1.0Kompetenz statt Demenzhttps://kompetenz-statt-demenz.dsgip.de/en/Jens Brünnlerhttps://kompetenz-statt-demenz.dsgip.de/en/author/j-bruennler/New trails on anti-Amyloid drug failed – Kompetenz statt Demenzrich600338<blockquote class="wp-embedded-content" data-secret="a3iSP8FGEi"><a href="https://kompetenz-statt-demenz.dsgip.de/en/anti-amyloid-drug-failed/">New trails on anti-Amyloid drug failed</a></blockquote><iframe sandbox="allow-scripts" security="restricted" src="https://kompetenz-statt-demenz.dsgip.de/en/anti-amyloid-drug-failed/embed/#?secret=a3iSP8FGEi" width="600" height="338" title="“New trails on anti-Amyloid drug failed” — Kompetenz statt Demenz" data-secret="a3iSP8FGEi" frameborder="0" marginwidth="0" marginheight="0" scrolling="no" class="wp-embedded-content"></iframe><script>
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https://kompetenz-statt-demenz.dsgip.de/wp-content/uploads/2019/12/microscope-1817641_1920.jpg19201280Lanabecestat is a potent inhibitor of Amyloid beta (Aβ) formation – the main component of amyloid plaques. Aβ is formed through cleavage of amyloid precursor protein (APP) by proteases known as secretases (β and γ). The Beta-site-APP-cleaving enzyme 1 (BACE1) cleaves APP at the β-secretase site, after which APP is cleaved by γ secretase to generate Aβ peptides. Lanabecestat inhibits BACE1 and was able to reduce levels of Aβ1-40 and Aβ1-42 in the brain, cerebrospinal fluid (CSF), and plasma in several animal models, as well as in human CSF and plasma. Besides that, Lanabecestat is brain permeable meaning that an adequate amount of this substance is able to reach the brain after oral intake.