Literature DB >> 7482354

Anti-interferon immunoglobulins can improve the trisomy 16 mouse phenotype.

L E Maroun1.   

Abstract

Mouse trisomy 16 is a well-studied model for human chromosome 21 trisomy (Down's syndrome). The late stage trisomy 16 mouse fetus exhibits significant growth retardation, inappropriately opened eyes, and convex rather than concave back curvature. The interferons (alpha, beta, and gamma) have potent growth retarding activity, and sensitivity to these cytokines is controlled by genes that map to mouse chromosome 16 and human chromosome 21. In experiments designed to determine if the interferons induce or aggravate the trisomy phenotype, mice pregnant with trisomy 16 fetuses were injected with a combination of anti-alpha, -beta, and -gamma interferon IgG. This maternal anti-interferon treatment was found to provide measurable benefit to the development and growth of the trisomic fetuses with significant return-toward-normal values observed for overall fetal growth, eye opening, and back curvature.

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Year:  1995        PMID: 7482354     DOI: 10.1002/tera.1420510509

Source DB:  PubMed          Journal:  Teratology        ISSN: 0040-3709


  8 in total

Review 1.  Exosomal biomarkers in Down syndrome and Alzheimer's disease.

Authors:  Eric D Hamlett; Aurélie Ledreux; Huntington Potter; Heidi J Chial; David Patterson; Joaquin M Espinosa; Brianne M Bettcher; Ann-Charlotte Granholm
Journal:  Free Radic Biol Med       Date:  2017-09-05       Impact factor: 7.376

Review 2.  Dendritic spine pathology and thrombospondin-1 deficits in Down syndrome.

Authors:  Maria D Torres; Octavio Garcia; Cindy Tang; Jorge Busciglio
Journal:  Free Radic Biol Med       Date:  2017-09-28       Impact factor: 7.376

3.  Neuroinflammation in the aging down syndrome brain; lessons from Alzheimer's disease.

Authors:  Donna M Wilcock
Journal:  Curr Gerontol Geriatr Res       Date:  2012-02-21

4.  Trisomy 21 consistently activates the interferon response.

Authors:  Kelly D Sullivan; Hannah C Lewis; Amanda A Hill; Ahwan Pandey; Leisa P Jackson; Joseph M Cabral; Keith P Smith; L Alexander Liggett; Eliana B Gomez; Matthew D Galbraith; James DeGregori; Joaquín M Espinosa
Journal:  Elife       Date:  2016-07-29       Impact factor: 8.140

5.  Rapamycin Treatment Ameliorates Age-Related Accumulation of Toxic Metabolic Intermediates in Brains of the Ts65Dn Mouse Model of Down Syndrome and Aging.

Authors:  Nathan Duval; Guido N Vacano; David Patterson
Journal:  Front Aging Neurosci       Date:  2018-09-06       Impact factor: 5.750

Review 6.  Down syndrome and type I interferon: not so simple.

Authors:  Louise Malle; Dusan Bogunovic
Journal:  Curr Opin Immunol       Date:  2021-06-23       Impact factor: 7.268

Review 7.  Down's syndrome, neuroinflammation, and Alzheimer neuropathogenesis.

Authors:  Donna M Wilcock; W Sue T Griffin
Journal:  J Neuroinflammation       Date:  2013-07-16       Impact factor: 8.322

Review 8.  Potential Role of JAK-STAT Signaling Pathway in the Neurogenic-to-Gliogenic Shift in Down Syndrome Brain.

Authors:  Han-Chung Lee; Kai-Leng Tan; Pike-See Cheah; King-Hwa Ling
Journal:  Neural Plast       Date:  2016-01-12       Impact factor: 3.599

  8 in total

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