Direct evidence for this was produced in 2005 when Cartier et al. showed elevated levels of pro-inflammatory and apoptotic molecules (IL-1α, CXCR2, CCR3, CCR5, and TGF-β) in post-mortem brain tissue in subjects with Alzheimer’s disease (AD) compared to age-matched controls [50]. The gene discussed is IL1A; the disease is Alzheimer disease.