Hospitalization for major surgery or critical illness is often associated with cognitive decline. Inflammation is considered to participate in the mechanisms underlying memory impairment after surgery, but the mechanisms remain poorly understood.

Using a mouse model of surgery-induced cognitive decline, the authors of this study report that orthopedic surgery affects hippocampal neuronal-glial function, including synaptic transmission and plasticity.

The authors found that aspirin-triggered resolvin D1 production improved memory decline after surgery and abolished signs of synaptic dysfunction. Delayed administration 24 h after surgery also attenuated signs of neuronal dysfunction postoperatively. Resolvin D1 also limited peripheral damage by modulating the release of systemic interleukin (IL)-6 and improved other clinical markers of tissue injury. Resolvins are endogenous lipid mediators biosynthesized during the resolution phase of acute inflammation which produce immunoresolvent actions.

The paper concluded that aspirin-triggered resolvin D1 may modulate the proinflammatory milieu after aseptic injury and protect the brain from neuroinflammation, synaptic dysfunction and cognitive decline. Postoperative cognitive decline and other forms of memory dysfunction may benefit from further developments in this treatment approach.

Terrando N, Gómez-Galán M, Yang T, Carlström M, Gustavsson D, Harding RE, Lindskog M, Eriksson LI: Aspirin-triggered resolvin D1 prevents surgery-induced cognitive decline. FASEB J. [Epub ahead of print, May 24, 2013].

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