Accumulation of amyloid-β protein in exocrine glands of transgenic mice overexpressing a carboxyl terminal portion of amyloid protein precursor

Amyloid-beta protein (A beta) and its precursor (beta PP) play important roles in the pathogenesis of Alzheimer disease and inclusion-body myositis. In humans, A beta deposits are found in brain, skeletal muscle, and skin. Therefore, we have investigated possible A beta deposits in multiple tissues of two transgenic mouse lines overexpressing the signal plus A beta-bearing 99-amino acid carboxyl terminal sequences of beta PP under the control of a cytomegalovirus enhancer/beta-actin promoter. One of the lines developed A beta-immunoreactive intracellular deposits consistently in the pancreas and lacrimal gland, and occasionally in gastric, DeSteno's, and lingual glands. Although the A beta deposits increased during ageing and degenerative changes of the tissues were observed, little or no extracellular A beta 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 A beta deposits.