Login Register Cart 0
Generic placeholder image

CNS & Neurological Disorders - Drug Targets

Editor-in-Chief

ISSN (Print): 1871-5273
ISSN (Online): 1996-3181

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe
Review Article

Pharmacotherapy of Down’s Syndrome: When and Which?

Author(s): Seyed K. Tayebati*, Alessandro Cecchi, Ilenia Martinelli, Elisa Carboni and Francesco Amenta

Volume 18, Issue 10, 2019

Page: [750 - 757] Pages: 8

DOI: 10.2174/1871527318666191114092924

Price: $65

Abstract

Down Syndrome (DS) is an essential genetic disease that involves many other body systems along with cerebral functions. The postnatal approach to treat this genetic disease includes intervention on various related disorders (e.g., heart failure, respiratory, oral, ear, and hearing disorders). However, different proposed treatments do not significantly improve the quality of life of these subjects. Another approach to the treatment of DS considering the possibility to intervene on the embryo was recently introduced. As of this, the current study has reviewed different outcomes regarding DS treatment in an animal model, namely the Ts65Dn mouse. The obtained results encouraged spending more time, efforts, and resources in this field. Besides, various treatment strategies were tried to include genetic modification, treatment with vasoactive intestinal peptide derivatives or fluoxetine. However, the main obstacle to the use of these possible treatments is the ethical issues it raises. The progression of the pregnancy in spite of awareness that DS affects the unborn and prenatal treatment of DS injured embryo are relevant dilemmas. Thus, talented researchers should spend more efforts to improve the quality of life for people affected by DS, which will allow probably a better approach to the ethical issues.

Keywords: Down’s syndrome, associated disorders, animal models, prenatal and postnatal therapies, pharmacotherapy, DS-induced disorders.

