While psychosocial factors, such as adjusting to a new disability or the loss of independence, are certainly important contributors to post-stroke depression, there is also evidence that depression may be rooted in neurochemical abnormalities consistent with a pro-inflammatory state, including elevations in C-reactive protein and cytokines such as interleukin 6 and tumour necrosis factor alpha (TNF-α)(24). This evidence concerns the gene CRP and depressive symptom measurement.