Amyloid beta-protein deposition in tissues other than brain in Alzheimer's disease.

摘要: ALZHEIMER'S disease is the most common cause of progressive intellectual failure in aged humans. The filamentous brain lesions which define occur within neurons (neurofibrillary tangles), extracellular cerebral deposits (amyloid plaques) and meningocerebral blood vessels angiopathy)1,2. They are found lesser numbers brains virtually all old humans1. A protein with a relative molecular mass (Mr) ∼4,000, designated amyloid β-protein or A4 protein, subunit vascular plaque filaments individuals Alzheimer's disease3–5, normal ageing6 trisomy 21 (Down's syndrome) 7. small fragment membrane-associated glycoprotein8–13, encoded by gene on human chromosome telomeric to genetic defect that causes at least some cases familial disease14,15. Until now, pathological have been only brain, although reports phenotypic abnormalities non-neural tissues16–20 suggested may be widespread, systemic disorder. Here we report detection tissues patients, including skin, subcutaneous tissue intestine. was also present proportion aged, subjects. Our findings indicate principal feature process expressed subclinically other than brain. occurrence β- multiple suggests produced locally numerous organs may, as amyloidoses, derived from circulating precursor. These observations affect rationale for many experiments analysing precursor its messenger RNAs major implications pathogenesis treatment disease.