« Previous Next »
Graphical Abstract

[1]
O’Neill KL, Shults J, Stallings VA, Stettler N. Child-feeding practices in children with Down syndrome and their siblings. J Pediatr 2005; 146(2): 234-8.
[http://dx.doi.org/10.1016/j.jpeds.2004.10.045] [PMID: 15689916]
[2]
Sadowska L, Mysłek-Prucnal M, Choińska AM, Mazurek A. Diagnosis and treatment of children with down syndrome in the light of their own and review of literature. Przegl Med Uniw Rzesz 2009; 1: 8-30.
[3]
Mazurek D, Wyka J. Down syndrome--genetic and nutritional aspects of accompanying disorders. Rocz Panstw Zakl Hig 2015; 66(3): 189-94.
[PMID: 26400113]
[4]
Bernal JE, Briceno I. Genetic and other diseases in the pottery of Tumaco-La Tolita culture in Colombia-Ecuador. Clin Genet 2006; 70(3): 188-91.
[http://dx.doi.org/10.1111/j.1399-0004.2006.00670.x] [PMID: 16922718]
[5]
Levitas AS, Reid CS. An angel with Down syndrome in a sixteenth century Flemish Nativity painting. Am J Med Genet A 2003; 116A(4): 399-405.
[http://dx.doi.org/10.1002/ajmg.a.10043] [PMID: 12522800]
[6]
Mégarbané A, Ravel A, Mircher C, et al. The 50th anniversary of the discovery of trisomy 21: The past, present, and future of research and treatment of Down syndrome. Genet Med 2009; 11(9): 611-6.
[http://dx.doi.org/10.1097/GIM.0b013e3181b2e34c] [PMID: 19636252]
[7]
Rivollat M, Castex D, Hauret L, Tillier AM. Ancient Down syndrome: An osteological case from Saint-Jean-des-Vignes, northeastern France, from the 5-6th century AD. Int J Paleopathol 2014; 7: 8-14.
[http://dx.doi.org/10.1016/j.ijpp.2014.05.004] [PMID: 29539495]
[8]
Kazemi M, Salehi M, Kheirollahi M. Down syndrome: Current status, challenges and future perspectives. Int J Mol Cell Med 2016; 5(3): 125-33.
[PMID: 27942498]
[9]
Antonarakis SE. Human chromosome 21: Genome mapping and exploration, circa 1993. Trends Genet 1993; 9(4): 142-8.
[http://dx.doi.org/10.1016/0168-9525(93)90210-9] [PMID: 8516850]
[10]
Hattori M, Fujiyama A, Taylor TD, et al. Chromosome 21 mapping and sequencing consortium. The DNA sequence of human chromosome 21. Nature 2000; 405(6784): 311-9.
[http://dx.doi.org/10.1038/35012518] [PMID: 10830953]
[11]
Lyle R, Béna F, Gagos S, et al. Genotype-phenotype correlations in Down syndrome identified by array CGH in 30 cases of partial trisomy and partial monosomy chromosome 21. Eur J Hum Genet 2009; 17(4): 454-66.
[http://dx.doi.org/10.1038/ejhg.2008.214] [PMID: 19002211]
[12]
Oster J, Mikkelsen M, Nielsen A. Mortality and life-table in Down’s syndrome. Acta Paediatr Scand 1975; 64(2): 322-6.
[http://dx.doi.org/10.1111/j.1651-2227.1975.tb03842.x] [PMID: 124122]
[13]
Englund A, Jonsson B, Zander CS, Gustafsson J, Annerén G. Changes in mortality and causes of death in the Swedish Down syndrome population. Am J Med Genet A 2013; 161A(4): 642-9.
[http://dx.doi.org/10.1002/ajmg.a.35706] [PMID: 23436430]
[14]
Arumugam A, Raja K, Venugopalan M, et al. Down syndrome-A narrative review with a focus on anatomical features. Clin Anat 2016; 29(5): 568-77.
[http://dx.doi.org/10.1002/ca.22672] [PMID: 26599319]
[15]
Roizen NJ, Patterson D. Down’s syndrome. Lancet 2003; 361(9365): 1281-9.
[http://dx.doi.org/10.1016/S0140-6736(03)12987-X] [PMID: 12699967]
[16]
