Summary
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder, characterized by neurofibrillary tangles, β-amyloid (Aβ) plaques, and astrocyte dysfunction. Astrocytes play critical roles in AD pathophysiology, including Aβ clearance and modulation of neuroinflammation. Thus, astrocytes are essential in the pathogenesis of AD, yet the molecular mechanisms underlying astrocyte pathology in AD are not fully understood. Robust evidence from the literature and our preliminary data in human AD tissue and an AD mouse model shows an increase in a population of astrocytes characterized by e
