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The resolution of conflict is one of the most immediate international issues of our time. We are living in a period of great change. Powers decline while others emerge as the world moves to a new strategic accommodation. During the twentieth century, the strategic shifts have been marked by the two world wars and the Cold War. Each unleashed its own set of dynamics which led to the confrontation that followed. While the current strategic shift has seen the threat of global nuclear war recede, the end of the Cold War has also weakened the influence of the superpowers on their client-states and proxies. In the SO years after 1945, the Cold War seemed to contain many of the deep ethnic, religious and cultural tensions that have plagued modern history. The collapse of the Soviet Union’s capacity to pursue a global strategy led to the disintegration of the Soviet bloc and the fragmentation of the Soviet Union itself. The world’s remaining superpower, relieved of the security burdens imposed by its former adversary and denied the crystalline certainty of its role as the defender of freedom, is itself divided. It moves towards a new role only with uncertainty, while burgeoning domestic problems cast a shadow over its ability to sustain a coherent international commitment.

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Spatially heterogeneous synapse loss is a characteristic of many psychiatric and neurological disorders, but the underlying mechanisms are unclear. Here, we show that spatially-restricted complement activation mediates stress-induced heterogeneous microglia activation and synapse loss localized to the upper layers of the mouse medial prefrontal cortex (mPFC). Single cell RNA sequencing also reveals a stress-associated microglia state marked by high expression of the apolipoprotein E gene (ApoE high ) localized to the upper layers of the mPFC. Mice lacking complement component C3 are protected from stress-induced layer-specific synapse loss, and the ApoE high microglia population is markedly reduced in the mPFC of these mice. Furthermore, C3 knockout mice are also resilient to stress-induced anhedonia and working memory behavioral deficits. Our findings suggest that region-specific complement and microglia activation can contribute to the disease-specific spatially restricted patterns of synapse loss and clinical symptoms found in many brain diseases.