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MICROGLIAL TAM RECEPTORS MODULATE ALS PATHOLOGY IN SOD1<SUP >G93A</SUP> MOUSE MODEL
Youtong Huangand 3 co-authors
Boston Children’s Hospital
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-044
Presentation
Date TBA
Board: PS04-08PM-044
Event Information
Poster Board
PS04-08PM-044
Poster
View posterAbstract
Activation of microglia, the tissue macrophages of the central nervous system, is a prominent feature of Amyotrophic Lateral Sclerosis (ALS), a neurodegenerative disease that leads to the progressive loss of motor neurons. However, whether and how microglia are involved in ALS pathogenesis has been elusive. A key component of this activation is the engagement of the microglial TAM receptor tyrosine kinases Mer (gene name Mertk) and Axl, which are phagocytic receptors that detect the externalized “eat-me” signal, phosphatidylserine (PtdSer). Interestingly, using SOD1G93A mice, a well-characterized mouse model of ALS, we showed the absence of Axl and Mer has dramatically altered the disease course and extended the arrival of the end stage of the disease from that of TAM-expressing SOD1G93A mice. We showed this delayed end stage of disease may be accompanied by dampened microglial activation and partial rescue of ALS-vulnerable motor neurons and preservation of neuromuscular junctions in the spinal cord. Our recent efforts have been focused on identifying and manipulating potential neuronal upstream mechanisms that drive local non-apoptotic PtdSer externalization in early stage of the disease. This work demonstrates a critical role of microglial TAM receptors in ALS pathogenesis that drives vulnerable motor circuit degeneration.
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