Day SM, Strauss DJ, Shavelle RM, Reynolds RJ. Mortality and causes of death in persons with Down syndrome in California. Dev Med Child Neurol 2005; 47(3): 171-6.
[http://dx.doi.org/10.1017/S0012162205000319] [PMID: 15739721]
[17]
Rankin J, Tennant PWG, Bythell M, Pearce MS. Predictors of survival in children born with Down syndrome: A registry-based study. Pediatrics 2012; 129(6): e1373-81.
[http://dx.doi.org/10.1542/peds.2011-3051] [PMID: 22614780]
[18]
Caballero-Villarraso J, Galvan A, Escribano BM, Tunez I. Interrelationships among gut microbiota and host: Paradigms, role in neurodegenerative diseases and future prospects. CNS Neurol Disord Drug Targets 2017; 16(8): 945-64.
[PMID: 28714393]
[19]
Marin-Padilla M. Structural abnormalities of the cerebral cortex in human chromosomal aberrations: A Golgi study. Brain Res 1972; 44(2): 625-9.
[http://dx.doi.org/10.1016/0006-8993(72)90324-1] [PMID: 4263073]
[20]
Coyle JT, Oster-Granite ML, Gearhart JD. The neurobiologic consequences of Down syndrome. Brain Res Bull 1986; 16(6): 773-87.
[http://dx.doi.org/10.1016/0361-9230(86)90074-2] [PMID: 2875770]
[21]
Golden JA, Hyman BT. Development of the superior temporal neocortex is anomalous in trisomy 21. J Neuropathol Exp Neurol 1994; 53(5): 513-20.
[http://dx.doi.org/10.1097/00005072-199409000-00011] [PMID: 8083693]
[22]
Chakrabarti L, Scafidi J, Gallo V, Haydar TF. Environmental enrichment rescues postnatal neurogenesis defect in the male and female Ts65Dn mouse model of Down syndrome. Dev Neurosci 2011; 33(5): 428-41.
[http://dx.doi.org/10.1159/000329423] [PMID: 21865665]
[23]
Nadel L. Down’s syndrome: A genetic disorder in biobehavioral perspective. Genes Brain Behav 2003; 2(3): 156-66.
[http://dx.doi.org/10.1034/j.1601-183X.2003.00026.x] [PMID: 12931789]
[24]
Benavides-Piccione R, Ballesteros-Yáñez I, de Lagrán MM, et al. On dendrites in Down syndrome and DS murine models: A spiny way to learn. Prog Neurobiol 2004; 74(2): 111-26.
[http://dx.doi.org/10.1016/j.pneurobio.2004.08.001] [PMID: 15518956]
[25]
Torres MD, Garcia O, Tang C, Busciglio J. Dendritic spine pathology and thrombospondin-1 deficits in Down syndrome. Free Radic Biol Med 2018; 114: 10-4.
[http://dx.doi.org/10.1016/j.freeradbiomed.2017.09.025] [PMID: 28965914]
[26]
Iulita MF, Caraci F, Cuello AC. A link between nerve growth factor metabolic deregulation and amyloid-β-driven inflammation in Down syndrome. CNS Neurol Disord Drug Targets 2016; 15(4): 434-47.
[http://dx.doi.org/10.2174/1871527315666160321104916] [PMID: 26996175]
[27]
Ballard C, Mobley W, Hardy J, Williams G, Corbett A. Dementia in Down’s syndrome. Lancet Neurol 2016; 15(6): 622-36.
[http://dx.doi.org/10.1016/S1474-4422(16)00063-6] [PMID: 27302127]
[28]
Vicari S, Bellucci S, Carlesimo GA. Visual and spatial long-term memory: Differential pattern of impairments in Williams and Down syndromes. Dev Med Child Neurol 2005; 47(5): 305-11.
[http://dx.doi.org/10.1017/S0012162205000599] [PMID: 15892372]
[29]
Contestabile A, Benfenati F, Gasparini L. Communication breaks-Down: From neurodevelopment defects to cognitive disabilities in Down syndrome. Prog Neurobiol 2010; 91(1): 1-22.
[http://dx.doi.org/10.1016/j.pneurobio.2010.01.003] [PMID: 20097253]
[30]
