Abstract
Alzheimer's disease and other cognitive impairments are a growing problem in the healthcare world with the ageing population. There are currently no effective treatments available; however, it has been suggested that targeting neuroinflammation may be a successful approach in slowing the progression of neurodegeneration. Reducing the destructive hyperinflammatory pathology to maintain homeostasis in neural tissue is a promising option to consider. This review explores the mechanisms behind neuroinflammation and the effectiveness of immunotherapy in slowing the progression of cognitive decline in patients with Alzheimer's disease. The key components of neuroinflammation in Alzheimer's disease researched are microglia, astrocytes, cytokines and CD8+ effector T cells. The role of oxidative stress on modulating regulatory T cells and some of the limitations of regulatory T cell-based therapies are also explored. Increasing regulatory T cells can decrease activation of microglia, proinflammatory cytokines and astrocytes; however, it can also increase levels of inflammatory cytokines. There is a complex network of regulatory T cell interactions that reduce Alzheimer's disease pathology, which is not fully understood. Exploring the current literature, further research into the use of immunotherapy in Alzheimer's disease is vital to determine the potential of these techniques; however, there is sufficient evidence to suggest that increasing regulatory T cells count does prevent Alzheimer's disease symptoms and pathology in patients with Alzheimer's disease. Some exciting innovative therapies are muted to explore in the future. The function of regulatory T cells in the presence of reactive oxygen species and oxidative stress should be investigated further in patients with neurogenerative disorders to ascertain if combination therapies could reduce oxidative stress while also enhancing regulatory T cells function. Could methods of immunotherapy infuse exogenous functional Tregs or enhance the immune environment in favour of endogenous regulatory T cells differentiation, thus reducing neuroinflammation in neurodegenerative pathology, inhibiting the progression of Alzheimer's disease?