In the past, the role of neuroinammation in Alzheimer’s disease (AD) was considered to be a simple response to the well-established neuropathological features (e.g. the neuritic plaques or tangles) of the disease. However, emerging evidence now shows it is a major contributor to the progression and development of the disease. Indeed, both preclinical and clinical research support an early and substantial involvement of neuroinammation in AD pathogenesis that changes in character as the disease progresses. e term ‘neuroinammation’, in its broadest sense, encompasses any inammatory process, whether acute or chronic, involving the nervous system. Depending on the nature of the inammatory process diverse cell types may be involved. e central nervous system (CNS) resident cells (microglia and astrocytes) are a major component of this inammatory response. However, in some circumstances, e.g. where the blood-brain barrier (BBB) is damaged or in areas surrounding the vasculature of the brain, other peripherally derived cells (neutrophils, lymphocytes, plasma cells, macrophages and monocytes) may also be involved. In AD, the key cellular players are thought to be the CNS resident cells with its key mediators being cytokine proteins. However, there is also a developing interest in the potential role for peripherally derived cells and other mediators of inammation. Furthermore, there is increasing recognition that neuroinammatory processes in the AD brain are markedly inuenced by inammation that occurs outside the CNS. A greater understanding of the central and peripheral inammatory processes involved in AD will undoubtedly enable the development of clinical tools allowing the early detection of the disease but will, most importantly, lead to new preventative strategies and treatment approaches.