Ina Tesseur, Kun Zou, Luke Esposito, Frederique Bard, Elisabeth Berber, Judith Van Can, Amy H. Lin, Leslie Crews, Patrick Tremblay, Paul Mathews, Lennart Mucke, Eliezer Masliah, Tony Wyss-Coray
J Clin Invest.
2006;
116(11):3060–3069
doi:10.1172/JCI27341
This article Copyright © 2006, The American Society for Clinical Investigation
Abstract
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lzheimer’s disease (AD) is characterized by progressive neurodegeneration and cerebral accumulation of the β-amyloid peptide (Aβ), but it is unknown what makes neurons susceptible to degeneration. We report that the TGF-β type II receptor (TβRII) is mainly expressed by neurons, and that TβRII levels are reduced in human AD brain and correlate with pathological hallmarks of the disease. Reducing neuronal TGF-β signaling in mice resulted in age-dependent neurodegeneration and promoted Aβ accumulation and dendritic loss in a mouse model of AD. In cultured cells, reduced TGF-β signaling caused neuronal degeneration and resulted in increased levels of secreted Aβ and β-secretase–cleaved soluble amyloid precursor protein. These results show that reduced neuronal TGF-β signaling increases age-dependent neurodegeneration and AD-like disease in vivo. Increasing neuronal TGF-β signaling may thus reduce neurodegeneration and be beneficial in AD.
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