Publication: APPsα rescues Tau-induced synaptic pathology
APPsα rescues Tau-induced synaptic pathology
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Bold, C. S., Baltissen, D., Ludewig, S., Back, M. K., Just, J., Kilian, L., Erdinger, S., Banicevic, M., Rehra, L., Almouhanna, F., Nigri, M., Wolfer, D. P., Spilger, R., Rohr, K., Kann, O., Buchholz, C. J., von Engelhardt, J., Korte, M., & Müller, U. C. (2022). APPsα rescues Tau-induced synaptic pathology. Journal of Neuroscience, 42(29), 5782–5802. https://doi.org/10.1523/JNEUROSCI.2200-21.2022
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Alzheimer's disease (AD) is histopathologically characterized by Aβ plaques and the accumulation of hyperphosphorylated Tau species, the latter also constituting key hallmarks of primary tauopathies. Whereas Aβ is produced by amyloidogenic APP processing, APP processing along the competing non-amyloidogenic pathway results in the secretion of neurotrophic and synaptotrophic APPsα. Recently, we demonstrated that APPsα has therapeutic effects in transgenic AD model mice and rescues Aβ-dependent impairments. Here, we examined the potenti
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Bold, C. S., Baltissen, D., Ludewig, S., Back, M. K., Just, J., Kilian, L., Erdinger, S., Banicevic, M., Rehra, L., Almouhanna, F., Nigri, M., Wolfer, D. P., Spilger, R., Rohr, K., Kann, O., Buchholz, C. J., von Engelhardt, J., Korte, M., & Müller, U. C. (2022). APPsα rescues Tau-induced synaptic pathology. Journal of Neuroscience, 42(29), 5782–5802. https://doi.org/10.1523/JNEUROSCI.2200-21.2022