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Functional loss of the microglial receptor TREM2 has been linked to the development of Alzheimer’s disease (AD) (1). A recent study by Ewers et al. reported that increased soluble TREM2 (sTREM2) measured in cerebrospinal fluid (CSF) was associated with lower rates of cognitive and clinical decline and progression in people with AD or mild cognitive impairment (MCI) (2). Importantly, an increased ratio of CSF sTREM2 to p-tau181 concentrations was useful as a predictor of slowed conversion of normal to compromised cognition or from MCI to AD in individuals with CSF Aβ1-42 and CSF p-tau181 expression. This work presents a very exciting perspective on the relationship between AD and the innate immune system, as well as encouraging further research into TREM2 signaling as a potential therapeutic approach for AD.
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