Grieco J, Pulsifer M, Seligsohn K, Skotko B, Schwartz A. Down syndrome: Cognitive and behavioral functioning across the lifespan. Am J Med Genet C Semin Med Genet 2015; 169(2): 135-49.
[http://dx.doi.org/10.1002/ajmg.c.31439] [PMID: 25989505]
[31]
Pulsifer MB. The neuropsychology of mental retardation. J Int Neuropsychol Soc 1996; 2(2): 159-76.
[http://dx.doi.org/10.1017/S1355617700001016] [PMID: 9375201]
[32]
Anderson JS, Nielsen JA, Ferguson MA, et al. Abnormal brain synchrony in Down Syndrome. Neuroimage Clin 2013; 2: 703-15.
[http://dx.doi.org/10.1016/j.nicl.2013.05.006] [PMID: 24179822]
[33]
Daunhauer LA, Fidler DJ, Hahn L, Will E, Lee NR, Hepburn S. Profiles of everyday executive functioning in young children with down syndrome. Am J Intellect Dev Disabil 2014; 119(4): 303-18.
[http://dx.doi.org/10.1352/1944-7558-119.4.303] [PMID: 25007296]
[34]
Tayebati SK. Animal models of cognitive dysfunction. Mech Ageing Dev 2006; 127(2): 100-8.
[http://dx.doi.org/10.1016/j.mad.2005.09.026] [PMID: 16293295]
[35]
Reeves RH. Down syndrome mouse models are looking up. Trends Mol Med 2006; 12(6): 237-40.
[http://dx.doi.org/10.1016/j.molmed.2006.04.005] [PMID: 16677859]
[36]
Roncacé V, Burattini C, Stagni F, et al. Neuroanatomical alterations and synaptic plasticity impairment in the perirhinal cortex of the Ts65Dn mouse model of Down syndrome. Neurobiol Dis 2017; 106: 89-100.
[http://dx.doi.org/10.1016/j.nbd.2017.06.017] [PMID: 28651891]
[37]
Reeves RH, Irving NG, Moran TH, et al. A mouse model for Down syndrome exhibits learning and behaviour deficits. Nat Genet 1995; 11(2): 177-84.
[http://dx.doi.org/10.1038/ng1095-177] [PMID: 7550346]
[38]
Demas GE, Nelson RJ, Krueger BK, Yarowsky PJ. Spatial memory deficits in segmental trisomic Ts65Dn mice. Behav Brain Res 1996; 82(1): 85-92.
[http://dx.doi.org/10.1016/S0166-4328(97)81111-4] [PMID: 9021073]
[39]
Belichenko PV, Kleschevnikov AM, Salehi A, Epstein CJ, Mobley WC. Synaptic and cognitive abnormalities in mouse models of Down syndrome: Exploring genotype-phenotype relationships. J Comp Neurol 2007; 504(4): 329-45.
[http://dx.doi.org/10.1002/cne.21433] [PMID: 17663443]
[40]
Salehi A, Faizi M, Colas D, et al. Restoration of norepinephrine-modulated contextual memory in a mouse model of Down syndrome. Sci Transl Med 2009; 1(7): 7ra17.
[http://dx.doi.org/10.1126/scitranslmed.3000258] [PMID: 20368182]
[41]
Bianchi P, Ciani E, Guidi S, et al. Early pharmacotherapy restores neurogenesis and cognitive performance in the Ts65Dn mouse model for Down syndrome. J Neurosci 2010; 30(26): 8769-79.
[http://dx.doi.org/10.1523/JNEUROSCI.0534-10.2010] [PMID: 20592198]
[42]
Gruart A, Leal-Campanario R, López-Ramos JC, Delgado-García JM. Functional basis of associative learning and its relationships with long-term potentiation evoked in the involved neural circuits: Lessons from studies in behaving mammals. Neurobiol Learn Mem 2015; 124: 3-18.
[http://dx.doi.org/10.1016/j.nlm.2015.04.006] [PMID: 25916668]
[43]
Siarey RJ, Stoll J, Rapoport SI, Galdzicki Z. Altered long-term potentiation in the young and old Ts65Dn mouse, a model for Down Syndrome. Neuropharmacology 1997; 36(11-12): 1549-54.
[http://dx.doi.org/10.1016/S0028-3908(97)00157-3] [PMID: 9517425]
[44]
