Alzheimer's disease (AD) is a severe brain disorder characterized by beta-amyloid plaques, tau pathology, inflammation, neurodegeneration, and cerebrovascular dysfunction. Chronic neuroinflammation, breaches in the blood-brain barrier (BBB), and elevated levels of inflammatory mediators are central to AD pathogenesis. Peripheral immune cells, including neutrophils, T lymphocytes, B lymphocytes, NK cells, and monocytes, play crucial roles in this inflammation. This review aims to provide a comprehensive overview of these peripheral immune cells' contributions to neuroinflammation in AD. Neutrophils, the primary defense against infections, can accumulate and adhere to vascular walls, potentially obstructing blood flow. They can also enter the brain through a compromised BBB, releasing inflammatory cytokines and neutrophil extracellular traps (NETs). T lymphocytes, particularly CD4+ and CD8+ cells, contribute to disease progression by affecting glial cell function and releasing inflammatory cytokines. B lymphocytes impact the disease by secreting inflammatory cytokines and antibodies, while NK cells release inflammatory mediators and interact with microglia. These cells' activities drive the pathogenesis of AD and suggest potential therapeutic targets. The review also discusses specific biomarkers associated with AD, such as NETs, myeloperoxidase (MPO), neutrophil gelatinase-associated lipocalin (NGAL), and the neutrophil-to-lymphocyte ratio (NLR). These biomarkers show promise as markers for disease progression and prognosis. For T lymphocytes, the review explores the roles of CD8+ and CD4+ T cells, regulatory T cells (Tregs), and the potential of T cell-based therapies. CD8+ T cells can directly damage neurons and the BBB, while CD4+ T cells, particularly Th17 cells, contribute to neuroinflammation. Tregs, with their anti-inflammatory properties, show potential in protecting against neurodegenerative diseases. B lymphocytes, as antigen-presenting cells, can be activated by Aβ and other pathogens, leading to chronic microglial dysfunction and amyloid plaque buildup. They produce antibodies that can interfere with Aβ aggregation and toxicity, but their effectiveness in reversing cognitive impairments is limited. Overall, understanding the role of peripheral immune cells in neuroinflammation is vital for developing new diagnostic markers and therapeutic targets to enhance the diagnosis and treatment of AD.Alzheimer's disease (AD) is a severe brain disorder characterized by beta-amyloid plaques, tau pathology, inflammation, neurodegeneration, and cerebrovascular dysfunction. Chronic neuroinflammation, breaches in the blood-brain barrier (BBB), and elevated levels of inflammatory mediators are central to AD pathogenesis. Peripheral immune cells, including neutrophils, T lymphocytes, B lymphocytes, NK cells, and monocytes, play crucial roles in this inflammation. This review aims to provide a comprehensive overview of these peripheral immune cells' contributions to neuroinflammation in AD. Neutrophils, the primary defense against infections, can accumulate and adhere to vascular walls, potentially obstructing blood flow. They can also enter the brain through a compromised BBB, releasing inflammatory cytokines and neutrophil extracellular traps (NETs). T lymphocytes, particularly CD4+ and CD8+ cells, contribute to disease progression by affecting glial cell function and releasing inflammatory cytokines. B lymphocytes impact the disease by secreting inflammatory cytokines and antibodies, while NK cells release inflammatory mediators and interact with microglia. These cells' activities drive the pathogenesis of AD and suggest potential therapeutic targets. The review also discusses specific biomarkers associated with AD, such as NETs, myeloperoxidase (MPO), neutrophil gelatinase-associated lipocalin (NGAL), and the neutrophil-to-lymphocyte ratio (NLR). These biomarkers show promise as markers for disease progression and prognosis. For T lymphocytes, the review explores the roles of CD8+ and CD4+ T cells, regulatory T cells (Tregs), and the potential of T cell-based therapies. CD8+ T cells can directly damage neurons and the BBB, while CD4+ T cells, particularly Th17 cells, contribute to neuroinflammation. Tregs, with their anti-inflammatory properties, show potential in protecting against neurodegenerative diseases. B lymphocytes, as antigen-presenting cells, can be activated by Aβ and other pathogens, leading to chronic microglial dysfunction and amyloid plaque buildup. They produce antibodies that can interfere with Aβ aggregation and toxicity, but their effectiveness in reversing cognitive impairments is limited. Overall, understanding the role of peripheral immune cells in neuroinflammation is vital for developing new diagnostic markers and therapeutic targets to enhance the diagnosis and treatment of AD.