9 October 1997. 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.
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