## Abstract The etiology of Alzheimer's disease (AD) involves a significant inflammatory component as evidenced by the presence of elevated levels of a diverse range of proinflammatory molecules in the AD brain. These inflammatory molecules are produced principally by activated microglia, which are
APOLIPOPROTEIN E IS ASSOCIATED WITH ISLET AMYLOID AND OTHER AMYLOIDOSES: IMPLICATIONS FOR ALZHEIMER'S DISEASE
✍ Scribed by CHARGÉ, SOPHIE B. P.; ESIRI, MARGARET M.; BETHUNE, CLAIRE A.; HANSEN, BARBARA C.; CLARK, ANNE
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 652 KB
- Volume
- 179
- Category
- Article
- ISSN
- 0022-3417
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✦ Synopsis
Apolipoprotein E (ApoE) has recently been proposed as an aetiological factor of Alzheimer's disease (AD): ApoE is co-localized to amyloid plaques and neurofibrillary tangles in the brain and binds to AP-protein in vitvo. An association of ApoE e4 allele with the development of AD has been reported. Islet amyloid is formed from islet amyloid polypeptide (IAPP) in pancreatic islets of 90 per cent of patients with non-insulin-dependent diabetes mellitus (NIDDM) which, like AD, is an age-dependent pathology. The relationship of ApoE to islet amyloid and other amyloidoses is largely unknown. In this study, ApoE was localized by immunocytochemistry on pancreatic specimens from non-diabetic man, monkey, and mouse, and on amyloid-containing human tissues from pancreas, heart, brain, and intestine. All types of amyloid deposits, irrespective of the constituent peptide, site of deposition, or species, showed immunoreactivity for ApoE (ApoE-IR). Quantitative morphometry showed that similar proportions of islet amyloid were labelled for IAPP and ApoE in monkey islets. ApoE-IR was observed in pancreatic islet cells of non-diabetics. These results suggest that the association of ApoE with amyloid is nou-specific for AD or to the component peptide of amyloid fibrils. If ApoE promotes amyloid formation, its synthesis in pancreatic islets could be important for the initiation or the development of pancreatic amyloid in NIDDM.
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