Neuroinflammation and neuroimmunology in Alzheimer's disease: The role of T-lymphocytes in Alzheimer's disease

Alzheimer's disease (AD) is the leading cause of dementia, with the number of patients with AD expected to double in the next quarter-century. Brain deposition of amyloid-β (Aβ) and tau proteins is a necessary but insufficient condition for AD pathogenesis. There is also growing evidence to suggest that chronic neuroinflammation due to excessive microglial activation and astrocyte dysfunction exacerbates the pathophysiology of AD, but the factors that disrupt these homeostatic processes remain unclear. Research into AD pathophysiology has shown interest in the changes in adaptive T-cells, which play a pivotal role in immunity. The immune alterations in the peripheral circulation and increased blood–brain-barrier permeability observed in patients with AD, even in the initial stages of the disease, require investigation of the immune mechanisms resulting from T-cell infiltration into the central nervous system (CNS) during disease initiation and exacerbation. Since T-cells play a two-faceted role in the CNS immune response, including pathogenic and neuroprotective roles, the role of T-cells in AD has been debated. Memory T-cells reside in the brain and communicate with glial cells and neurons. In this review, the role of immune responses in AD is discussed, focusing on the contribution of T-cells.