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Accumulation of amyloid‐β protein in exocrine glands of transgenic mice overexpressing a carboxyl terminal portion of amyloid protein precursor
Author(s) -
Fukuchi KenIchiro,
Li Ling,
Hart Michael,
Lindsey J. Russell
Publication year - 2000
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1046/j.1365-2613.2000.00156.x
Subject(s) - genetically modified mouse , transgene , intracellular , extracellular , biology , amyloid (mycology) , pancreas , pathogenesis , microbiology and biotechnology , endocrinology , biochemistry , gene , immunology , botany
Amyloid‐β protein (Aβ) and its precursor (βPP) play important roles in the pathogenesis of Alzheimer disease and inclusion‐body myositis. In humans, Aβ deposits are found in brain, skeletal muscle, and skin. Therefore, we have investigated possible Aβ deposits in multiple tissues of two transgenic mouse lines overexpressing the signal plus Aβ‐bearing 99‐amino acid carboxyl terminal sequences of βPP under the control of a cytomegalovirus enhancer/β‐actin promoter. One of the lines developed Aβ‐immunoreactive intracellular deposits consistently in the pancreas and lacrimal gland, and occasionally in gastric, DeSteno's, and lingual glands. Although the Aβ deposits increased during ageing and degenerative changes of the tissues were observed, little or no extracellular Aβ deposits were observed up to the age of 25 months. These lines of transgenic mice are useful for studying the molecular mechanisms of development and clearance of intracellular Aβ deposits.