Abstract
Alzheimer’s disease (AD) is one of the neurodegenerative diseases associated with neuroinflammation. Tau neurofibrillary tangles and amyloid beta (Aβ) plaques can activate microglia and then elevate the levels of neuroinflammatory mediators in AD models. The elevation of cytokines levels can lead to increased Aβ 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.
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Acknowledgment
The book chapter was written during the period of fund supported by the International Scientific Partnership Program (ISPP-146) from the Deanship of Scientific Research, King Saud University.
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Alasmari, F., Al-Harbi, N.O., Alanazi, M.M., Alasmari, A.F., Sari, Y. (2019). Memory Dysfunction Correlates with the Dysregulated Dopaminergic System in the Ventral Tegmental Area in Alzheimer’s Disease. In: Paul, S. (eds) Application of Biomedical Engineering in Neuroscience. Springer, Singapore. https://doi.org/10.1007/978-981-13-7142-4_5
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