Inhibition of Bone Morphogenetic Protein Signaling Prevents Tau Pathology in iPSC Derived Neurons and PS19 Mice.

Amira Affaneh, Anne K Linden, Elif Tunc-Ozcan, Yung-Hsu Tsai, Chian-Yu Peng, John A Kessler

Davee Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL.Davee Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL. · pubmed

Paper

Abstract

Many neurodegenerative disorders share a common pathologic feature involving the deposition of abnormal tau protein in the brain (tauopathies). This suggests that there may be some shared pathophysiologic mechanism(s). The largest risk factor for the majority of these disorders is aging, suggesting involvement of the aging process in the shared pathophysiology. We test the hypothesis that an increase in bone morphogenetic protein (BMP) signaling that occurs during aging contributes to the onset and progression of tauopathies.

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Research summary

The paper investigates the role of bone morphogenetic protein (BMP) signaling in the context of tauopathies, which are associated with aging. By exploring the potential link between BMP signaling and tau pathology, the research addresses a mechanism that could contribute to age-related neurodegenerative diseases. However, while the findings may provide insights into the underlying processes of tauopathies, the impact appears to be solid but limited, as it does not propose a direct intervention for aging itself or a significant breakthrough in longevity research.

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