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Drs. Flanders and Lippa are co-senior authors.
From the Laboratory of Chemoprevention (Drs. Flanders and Sporn), National Cancer Institute, Bethesda, MD; and the Departments of Neurology (Drs. Lippa, Smith, and Pollen) and Pathology (Drs. Lippa and Smith), University of Massachusetts Medical Center, Worcester, MA.
Received October 27, 1994. Accepted in final form January 12, 1995.
Address correspondence and reprint requests to Dr. Carol F. Lippa, Department of Neurology, University of Massachusetts Medical Center, Worcester, MA 01655.
We compared immunohistochemical expression of the transforming growth factor-beta s (TGF-beta 1, TGF-beta 2, and TGF-beta 3) using brain tissue from patients with nondominantly inherited Alzheimer's disease (NDAD) (n equals 9), autosomal dominantly inherited Alzheimer's disease with linkage to 14q24.3 (FAD-14) (n equals 4), and cognitively normal controls (n equals 10) to determine whether their pathologic changes are associated with an altered distribution of the TGF-beta s. We found increased expression of TGF-beta 2 in large, tangle-bearing neurons with widespread staining of glia in NDAD and FAD-14 patients compared with control cases. This result was confirmed with sandwich ELISA assays of brain tissue, which showed TGF-beta 2 levels in AD and NDAD to average 3.2 times the average level of control cases. Despite proximity of TGF-beta 1 and TGF-beta 3 to the sites of susceptibility loci on chromosomes 19 and 14, we did not find that TGF-beta 1 and TGF-beta 3 were selectively altered in any AD subtypes. However, selective induction of TGF-beta 2 may occur in NDAD and FAD-14.
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