@entity32 and anti-inflammatory strategies for XXXX --a mini-review.

@entity32 @entity6220 @entity527 @entity73 @entity3072 @entity195 @entity528
Until recently, the central nervous system (CNS) has been thought to be an immune privileged organ. However, it is now understood that neuroinflammation is linked with the development of several @entity6220 including late-onset @entity195 (LOAD). The development of @entity32 is a complex process involving a wide array of molecular interactions which in the CNS remains to be further characterized. The development of neuroinflammation may represent an important link between the early stages of LOAD and its pathological outcome. It is proposed that risks for LOAD, which include genetic, biological and environmental factors can each contribute to impairment of normal CNS regulation and function. The links between risk factors and the development of neuroinflammation are numerous and involve many complex interactions which contribute to vascular compromise, oxidative stress and ultimately neuroinflammation. Once this cascade of events is initiated, the process of neuroinflammation can become overactivated resulting in further cellular damage and @entity528 . Additionally, neuroinflammation has been associated with the formation of @entity527 and @entity3072 , the pathological hallmarks of LOAD. Increased levels of inflammatory markers have been correlated with an advanced @entity73 . Based on this knowledge, new therapies aimed at limiting onset of neuroinflammation could arrest or even reverse the development of the disease.
