Amyloidogenic role of cytokine TGF-β1 in transgenic mice and in Alzheimer's disease

Tony Wyss-Coray (), Eliezer Masliah, Margaret Mallory, Lisa McConlogue, Kelly Johnson-Wood, Carol Lin and Lennart Mucke
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Tony Wyss-Coray: University of California
Eliezer Masliah: University of California
Margaret Mallory: University of California
Lisa McConlogue: Athena Neurosciences Inc.
Kelly Johnson-Wood: Athena Neurosciences Inc.
Carol Lin: University of California
Lennart Mucke: University of California

Nature, 1997, vol. 389, issue 6651, 603-606

Abstract: Abstract Deposition of amyloid-β peptide in the central nervous system is a hallmark of Alzheimer's disease and a possible cause of neurodegeneration1,2,3. The factors that initiate or promote deposition of amyloid-β peptide are not known. The transforming growth factor TGF-β1 plays a central role in the response of the brain to injury4,5, and increased TGF-β1 has been found in the central nervous system of patients with Alzheimer's disease6,7,8. Here we report that TGF-β1 induces amyloid-β deposition in cerebral blood vessels and meninges of aged transgenic mice overexpressing this cytokine from astrocytes. Co-expression of TGF-β1 in transgenic mice overexpressing amyloid-precursor protein, which develop Alzheimer's like pathology9,10,11, accelerated the deposition of amyloid-β peptide. More TGF-β1 messenger RNA was present in post-mortem brain tissue of Alzheimer's patients than in controls, the levels correlating strongly with amyloid-β deposition in the damaged cerebral blood vessels of patients with cerebral amyloid angiopathy. These results indicate that overexpression of TGF-β1 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.

Date: 1997
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DOI: 10.1038/39321

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