Abstract

Neuroinflammation, AD, and Dementia

Highlights

  • Immunohistochemical and molecular biological evidence accumulated over the past two decades has shown that the brain is capable of sustaining an innate immune response and that the result may be damaging to host cells

  • The concept that neuroinflammation is detrimental implies that glial cell activation precedes and causes neuronal degeneration, a sequence of events that appears to be at odds with experimental models of neurodegeneration in which glial cell activation occurs secondary to neuronal damage

  • What distinguishes Alzheimer disease (AD) from other neurodegenerative diseases is the conspicuous presence of extracellular amyloid deposits in senile plaques, dystrophic neurite growth, and excessive tau phosphorylation

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Summary

Introduction

These articles focus on selected topics but the mixture of contributions on signaling pathways, mediators, and articles addressing cell lines provides an overview and an insight into current areas of debate in inflammation and neurodegeneration. Immunohistochemical and molecular biological evidence accumulated over the past two decades has shown that the brain is capable of sustaining an innate immune response and that the result may be damaging to host cells. Neuroinflammation is a characteristic feature of both acute and chronic CNS disorders and is a process that results primarily from the presence of chronically activated glial cells (astrocytes and microglia) in the brain, and is a common feature of several neurodegenerative conditions.

Results
Conclusion

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