Down’s Syndrome and Alzheimer’s Disease: Are Common Genes From Human Chromosome 21 Involved In Both Disorders?

Groner, Yoram; Dafni, Naomi; Sherman, Levana; Levanon, Ditsa; Bernstein, Yael; Danciger, E.; Elroy‐Stein, Orna; Neer, Ada

doi:10.1007/978-1-4613-2179-8_34

Advances in Behavioral Biology

1986

DOI: 10.1007/978-1-4613-2179-8_34

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Down’s Syndrome and Alzheimer’s Disease: Are Common Genes From Human Chromosome 21 Involved In Both Disorders?

Yoram Groner

Naomi Dafni

Levana Sherman

et al.

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1987

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Cited by 3 publications

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“…The overexpression of the CuZnSOD gene could disturb the steady-state equilibrium of active oxygen species within the cell, resulting in oxidative damage to biologically important molecules (10,11). It has been suggested that such a mechanism may be responsible for or contributory to either the mental retardation or Alzheimer disease, or both, which are part of the DS phenotype (12)(13)(14)(15).…”

mentioning

confidence: 99%

Transgenic mice with increased Cu/Zn-superoxide dismutase activity: animal model of dosage effects in Down syndrome.

Epstein

Avraham

Lovett

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

407

210

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Down syndrome, the phenotypic expression of human trisomy 21, is presumed to result from a 1.5-fold increase in the expression of the genes on human chromosome 21. As an approach to the development of an animal model for Down syndrome, several strains of transgenic mice that carry the human Cu/Zn-superoxide dismutase gene have been prepared. These animals express the transgene in a manner similar to that of humans, with 0.9-and 0.7-kilobase transcripts in a 1:4 ratio, and synthesize the human enzyme in an active form capable offorming human-mouse enzyme heterodimers. Cu/Znsuperoxide dismutase activity is increased from 1.6-to 6.0-fold in the brains of four transgenic strains and to an equal or lesser extent in several other tissues. These animals provide a unique system for studying the consequences of increased dosage of the Cu/Zn-superoxide dismutase gene in Down syndrome and the role of this enzyme in a variety of other pathological processes.

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mentioning

confidence: 99%

Transgenic mice with increased Cu/Zn-superoxide dismutase activity: animal model of dosage effects in Down syndrome.

Epstein

Avraham

Lovett

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

407

210

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Down's syndrome: morphological remodelling and increased complexity in the neuromuscular junction of transgenic CuZn-superoxide dismutase mice

et al. 1991

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Transgenic mice carrying the human CuZn-superoxide dismutase gene were used to investigate whether CuZn-superoxide dismutase gene dosage is involved in the signs of neuromuscular junction deterioration associated with Down's syndrome. Three parameters of neuromuscular junction morphology were studied in hindlimb muscles of CuZn-superoxide dismutase-transgenic mice and their non-transgenic littermates: nerve terminal length, number of nerve terminal branching points and incidence of sprouting that results in synapse formation. These parameters increased with advanced age and the increase occurred earlier in CuZn-superoxide dismutase-transgenic mice. Therefore, the data is in line with the possibility that CuZn-superoxide dismutase-transgenic mice are undergoing premature ageing with respect to neuromuscular junction morphology, most probably owing to a gene dosage effect of CuZn-superoxide dismutase.

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Premature thymic involution, observed at the ultrastructural level, in two lineages of human-SOD-1 transgenic mice

Nabarra

Casanova

Paris

et al. 1997

Mechanisms of Ageing and Development

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Down’s Syndrome and Alzheimer’s Disease: Are Common Genes From Human Chromosome 21 Involved In Both Disorders?

Cited by 3 publications

References 62 publications

Transgenic mice with increased Cu/Zn-superoxide dismutase activity: animal model of dosage effects in Down syndrome.

Transgenic mice with increased Cu/Zn-superoxide dismutase activity: animal model of dosage effects in Down syndrome.

Down's syndrome: morphological remodelling and increased complexity in the neuromuscular junction of transgenic CuZn-superoxide dismutase mice

Premature thymic involution, observed at the ultrastructural level, in two lineages of human-SOD-1 transgenic mice

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