In the past the role of neuroinflammation in Alzheimer’s disease (AD) was considered to be a simple response to the established neuropathological features (e.g., the extracellular deposits of amyloid beta: neuritic plaques) 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 supports an early and substantial involvement of neuroinflammation in AD pathogenesis that changes in character as the disease progresses. Here, the term ‘neuroinflammation’, is used in its broadest sense to encompass any inflammatory process, whether acute or chronic, involving the nervous system. Depending on the nature of the inflammatory process diverse cell types may be involved. The central nervous system (CNS) resident cells (microglia and astrocytes) are a major component of this inflammatory 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 (e.g., lymphocytes, 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 cytokines but also chemokines, nitric oxide, hydrogen peroxide, complement and anti-microbial peptides (AMPS). However, there is also a developing interest in the potential role of adaptive immunity in the development of AD. In addition, there is increasing recognition that the neuroinflammatory processes within the AD brain are markedly influenced by genetic factors and by inflammatory processes that occur outside the CNS.