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Zoology and wildlife conservation

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Abstracts » Zoology and wildlife conservation

Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene

Article Abstract:

Amino-acid and structural similarities between the newly discovered E5-1 gene on chromosome 1 and the S182 gene on chromosome 14q24.3 along with their associations with early-onset familial Alzheimer's disease subtype AD3 indicate the existence of other AD susceptibility genes. Both genes have missense mutations that are present in persons with AD3, suggesting that they serve similar functions on the same biochemical pathway with aberrations leading to heightened Alzheimer's risk.

Author: Ikeda, M., Lannfelt, L., St. George-Hyslop, P.H., Sorbi, S., Liang, Y., Sherrington, R., Rogaev, E.I., Rogaeva, E.A., Chi, H., Lin, C., Holman, K., Tsuda, T., Mar, L., Chumakov, I., Fraser, P.E., Rommens, J.M., Levesque G., Nacmias, B., Piacentini, S., Amaducci, L., Cohen, D.
Publisher: Macmillan Publishing Ltd.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1995
Research, Animal mutation

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Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimer's disease gene

Article Abstract:

The resemblance of the sel-12 gene, which codes a protein with many transmembrane domains, to the S182 gene from Caenorhabditis (C.) elegans which is probably responsible for familial Alzheimer's disease, indicates that their proteins' functions are also probably conserved. The sel-12 gene has been identified by screening the suppressors of the lin-12 gene. The lin-12 and glp-1 genes of C. elegans belong to a family of receptors responsible for signals that take care of cell fate.

Author: Levitan, Diane, Greenwald, Iva
Publisher: Macmillan Publishing Ltd.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1995
Caenorhabditis elegans

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Presenilin-1 mutations in Alzheimer's disease

Article Abstract:

It has been established that an unusual form of beta-amyloid that does not have the first 10 amino acids accumulates in the brains of people carrying presenilin-1 mutations, which are the most common cause of familial Alzheimer's disease. This form is more common in these people than in people affected by other forms of Alzheimer's.

Author: Russo, C., Schettini, G., Saido, T.C., Hulette, C., Lippa, C., Lannfelt, L., Ghetti, B., Gambetti, P., Tabaton, M., Teller, J.K.
Publisher: Macmillan Publishing Ltd.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 2000

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Subjects list: Genetic aspects, Alzheimer's disease
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