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Fig. 1 | Genome Medicine

Fig. 1

From: The neuroimmune axis of Alzheimer’s disease

Fig. 1

Neuroimmune interactions in AD neuropathology. AD is a heterogeneous and multifactorial complex neurodegenerative disease that is characterized by the abnormal aggregation of extracellular β-amyloid plaques and intracellular neurofibrillary tangles. This leads to neuronal cell death, synaptic degradation, and gliosis (microglia and astrocytes), further exacerbating neurodegeneration and ultimately leading to dementia. Under homeostatic conditions, microglia have a predominantly protective role, including phagocytosis and degradation of Aβ, secretion of anti-inflammatory cytokines, and neural network remodeling. However, excessive β-amyloid deposition and neuronal cell death can trigger robust pro-neuroinflammatory activation of microglia, leading to the release of pro-inflammatory cytokines and complement. A vicious cycle of neuropathology, pro-inflammatory glial activation, and excessive neurodegeneration ensues. This pathological cycle affects the BBB integrity and lymphatic drainage, which leads to immune cell infiltration (e.g., T cells) in the brain parenchyma and border zone, immune cell activation, antigen accumulation, and TCR clonal expansion. In this neuroimmune axis model, immunopathogenesis changes can therefore serve as a foundation for designing and developing of disease-modifying therapies for AD. APC, antigen-presenting cells; TCR, T cell receptor

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