Abstract

Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) plaques, neurofibrillary tangles, and neurodegeneration. Microglia, the resident immune cells of the central nervous system (CNS), play a crucial role in AD pathogenesis by containing the spreading of Aβ plaques. Genetic studies have associated a variant of the receptor Paired Immunoglobulin-like Type 2 Receptor Alpha (PILRα) with reduced risk for AD. PILRα is a receptor found on myeloid cells, such as microglia, that binds to endogenous cell surface glycoproteins and sends inhibitory signals within the cell. Additionally, it serves as an entry receptor for Herpes Simplex Virus 1. To elucidate the role of PILRα in microglial responses to brain pathology, here we used the cuprizone (CPZ) model of demyelination in Pilrα–/– mice. In this model, CPZ-fed mice experience oligodendrocyte death and demyelination of brain white matter, with microglia crucially clearing damaged myelin and promoting remyelination by oligodendrocyte progenitor cells (OPCs) after CPZ exposure ceases. Among mouse brain cells, PILRα expression was specifically observed in microglia. Deficiency of PILRα reduced microglia response to demyelination and myelin remodeling. This defect was associated with increased proliferation of OPCs. Co-immunoprecipitation experiments corroborated a direct interaction of PILRα with the inhibitory phosphatase SHP1. Hence, PILRα plays a key role in balancing the microglial response and promoting myelin regeneration by OPCs. This reveals an unexpected function in regulating repair mechanisms during brain pathology.

Committee Chair

Marco Colonna

Committee Members

Claudia Han; Fumihiko Urano; Gregory Wu; Michael Holtzman; Robert Schmidt

Degree

Doctor of Philosophy (PhD)

Author's Department

Biology & Biomedical Sciences (Molecular Cell Biology)

Author's School

Graduate School of Arts and Sciences

Document Type

Dissertation

Date of Award

4-9-2025

Language

English (en)

Author's ORCID

https://orcid.org/0009-0001-1463-1909

Available for download on Wednesday, April 08, 2026

Included in

Biology Commons

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