Kleschevnikov AM, Belichenko PV, Villar AJ, Epstein CJ, Malenka RC, Mobley WC. Hippocampal long-term potentiation suppressed by increased inhibition in the Ts65Dn mouse, a genetic model of Down syndrome. J Neurosci 2004; 24(37): 8153-60.
[http://dx.doi.org/10.1523/JNEUROSCI.1766-04.2004] [PMID: 15371516]
[45]
Kleschevnikov AM, Belichenko PV, Faizi M, et al. Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists. J Neurosci 2012; 32(27): 9217-27.
[http://dx.doi.org/10.1523/JNEUROSCI.1673-12.2012] [PMID: 22764230]
[46]
Costa AC, Grybko MJ. Deficits in hippocampal CA1 LTP induced by TBS but not HFS in the Ts65Dn mouse: A model of Down syndrome. Neurosci Lett 2005; 382(3): 317-22.
[http://dx.doi.org/10.1016/j.neulet.2005.03.031] [PMID: 15925111]
[47]
Begenisic T, Baroncelli L, Sansevero G, et al. Fluoxetine in adulthood normalizes GABA release and rescues hippocampal synaptic plasticity and spatial memory in a mouse model of Down syndrome. Neurobiol Dis 2014; 63: 12-9.
[http://dx.doi.org/10.1016/j.nbd.2013.11.010] [PMID: 24269730]
[48]
Kleschevnikov AM, Belichenko PV, Salehi A, Wu C. Discoveries in Down syndrome: Moving basic science to clinical care. Prog Brain Res In: 2012; 197: pp. 199-221.
[http://dx.doi.org/10.1016/B978-0-444-54299-1.00010-8] [PMID: 22541294]
[49]
Dierssen M, Vallina IF, Baamonde C, García-Calatayud S, Lumbreras MA, Flórez J. Alterations of central noradrenergic transmission in Ts65Dn mouse, a model for Down syndrome. Brain Res 1997; 749(2): 238-44.
[http://dx.doi.org/10.1016/S0006-8993(96)01173-0] [PMID: 9138724]
[50]
Lockrow J, Boger H, Gerhardt G, Aston-Jones G, Bachman D, Granholm AC. A noradrenergic lesion exacerbates neurodegeneration in a Down syndrome mouse model. J Alzheimers Dis 2011; 23(3): 471-89.
[http://dx.doi.org/10.3233/JAD-2010-101218] [PMID: 21098982]
[51]
Dekker AD, Vermeiren Y, Albac C, et al. Aging rather than aneuploidy affects monoamine neurotransmitters in brain regions of Down syndrome mouse models. Neurobiol Dis 2017; 105: 235-44.
[http://dx.doi.org/10.1016/j.nbd.2017.06.007] [PMID: 28624415]
[52]
Lana-Elola E, Watson-Scales S, Slender A, et al. Genetic dissection of Down syndrome-associated congenital heart defects using a new mouse mapping panel. eLife 2016; 5: e11614.
[http://dx.doi.org/10.7554/eLife.11614] [PMID: 26765563]
[53]
Davisson MT, Schmidt C, Akeson EC. Segmental trisomy of murine chromosome 16: A new model system for studying Down syndrome. Prog Clin Biol Res 1990; 360: 263-80.
[PMID: 2147289]
[54]
Duchon A, Raveau M, Chevalier C, Nalesso V, Sharp AJ, Herault Y. Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: Relevance for modeling Down syndrome. Mamm Genome 2011; 22(11-12): 674-84.
[http://dx.doi.org/10.1007/s00335-011-9356-0] [PMID: 21953411]
[55]
Fortress AM, Hamlett ED, Vazey EM, et al. Designer receptors enhance memory in a mouse model of Down syndrome. J Neurosci 2015; 35(4): 1343-53.
[http://dx.doi.org/10.1523/JNEUROSCI.2658-14.2015] [PMID: 25632113]
[56]
Phillips C, Fahimi A, Das D, Mojabi FS, Ponnusamy R, Salehi A. Noradrenergic system in Down syndrome and Alzheimer’s disease: a target for therapy. Curr Alzheimer Res 2016; 13(1): 68-83.
[http://dx.doi.org/10.2174/1567205012666150921095924] [PMID: 26391048]
[57]
