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Astrocytes respond dramatically to pathological alterations in the brain including Alzheimer’s disease (AD) through a highly heterogeneous process called astrocyte reactivity. Astrocyte reactivity is characterized by changes in morphological, transcriptional and biochemical levels. The reactive astrocytes secrete a plethora of cytokines that regulate neuronal health through disease stages. Recently, we showed that oligomeric Aβ_1‐42 (Aβ) treatment to primary astrocytes induced an early reactivity and detected tissue inhibitor of matrix metalloproteinase‐1 (TIMP‐1) as the major candidate in the astrocyte secretome that promoted neuronal viability against Aβ toxicity. Moreover, in Aβ‐injected rats, TIMP‐1 recovered cognitive functions (Brain Behav Immun. 2020 87:804‐819). However, the mechanisms underlying TIMP‐1’s neuroprotective role remained to be revealed which we aim to achieve through our …