Currently, chronic traumatic encephalopathy (CTE) is widely recognized as a neurodegenerative syndrome caused by constant exposure to events of acceleration and deceleration. CTE produces a myriad of neurological alterations in both the short-and long term; some of these alterations disturb the homeostasis of the central nervous system, and trigger several behavioral and cognitive deficits. The pathology of CTE resembles that of Alzheimer's, Parkinson's and Huntington's disease (among many others), which are characterized by the important role of the immune response in the development of the disease and the deposition of proteins, such as amyloid beta and tau. In the present article, we review the succession of events that develop after exposure to acceleration/deceleration events, and how such events affect the distinct cellular types in the central nervous system and their role in the activation of the immune system. We also review how the activation of the immune system affects mechanisms, such as neurogenesis and neurodegeneration, and how this in turn could generate the behavioral and cognitive deficits associated with this pathology. ClassificationChronic traumatic encephalopathy, such as posttraumatic encephalopathy, is part of TBI, the latter is