Guidi S, Bianchi P, Stagni F, et al. Lithium restores age-related olfactory impairment in the Ts65Dn mouse model of Down Syndrome. CNS Neurol Disord Drug Targets 2017; 16(7): 812-9.
[http://dx.doi.org/10.2174/1871527315666160801143108] [PMID: 27488422]
[58]
Stagni F, Giacomini A, Guidi S, Ciani E, Bartesaghi R. Timing of therapies for Down syndrome: The sooner, the better. Front Behav Neurosci 2015; 9: 265.
[http://dx.doi.org/10.3389/fnbeh.2015.00265] [PMID: 26500515]
[59]
Rueda N, Flórez J, Martínez-Cué C. Chronic pentylenetetrazole but not donepezil treatment rescues spatial cognition in Ts65Dn mice, a model for Down syndrome. Neurosci Lett 2008; 433(1): 22-7.
[http://dx.doi.org/10.1016/j.neulet.2007.12.039] [PMID: 18226451]
[60]
de Souza FM, Busquet N, Blatner M, Maclean KN, Restrepo D, Restrepot D. Galantamine improves olfactory learning in the Ts65Dn mouse model of Down syndrome. Sci Rep 2011; 1: 137.
[http://dx.doi.org/10.1038/srep00137] [PMID: 22355654]
[61]
Vidal V, García S, Martínez P, et al. Lack of behavioral and cognitive effects of chronic ethosuximide and gabapentin treatment in the Ts65Dn mouse model of Down syndrome. Neuroscience 2012; 220: 158-68.
[http://dx.doi.org/10.1016/j.neuroscience.2012.06.031] [PMID: 22728103]
[62]
Rueda N, Llorens-Martín M, Flórez J, et al. Memantine normalizes several phenotypic features in the Ts65Dn mouse model of Down syndrome. J Alzheimers Dis 2010; 21(1): 277-90.
[http://dx.doi.org/10.3233/JAD-2010-100240] [PMID: 20421694]
[63]
Incerti M, Toso L, Vink J, et al. Prevention of learning deficit in a Down syndrome model. Obstet Gynecol 2011; 117(2 Pt 1): 354-61.
[http://dx.doi.org/10.1097/AOG.0b013e3182051ca5] [PMID: 21252750]
[64]
Blanchard J, Bolognin S, Chohan MO, Rabe A, Iqbal K, Grundke-Iqbal I. Rescue of synaptic failure and alleviation of learning and memory impairments in a trisomic mouse model of down syndrome. J Neuropathol Exp Neurol 2011; 70(12): 1070-9.
[http://dx.doi.org/10.1097/NEN.0b013e318236e9ad] [PMID: 22082658]
[65]
Granholm AC, Ford KA, Hyde LA, et al. Estrogen restores cognition and cholinergic phenotype in an animal model of Down syndrome. Physiol Behav 2002; 77(2-3): 371-85.
[http://dx.doi.org/10.1016/S0031-9384(02)00884-3] [PMID: 12419414]
[66]
De la Torre R, De Sola S, Pons M, et al. Epigallocatechin-3-gallate, a DYRK1A inhibitor, rescues cognitive deficits in Down syndrome mouse models and in humans. Mol Nutr Food Res 2014; 58(2): 278-88.
[http://dx.doi.org/10.1002/mnfr.201300325] [PMID: 24039182]
[67]
Clark S, Schwalbe J, Stasko MR, Yarowsky PJ, Costa AC. Fluoxetine rescues deficient neurogenesis in hippocampus of the Ts65Dn mouse model for Down syndrome. Exp Neurol 2006; 200(1): 256-61.
[http://dx.doi.org/10.1016/j.expneurol.2006.02.005] [PMID: 16624293]
[68]
Lockrow J, Prakasam A, Huang P, Bimonte-Nelson H, Sambamurti K, Granholm AC. Cholinergic degeneration and memory loss delayed by vitamin E in a Down syndrome mouse model. Exp Neurol 2009; 216(2): 278-89.
[http://dx.doi.org/10.1016/j.expneurol.2008.11.021] [PMID: 19135442]
[69]
Nakano-Kobayashi A, Awaya T, Kii I, et al. Prenatal neurogenesis induction therapy normalizes brain structure and function in Down syndrome mice. Proc Natl Acad Sci USA 2017; 114(38): 10268-73.
[http://dx.doi.org/10.1073/pnas.1704143114] [PMID: 28874550]
[70]
