Previous studies have reported total leukocyte count to be a risk factor for coronary heart disease. The pattern of association between each class of leukocytes and the onset of the disease was investigated in the Paris Prospective Study II. The study population consisted of 3,779 male French employees aged 29-52 years working in the Paris area and recruited between 1980 and 1985 (end of follow-up: June 1989). A high monocyte count was strongly associated with the risk of coronary heart disease after adjustment for tobacco use and the other classical risk factors for the disease. The monocyte-macrophage is known to play an important part in the development of atherosclerosis. A high monocyte count seems to predict the premature occurrence of a coronary event in middle-aged men.

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Alzheimer's disease (AD), a neurodegenerative disorder, is the most common form of dementia in the elderly individuals. Among the pathogenic mechanisms in AD, chronic systemic inflammation is described and characterized by massive production of proinflammatory cytokines by peripheral blood mononuclear cells (PBMCs), which may contribute to an altered immune response and exacerbation of neurodegeneration. Studies have also reported increased double-stranded RNA-dependent protein kinase (PKR) activation in the PBMCs of patients with AD. Interestingly, PKR could be involved in NF-κB activation, leading to production of a wide range of cytokines. We proposed to decrease proinflammatory cytokines production and release by treating the PBMCs in 25 patients with AD with a specific inhibitor of PKR. Our results showed that PKR inhibition greatly decreased tumor necrosis factor α, interleukin (IL)-1α, IL-1β, and IL-6 production and release but did not affect the chemokine RANTES. Moreover, inhibition of the proinflammatory factors was correlated with prevention of caspase-3 activation. These results indicated that specific inhibition of PKR at the peripheral level might decrease the inflammatory response in AD.