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Pharmacological modulation of septins restores calcium homeostasis and is neuroprotective in models of Alzheimer's disease. 2024
Katrien Princen, and
Tom Van Dooren, and
Marit van Gorsel, and
Nikolaos Louros, and
Xiaojuan Yang, and
Michael Dumbacher, and
Ilse Bastiaens, and
Kristel Coupet, and
Shana Dupont, and
Eva Cuveliers, and
Annick Lauwers, and
Mohamed Laghmouchi, and
Thomas Vanwelden, and
Sofie Carmans, and
Nele Van Damme, and
Hein Duhamel, and
Seppe Vansteenkiste, and
Jovan Prerad, and
Karolien Pipeleers, and
Olivier Rodiers, and
Liese De Ridder, and
Sofie Claes, and
Yoni Busschots, and
Lentel Pringels, and
Vanessa Verhelst, and
Eveline Debroux, and
Marinka Brouwer, and
Sam Lievens, and
Jan Tavernier, and
Melissa Farinelli, and
Sandrine Hughes-Asceri, and
Marieke Voets, and
Joris Winderickx, and
Stefaan Wera, and
Joris de Wit, and
Joost Schymkowitz, and
Frederic Rousseau, and
Henrik Zetterberg, and
Jeffrey L Cummings, and
Wim Annaert, and
Tom Cornelissen, and
Hans De Winter, and
Koen De Witte, and
Marc Fivaz, and
Gerard Griffioen
reMYND NV, Bio-Incubator, 3001 Leuven-Heverlee, Belgium.
Abnormal calcium signaling is a central pathological component of Alzheimer's disease (AD). Here, we describe the identification of a class of compounds called ReS19-T, which are able to restore calcium homeostasis in cell-based models of tau pathology. Aberrant tau accumulation leads to uncontrolled activation of store-operated calcium channels (SOCCs) by remodeling septin filaments at the cell cortex. Binding of ReS19-T to septins restores filament assembly in the disease state and restrains calcium entry through SOCCs. In amyloid-β and tau-driven mouse models of disease, ReS19-T agents restored synaptic plasticity, normalized brain network activity, and attenuated the development of both amyloid-β and tau pathology. Our findings identify the septin cytoskeleton as a potential therapeutic target for the development of disease-modifying AD treatments.
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Olivier Rodiers, and
Liese De Ridder, and
Sofie Claes, and
Yoni Busschots, and
Lentel Pringels, and
Vanessa Verhelst, and
Eveline Debroux, and
Marinka Brouwer, and
Sam Lievens, and
Jan Tavernier, and
Melissa Farinelli, and
Sandrine Hughes-Asceri, and
Marieke Voets, and
Joris Winderickx, and
Stefaan Wera, and
Joris de Wit, and
Joost Schymkowitz, and
Frederic Rousseau, and
Henrik Zetterberg, and
Jeffrey L Cummings, and
Wim Annaert, and
Tom Cornelissen, and
Hans De Winter, and
Koen De Witte, and
Marc Fivaz, and
Gerard Griffioen
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Xiaojuan Yang, and
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Shana Dupont, and
Eva Cuveliers, and
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Thomas Vanwelden, and
Sofie Carmans, and
Nele Van Damme, and
Hein Duhamel, and
Seppe Vansteenkiste, and
Jovan Prerad, and
Karolien Pipeleers, and
Olivier Rodiers, and
Liese De Ridder, and
Sofie Claes, and
Yoni Busschots, and
Lentel Pringels, and
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Eveline Debroux, and
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Sandrine Hughes-Asceri, and
Marieke Voets, and
Joris Winderickx, and
Stefaan Wera, and
Joris de Wit, and
Joost Schymkowitz, and
Frederic Rousseau, and
Henrik Zetterberg, and
Jeffrey L Cummings, and
Wim Annaert, and
Tom Cornelissen, and
Hans De Winter, and
Koen De Witte, and
Marc Fivaz, and
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Shana Dupont, and
Eva Cuveliers, and
Annick Lauwers, and
Mohamed Laghmouchi, and
Thomas Vanwelden, and
Sofie Carmans, and
Nele Van Damme, and
Hein Duhamel, and
Seppe Vansteenkiste, and
Jovan Prerad, and
Karolien Pipeleers, and
Olivier Rodiers, and
Liese De Ridder, and
Sofie Claes, and
Yoni Busschots, and
Lentel Pringels, and
Vanessa Verhelst, and
Eveline Debroux, and
Marinka Brouwer, and
Sam Lievens, and
Jan Tavernier, and
Melissa Farinelli, and
Sandrine Hughes-Asceri, and
Marieke Voets, and
Joris Winderickx, and
Stefaan Wera, and
Joris de Wit, and
Joost Schymkowitz, and
Frederic Rousseau, and
Henrik Zetterberg, and
Jeffrey L Cummings, and
Wim Annaert, and
Tom Cornelissen, and
Hans De Winter, and
Koen De Witte, and
Marc Fivaz, and
Gerard Griffioen
January 1989,
Annals of the New York Academy of Sciences,