Vasudeva K, Chaurasia P, Singh S, Munshi A. Genetic signatures in ischemic stroke: Focus on aspirin resistance. CNS Neurol Disord Drug Targets 2017; 16(9): 974-82.
[PMID: 28969559]
[71]
Putteeraj M, Fairuz YM, Teoh SL. MicroRNA dysregulation in Alzheimer’s disease. CNS Neurol Disord Drug Targets 2017; 16(9): 1000-9.
[PMID: 28782488]
[72]
Ohno Y, Tokudome K. Therapeutic role of synaptic vesicle glycoprotein 2A (SV2A) in modulating epileptogenesis. CNS Neurol Disord Drug Targets 2017; 16(4): 463-71.
[http://dx.doi.org/10.2174/1871527316666170404115027] [PMID: 28393712]
[73]
Simmons DA, Longo FM, Massa SM. Neurotrophin receptor signaling as a therapeutic target for huntington’s disease. CNS Neurol Disord Drug Targets 2017; 16(3): 291-302.
[http://dx.doi.org/10.2174/1871527315666161107093047] [PMID: 27823570]
[74]
Busciglio J, Pelsman A, Helguera P, et al. NAP and ADNF-9 protect normal and Down’s syndrome cortical neurons from oxidative damage and apoptosis. Curr Pharm Des 2007; 13(11): 1091-8.
[http://dx.doi.org/10.2174/138161207780618957] [PMID: 17430172]
[75]
Incerti M, Horowitz K, Roberson R, et al. Prenatal treatment prevents learning deficit in Down syndrome model. PLoS One 2012; 7(11): e50724.
[http://dx.doi.org/10.1371/journal.pone.0050724] [PMID: 23209818]
[76]
Guidi S, Stagni F, Bianchi P, et al. Prenatal pharmacotherapy rescues brain development in a Down’s syndrome mouse model. Brain 2014; 137(Pt 2): 380-401.
[http://dx.doi.org/10.1093/brain/awt340] [PMID: 24334313]
[77]
Guedj F, Bianchi DW, Delabar JM. Prenatal treatment of Down syndrome: A reality? Curr Opin Obstet Gynecol 2014; 26(2): 92-103.
[http://dx.doi.org/10.1097/GCO.0000000000000056] [PMID: 24573065]
[78]
Guedj F, Pennings JL, Massingham LJ, et al. An integrated human/murine transcriptome and pathway approach to identify prenatal treatments for Down syndrome. Sci Rep 2016; 6: 32353.
[http://dx.doi.org/10.1038/srep32353] [PMID: 27586445]
[79]
Kuehn BM. Treating trisomies: Prenatal Down’s syndrome therapies explored in mice. Nat Med 2016; 22(1): 6-7.
[http://dx.doi.org/10.1038/nm0116-6] [PMID: 26735397]
[80]
Kazim SF, Blanchard J, Bianchi R, Iqbal K. Early neurotrophic pharmacotherapy rescues developmental delay and Alzheimer’s-like memory deficits in the Ts65Dn mouse model of Down syndrome. Sci Rep 2017; 7: 45561.
[http://dx.doi.org/10.1038/srep45561] [PMID: 28368015]
[81]
Velazquez R, Ash JA, Powers BE, et al. Maternal choline supplementation improves spatial learning and adult hippocampal neurogenesis in the Ts65Dn mouse model of Down syndrome. Neurobiol Dis 2013; 58: 92-101.
[http://dx.doi.org/10.1016/j.nbd.2013.04.016] [PMID: 23643842]
[82]
Endres M, Toso L, Roberson R, et al. Prevention of alcohol-induced developmental delays and learning abnormalities in a model of fetal alcohol syndrome. Am J Obstet Gynecol 2005; 193(3 Pt 2): 1028-34.
[http://dx.doi.org/10.1016/j.ajog.2005.05.052] [PMID: 16157106]
[83]
Toso L, Cameroni I, Roberson R, Abebe D, Bissell S, Spong CY. Prevention of developmental delays in a Down syndrome mouse model. Obstet Gynecol 2008; 112(6): 1242-51.
[http://dx.doi.org/10.1097/AOG.0b013e31818c91dc] [PMID: 19037032]

Rights & Permissions Print Cite
Article Metrics
23
1
© 2024 Bentham Science Publishers | Privacy Policy