Neuroinflammation, microglia and implications for anti-inflammatory treatment in Alzheimer's disease

Abstract

Neuroinflammation has been implicated in the pathology of Alzheimer's disease (AD) for decades. Still it has not been fully understood when and how inflammation arises in the course of AD. Whether inflammation is an underling cause or a resulting condition in AD remains unresolved. Mounting evidence indicates that microglial activation contributes to neuronal damage in neurodegenerative diseases. However, also beneficial aspects of microglial activation have been identified. The purpose of this review is to highlight new insights into the detrimental and beneficial role of neuroinflammation in AD. It is our intention to focus on newer controversies in the field of microglia activation. Precisely, we want to shed light on whether neuroinflammation is associated to brain tissue damage and functional impairment or is there also a damage limiting activity. In regard to this, we discuss the limitations and the advantages of anti-inflammatory treatment options and identify what future implications might result from this underling neuroinflammation for AD therapy.

Figure 1

possible interactions of COX-inhibitors and Alzheimer‘s disease pathology. The fair arrows show neurotoxic properties of Aβ, COX-expression cytokines. In addition it is indicated that COX-inhibitors block COX-expression, activated microglia, ROS, and Aβ. ROS: radical oxygen species; COX: cyclooxygenase; Aβ: amyloid β.