Abstract
Alzheimer's disease (AD) is one of the neurodegenerative diseases associated with neuroinflammation. Tau neurofibrillary tangles and amyloid beta (A beta) plaques can activate microglia and then elevate the levels of neuroinflammatory mediators in AD models. The elevation of cytokines levels can lead to increased A beta production, which is one of the causes of the pathogenesis of AD. Although it is noteworthy that AD is associated with deficit in cholinergic system, it also demonstrated that AD is associated with dopaminergic neurodegeneration in the ventral tegmental area (VTA). The VTA sends dopaminergic inputs into the hippocampus and regulates the memory and learning functions. The depletion of dopaminergic neurons in the VTA in AD models might lead to memory impairments and cognition deficit. We suggest here that that neurodegeneration in the dopamine neurons is involved in the development of dysregulated behaviors in AD animal models. In this chapter, we illustrate the role of AD-associated neuroinflammation in dopaminergic neurodegeneration in the VTA.