Amyloid β protein (Aβ) is the main component of neuritic plaques in Alzheimer’s disease (AD), and its accumulation has been considered as the molecular driver of Alzheimer’s pathogenesis and progression. It is generated from the amyloid precursor protein (APP) by sequential cleavage of β- and γ-secretase.
Did someone investigate the differences in amyloid formation kinetics and fibril morphology between microgravity-grown and ground-grown amyloids?
It’s a similar mechanism for Age-Related Macular Degeneration (AMD), a leading cause of vision loss in adults over the age of 50.
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Great questions Shai! For further posts/discussion, you also can @ specific communities of AWG members - for example I think this post could use @AnimalAWG and @ALSDAawg (which is the phenotypic/physiolgoical-centric AWG)
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