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Amyloidogenic role of cytokine TGF-beta1 in transgenic mice and in Alzheimer's disease.

Deposition of amyoid-beta peptide in the central nervous system is a hallmark of Alzheimer's disease and a possible cause of neurodegeneration. The factors that initiate or promote deposition of amyloid-beta peptide are not known. The transforming growth factor TGF-beta1 plays a central role in the response of the brain to injury, and increased TGF-beta1 has been found in the central nervous system of patients with Alzheimer's disease. Here we report that TGF-beta1 induces amyloid-beta deposition in cerebral blood vessels and meninges of aged transgenic mice overexpressing this cytokine from astrocytes. Co-expression of TGF-beta1 in transgenic mice overexpressing amyloid-precursor protein, which develop Alzheimer's like pathology, accelerated the deposition of amyloid-beta peptide. More TGF-beta1 messenger RNA was present in post-mortem brain tissue of Alzheimer's patients than in controls, the levels correlating strongly with amyloid-beta deposition in the damaged cerebral blood vessels of patients with cerebral amyloid angiopathy. These results indicate that overexpression of TGF-beta1 may initiate or promote amyloidogenesis in Alzheimer's disease and in experimental models and so may be a risk factor for developing Alzheimer's disease.

Pubmed ID: 9335500

Authors

  • Wyss-Coray T
  • Masliah E
  • Mallory M
  • McConlogue L
  • Johnson-Wood K
  • Lin C
  • Mucke L

Journal

Nature

Publication Data

October 9, 1997

Associated Grants

None

Mesh Terms

  • Aged
  • Aging
  • Alzheimer Disease
  • Amyloid beta-Peptides
  • Amyloidosis
  • Animals
  • Astrocytes
  • Brain
  • Cerebral Amyloid Angiopathy
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • Mice, Transgenic
  • Thiazoles
  • Transforming Growth Factor beta