Alzheimer's disease (AD) is a complex disorder and the most common form of neurodegenerative dementia. Several genetic, environmental, and physiological factors, including inflammations and metabolic influences, are involved in the progression of AD. Inflammations are composed of complicated networks of many chemokines and cytokines with diverse cells. Inflammatory molecules are needed for the protection against pathogens, and maintaining their balances is important for normal physiological function. Recent studies demonstrated that inflammation may be involved in neurodegenerative dementia. Cellular immune components, such as microglia or astrocytes, mediate the release of inflammatory molecules, including tumor necrosis factor, growth factors, adhesion molecules, or chemokines. Over- and underexpression of pro- and anti-inflammatory molecules, respectively, may result in neuroinflammation and thus disease initiation and progression. In addition, levels of several inflammatory factors were reported to be altered in the brain or bodily fluids of patients with AD, reflecting their neuropathological changes. Therefore, simultaneous detection of several inflammatory molecules in the early or pre-symptomatic stage may improve the early diagnosis of AD. Further studies are needed to determine, how induction or inhibition of inflammatory factors could be used for AD therapies. This review summarizes the role or possible role of immune cells and inflammatory molecules in disease progression or prevention.