Microglia‐specific ApoE knock‐out does not alter Alzheimer's disease plaque pathogenesis or gene expression

A ~35% increase in average amyloid beta plaque size was observed with microglial-specific ApoE knock-out in a 5xFAD mouse model of Alzheimer's disease.

• Microglial-specific ApoE knock-out did not alter plaque load, microglial number, clustering around plaques, or the formation of cerebral amyloid angiopathy.
• ApoE protein was found in plaque-associated microglia despite the knock-out, indicating microglia can uptake ApoE from other cells.
• Lower synaptic protein levels were noted in mice lacking microglial-expressed ApoE compared to controls, suggesting its role in maintaining synapses.
• Few differentially expressed genes were identified in both 5xFAD and control mice after microglial-specific ApoE knock-out.
• Some evidence of rescue in neuronal networks associated with 5xFAD was indicated through gene co-expression analysis.

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