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Previous Findings Using Down Syndrome Mouse Models[edit]

Ts16[edit]

Ts65Dn[edit]

This model was studied to understand the neurological basis of its mental impairment. It was found that it exhibited inhibition in the dentate gyrus, and that GABAA antagonists were able to resolve some of this impairment[1]. These mice were found to experience a delay in development, exhibit unusual behaviors similar to human retardation, and eventually encounter astrocytic hypertrophy and other forms of Alzheimer's-related neurodegeneration[2]. They also contained abnormally large neural synapses and other structural changes[3]. The brains of these mice have higher levels of oxidative stress that can be remedied with vitamin E, which has antioxidant properties, thus leading to enhanced memory[4]. These mice have been used to study sleep-wake cycles in Down Syndrome, and they have earlier and increased number of movements while asleep[5]. They were also found to have significantly lower levels of long-term potentiation[6]. Studies have shown that mental retardation in this model may be related to abnormal neural circuit development[7].

Dp(16)1Yu/Dp(16)1Yey[edit]

  1. Pharmacotherapy for cognitive impairment in a mouse model of Down syndrome.
  2. Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome.
  3. Synaptic structural abnormalities in the Ts65Dn mouse model of down syndrome.
  4. Cholinergic degeneration and memory loss delayed by vitamin E in a Down syndrome mouse model.

http://www.pnas.org/content/95/11/6256.short - Another mouse model

http://science.sciencemag.org/content/309/5743/2033 - Another mouse model

  1. ^ Fernandez, Fabian; Morishita, Wade; Zuniga, Elizabeth; Nguyen, James; Blank, Martina; Malenka, Robert C.; Garner, Craig C. (2007-04-01). "Pharmacotherapy for cognitive impairment in a mouse model of Down syndrome". Nature Neuroscience. 10 (4): 411–413. doi:10.1038/nn1860. ISSN 1097-6256.
  2. ^ Holtzman, David M.; Santucci, Daniela; Kilbridge, Joshua; Chua-Couzens, Jane; Fontana, David J.; Daniels, Scott E.; Johnson, Randolph M.; Chen, Karen; Sun, Yuling (1996-01-01). "Developmental Abnormalities and Age-Related Neurodegeneration in a Mouse Model of down Syndrome". Proceedings of the National Academy of Sciences of the United States of America. 93 (23): 13333–13338.
  3. ^ Belichenko, Pavel V.; Masliah, Eliezer; Kleschevnikov, Alexander M.; Villar, Angela J.; Epstein, Charles J.; Salehi, Ahmad; Mobley, William C. (2004-12-13). "Synaptic structural abnormalities in the Ts65Dn mouse model of down syndrome". The Journal of Comparative Neurology. 480 (3): 281–298. doi:10.1002/cne.20337. ISSN 1096-9861.
  4. ^ Lockrow, Jason; Prakasam, Annamalai; Huang, Peng; Bimonte-Nelson, Heather; Sambamurti, Kumar; Granholm, Ann-Charlotte (2009-04-01). "Cholinergic degeneration and memory loss delayed by vitamin E in a Down syndrome mouse model". Experimental Neurology. 216 (2): 278–289. doi:10.1016/j.expneurol.2008.11.021. PMC 2704550. PMID 19135442.
  5. ^ Stewart, Lee S.; Persinger, Michael A.; Cortez, Miguel A.; Iii, O. Carter Snead (2006-12-05). "Chronobiometry of Behavioral Activity in the Ts65Dn Model of Down Syndrome". Behavior Genetics. 37 (2): 388–398. doi:10.1007/s10519-006-9119-y. ISSN 0001-8244.
  6. ^ Siarey, R. J.; Stoll, J.; Rapoport, S. I.; Galdzicki, Z. (1997-11-01). "Altered long-term potentiation in the young and old Ts65Dn mouse, a model for down syndrome". Neuropharmacology. 36 (11–12): 1549–1554. doi:10.1016/S0028-3908(97)00157-3.
  7. ^ Dierssen, M.; Benavides-Piccione, R.; Martínez-Cué, C.; Estivill, X.; Flórez, J.; Elston, G. N.; DeFelipe, J. (2003-07-01). "Alterations of Neocortical Pyramidal Cell Phenotype in the Ts65Dn Mouse Model of Down Syndrome: Effects of Environmental Enrichment". Cerebral Cortex. 13 (7): 758–764. doi:10.1093/cercor/13.7.758. ISSN 1047-3211. PMID 12816891.
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