The role of amyloid-β (Aβ) peptide in human physiology and pathology remains an unresolved subject of study; Aβ's role in Alzheimer's disease (AD) is particularly controversial. However, before we can more fully appreciate Aβ's role in AD, an understanding of its normal physiological role(s) must first be attained. This perspective appraises the current literature and concludes that Aβ is a cytokine. This conclusion was arrived at based on a comprehensive listing of 30 characteristic defining structural and functional properties of cytokines followed by a literature precedence-based demonstration that Aβ possesses all 30 properties; this categorization of cytokine characteristics enabled an organized comparison of cytokines and Aβ, thereby providing systematic justification for classifying Aβ as a cytokine. The conclusion that Aβ is a cytokine enables the merger of two leading hypotheses of AD (amyloid hypothesis and neuroinflammation) into a single process.