“Murine models do not consistently replicate human CNS physiology, thereby failing to reflect pathological characteristics such as [neurodegnerative] disease onset or progression accurately.”
“This discrepancy likely arises from inter-species variability in [CNS] complexity, structure, and inflammatory responses, which constrains a complete reproduction of the pathophysiological alterations seen in humans. Unlike other species, human microglia exhibit heterogeneity in transcriptional states.”
“Moreover, significant differences in various gene modules between rodent and primate microglia exist. These differences include genes associated with complement pathways, phagocytosis, and susceptibility to neurodegenerative conditions like AD and Parkinson’s disease.”
By integrating cerebral #organoids with microglia-like cells derived from familial Alzheimer’s disease patient iPSCs, @uthealthhouston.bsky.social scientists developed a neuroimmune #assembloid model that faithfully reproduces Alzheimer's inflammatory hallmarks.
#alzsky #neuroskyence 🧪