisher
    ..and hippocampal presynaptic nerve terminals (synaptosomes) from commonly used mouse models with AD-like phenotypes (J20 age 6 months, Tg2576 age 16 months, and APP/PS age 9 and 14 months) to age-matched controls...
  37. Verret L, Mann E, Hang G, Barth A, Cobos I, Ho K, et al. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model. Cell. 2012;149:708-21 pubmed publisher
    ..We conclude that reduced Nav1.1 levels and PV cell dysfunction critically contribute to abnormalities in oscillatory rhythms, network synchrony, and memory in hAPP mice and possibly in AD. ..
  38. Simón A, Schiapparelli L, Salazar Colocho P, Cuadrado Tejedor M, Escribano L, Lopez de Maturana R, et al. Overexpression of wild-type human APP in mice causes cognitive deficits and pathological features unrelated to Abeta levels. Neurobiol Dis. 2009;33:369-78 pubmed publisher
    ..The results support the notion of Abeta-independent pathogenic pathways in Alzheimer's disease. ..
  39. Gültner S, Laue M, Riemer C, Heise I, Baier M. Prion disease development in slow Wallerian degeneration (Wld(S)) mice. Neurosci Lett. 2009;456:93-8 pubmed publisher
    ..These findings distinguish the neurodegeneration occuring in this prion model from chronic neurodegenerative diseases, in which the Wld(S)-mutation provides axon protection and greatly improves the clinical outcome...
  40. Hong S, Quintero Monzon O, Ostaszewski B, Podlisny D, Cavanaugh W, Yang T, et al. Dynamic analysis of amyloid ?-protein in behaving mice reveals opposing changes in ISF versus parenchymal A? during age-related plaque formation. J Neurosci. 2011;31:15861-9 pubmed publisher
  41. Fang D, Wang Y, Zhang Z, Du H, Yan S, Sun Q, et al. Increased neuronal PreP activity reduces Aβ accumulation, attenuates neuroinflammation and improves mitochondrial and synaptic function in Alzheimer disease's mouse model. Hum Mol Genet. 2015;24:5198-210 pubmed publisher
    ..Thus, enhancing PreP activity/expression may be a new therapeutic avenue for treatment of AD. ..
  42. Du H, Guo L, Wu X, Sosunov A, McKhann G, Chen J, et al. Cyclophilin D deficiency rescues A?-impaired PKA/CREB signaling and alleviates synaptic degeneration. Biochim Biophys Acta. 2014;1842:2517-27 pubmed publisher
  43. Vega Flores G, Rubio S, Jurado Parras M, Gomez Climent M, Hampe C, Manto M, et al. The GABAergic septohippocampal pathway is directly involved in internal processes related to operant reward learning. Cereb Cortex. 2014;24:2093-107 pubmed publisher
    ..Self-stimulation was evoked in wild-type (WT) mice using instrumental conditioning procedures and in J20 mutant mice, a type of mouse with a significant deficit in GABAergic septohippocampal projections...
  44. Liu R, Lei J, Luo C, Lan X, Chi L, Deng P, et al. Increased EID1 nuclear translocation impairs synaptic plasticity and memory function associated with pathogenesis of Alzheimer's disease. Neurobiol Dis. 2012;45:902-12 pubmed publisher
    ..Together, our data raise the possibility that alteration of EID1 expression, particularly the increase of EID1 nuclear localization that inhibits CBP/p300 activity in neuronal cells, may play an important role in AD pathogenesis. ..
  45. Hazra A, Corbett B, You J, Aschmies S, Zhao L, Li K, et al. Corticothalamic network dysfunction and behavioral deficits in a mouse model of Alzheimer's disease. Neurobiol Aging. 2016;44:96-107 pubmed publisher
  46. Aucoin J, Jiang P, Aznavour N, Tong X, Buttini M, Descarries L, et al. Selective cholinergic denervation, independent from oxidative stress, in a mouse model of Alzheimer's disease. Neuroscience. 2005;132:73-86 pubmed
  47. Beauquis J, Pavía P, Pomilio C, Vinuesa A, Podlutskaya N, Galvan V, et al. Environmental enrichment prevents astroglial pathological changes in the hippocampus of APP transgenic mice, model of Alzheimer's disease. Exp Neurol. 2013;239:28-37 pubmed publisher
    ..We thus characterized astroglial changes in the hippocampus of adult PDAPP-J20 transgenic mice, a model of AD, exposed for 3 months to an enriched environment, from 5 to 8 months of age...
