A history of brain injury raises a person’s risk of Alzheimer’s disease, and many researchers now suspect that the brain’s inflammatory responses to injury may magnify the neurodegenerative process. Now researchers have identified a substance that could explain how inflammation leads to the formation of amyloid plaques, which are a hallmark of Alzheimer’s disease.

Lennart Mucke and colleagues at the University of California, San Francisco, report that a substance called transforming growth factor TGF-β1 induces the accumulation of amyloid deposits in the cerebral blood vessels and meninges in aged transgenic mice that overexpress the substance. TGF-β1 is normally produced by brain cells in response to injury or infection. Mucke’s team report that transgenic mice expressing both excess TGF-β1 and a mutant form of amyloid precursor protein (APP), which causes an inherited form of Alzheimer’s disease, developed amyloid deposits by the age of two to three months. In contrast, animals that express only the mutant APP developed the deposits at six to eight months. In human Alzheimer's patients, levels of TGF-β1 in brain tissue are higher than in normal subjects.

The findings are reported in the 9 October 1997 issue of Nature.-June Kinoshita.

Reference:
Wyss-Coray T, Masliah E, Mallory M, McConlogue L, Johnson-Wood K, Lin C, Mucke L. Amyloidogenic role of cytokine TGF-beta1 in transgenic mice and in Alzheimer's disease. Nature 1997 Oct 9;389(6651):603-6. Abstract

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References

Paper Citations

  1. . Amyloidogenic role of cytokine TGF-beta1 in transgenic mice and in Alzheimer's disease. Nature. 1997 Oct 9;389(6651):603-6. PubMed.

Further Reading

Papers

  1. . Amyloidogenic role of cytokine TGF-beta1 in transgenic mice and in Alzheimer's disease. Nature. 1997 Oct 9;389(6651):603-6. PubMed.

Primary Papers

  1. . Amyloidogenic role of cytokine TGF-beta1 in transgenic mice and in Alzheimer's disease. Nature. 1997 Oct 9;389(6651):603-6. PubMed.