  48. Hébert F, Grand Maison M, Ho M, Lerch J, Hamel E, Bedell B. Cortical atrophy and hypoperfusion in a transgenic mouse model of Alzheimer's disease. Neurobiol Aging. 2013;34:1644-52 pubmed publisher
    ..Previously unreported regional genotype differences and age-related changes in cortical thickness and cerebral perfusion were identified in amyloid precursor protein transgenic and wild-type mice. ..
  49. Mueller Steiner S, Zhou Y, Arai H, Roberson E, Sun B, Chen J, et al. Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer's disease. Neuron. 2006;51:703-14 pubmed
    ..Thus, CatB likely fulfills antiamyloidogenic and neuroprotective functions. Insufficient CatB activity might promote AD; increasing CatB activity could counteract the neuropathology of this disease. ..
  50. Dong Q, Chen X, Li G. Effect of transcription factor ZBTB20 on mouse pituitary development. Genet Mol Res. 2015;14:17622-9 pubmed publisher
    ..The transcriptional factor ZBTB20 is widely expressed in brain tissues and participates in hippocampal development; however, the detailed molecular ..
  51. Roberson E, Halabisky B, Yoo J, Yao J, Chin J, Yan F, et al. Amyloid-?/Fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of Alzheimer's disease. J Neurosci. 2011;31:700-11 pubmed publisher
    ..Our results indicate that A?, tau, and Fyn jointly impair synaptic and network function and suggest that disrupting the copathogenic relationship between these factors could be of therapeutic benefit. ..
  52. Moreno H, Wu W, Lee T, Brickman A, Mayeux R, Brown T, et al. Imaging the Abeta-related neurotoxicity of Alzheimer disease. Arch Neurol. 2007;64:1467-77 pubmed
    ..Cross-sectional study comparing humans with AD and control subjects, cross-sectional study of J20 mice, a transgenic mouse model of AD, and a longitudinal study of flurbiprofen administration to transgenic mice...
  53. Tesseur I, Zou K, Esposito L, Bard F, Berber E, Can J, et al. Deficiency in neuronal TGF-beta signaling promotes neurodegeneration and Alzheimer's pathology. J Clin Invest. 2006;116:3060-9 pubmed
    ..These results show that reduced neuronal TGF-beta signaling increases age-dependent neurodegeneration and AD-like disease in vivo. Increasing neuronal TGF-beta signaling may thus reduce neurodegeneration and be beneficial in AD. ..
  54. Seabrook T, Jiang L, Maier M, Lemere C. Minocycline affects microglia activation, Abeta deposition, and behavior in APP-tg mice. Glia. 2006;53:776-82 pubmed
    ..Therefore, anti-inflammatory therapies to suppress microglial activation or function may reduce cytokine production but enhance Abeta plaque formation early in AD. ..
  55. Yamada M, Ihara M, Okamoto Y, Maki T, Washida K, Kitamura A, et al. The influence of chronic cerebral hypoperfusion on cognitive function and amyloid ? metabolism in APP overexpressing mice. PLoS ONE. 2011;6:e16567 pubmed publisher
    ..The results suggest interaction between chronic cerebral hypoperfusion and APP(Sw/Ind) overexpression in cognitive decline in mice through enhanced neuronal loss and altered amyloid ? metabolism. ..
  56. Belkacemi A, Ramassamy C. Time sequence of oxidative stress in the brain from transgenic mouse models of Alzheimer's disease related to the amyloid-? cascade. Free Radic Biol Med. 2012;52:593-600 pubmed publisher
    ..Here we review the evidence for increased free radical-mediated damage to the brain with particular attention to the stage of the disease in various transgenic models of AD related to the amyloid-? cascade. ..
  57. Baron R, Harpaz I, Nemirovsky A, Cohen H, Monsonego A. Immunity and neuronal repair in the progression of Alzheimer's disease: a brief overview. Exp Gerontol. 2007;42:64-9 pubmed
  58. Oue H, Miyamoto Y, Okada S, Koretake K, Jung C, Michikawa M, et al. Tooth loss induces memory impairment and neuronal cell loss in APP transgenic mice. Behav Brain Res. 2013;252:318-25 pubmed publisher
    ..Seventeen female transgenic mice (J20) were divided into the experimental (EX, n=10) and control (C, n=7) groups...
  59. Hargis K, Blalock E. Transcriptional signatures of brain aging and Alzheimer's disease: What are our rodent models telling us?. Behav Brain Res. 2017;322:311-328 pubmed publisher
    ..These results suggest that normal brain aging is similar in humans and research animals, and that different transgenic AD model mice may reflect selected aspects of AD pathology. ..
  60. Mairet Coello G, Courchet J, Pieraut S, Courchet V, Maximov A, Polleux F. The CAMKK2-AMPK kinase pathway mediates the synaptotoxic effects of A? oligomers through Tau phosphorylation. Neuron. 2013;78:94-108 pubmed publisher
    ..Our results identify a CAMKK2-AMPK-Tau pathway as a critical mediator of the synaptotoxic effects of A?42 oligomers. ..
  61. Frake R, Ricketts T, Menzies F, Rubinsztein D. Autophagy and neurodegeneration. J Clin Invest. 2015;125:65-74 pubmed publisher
    ..Finally, we briefly describe some of the signaling pathways that may be amenable to therapeutic targeting for these goals. ..
  62. Kam T, Park H, Gwon Y, Song S, Kim S, Moon S, et al. Fc?RIIb-SHIP2 axis links A? to tau pathology by disrupting phosphoinositide metabolism in Alzheimer's disease model. elife. 2016;5: pubmed publisher
    ..Thus, we concluded that the Fc?RIIb-SHIP2 axis links A? neurotoxicity to tau pathology by dysregulating PtdIns(3,4)P2 metabolism, providing insight into therapeutic potential against AD. ..
  63. Murakami K, Yokoyama S, Murata N, Ozawa Y, Irie K, Shirasawa T, et al. Insulin receptor mutation results in insulin resistance and hyperinsulinemia but does not exacerbate Alzheimer's-like phenotypes in mice. Biochem Biophys Res Commun. 2011;409:34-9 pubmed publisher
    ..Interestingly, the insulin receptor mutation reduced oxidative damage in the brains of the AD mice. These findings suggest that insulin resistance is not always involved in the pathogenesis of AD. ..
  64. Maier M, Peng Y, Jiang L, Seabrook T, Carroll M, Lemere C. Complement C3 deficiency leads to accelerated amyloid beta plaque deposition and neurodegeneration and modulation of the microglia/macrophage phenotype in amyloid precursor protein transgenic mice. J Neurosci. 2008;28:6333-41 pubmed publisher
    ..Our results suggest a beneficial role for complement C3 in plaque clearance and neuronal health as well as in modulation of the microglia phenotype. ..
  65. Durand D, Carniglia L, Beauquis J, Caruso C, Saravia F, Lasaga M. Astroglial mGlu3 receptors promote alpha-secretase-mediated amyloid precursor protein cleavage. Neuropharmacology. 2014;79:180-9 pubmed publisher
    ..Using the PDAPP-J20 murine model of AD we described a strong reduction in mGlu2/3 receptor expression in the hippocampus of 5- and 14-..
  66. Bien Ly N, Andrews Zwilling Y, Xu Q, Bernardo A, Wang C, Huang Y. C-terminal-truncated apolipoprotein (apo) E4 inefficiently clears amyloid-beta (Abeta) and acts in concert with Abeta to elicit neuronal and behavioral deficits in mice. Proc Natl Acad Sci U S A. 2011;108:4236-41 pubmed publisher
    ..Thus, the C-terminal-truncated apoE4 fragment inefficiently clears A? peptides and acts in concert with low levels of A? to elicit neuronal and behavioral deficits in mice. ..
  67. Zou K, Liu J, Watanabe A, Hiraga S, Liu S, Tanabe C, et al. A?43 is the earliest-depositing A? species in APP transgenic mouse brain and is converted to A?41 by two active domains of ACE. Am J Pathol. 2013;182:2322-31 pubmed publisher
    ..Activities of both ACE domains may be important for reducing A?43 levels in serum and reducing brain A?43 deposition. ..
  68. Chin J, Palop J, Yu G, Kojima N, Masliah E, Mucke L. Fyn kinase modulates synaptotoxicity, but not aberrant sprouting, in human amyloid precursor protein transgenic mice. J Neurosci. 2004;24:4692-7 pubmed
    ..We conclude that Fyn-dependent pathways are critical in AD-related synaptotoxicity and that the pathogenesis of hAPP/Abeta-induced neuronal alterations may be mechanistically heterogenous. ..
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