@entity12578 /   and y in a @entity35 Model of XXXX : Possible Involvement in @entity1726 Symptoms.

@entity1 @entity2136 @entity146 @entity16 @entity12578 @entity191 @entity1726 @entity179 @entity35 @entity2955 @entity528
UNASSIGNED: @entity191 is one of the most common @entity16 , affecting about 1-4% of @entity1 older than 60 years. Among the proposed mechanisms of @entity1726 generation, free @entity16 is believed to play a pivotal role in the development and/or progression of the disease. Recently, PPARs, a class of transcription factors involved in several pathways both in physiological and pathological conditions, have been linked by us and others to @entity179 . Particularly, PPARy and its ligands have been indicated as potential therapeutic targets for the treatment of several pathological conditions associated with neuroinflammation within the CNS. The anti-inflammatory function of PPARy has attracted attention since agonists exert a broad spectrum of protective effects in several animal models of @entity16 , including @entity146 . On the other hand a detrimental role for @entity12578 /   has been proposed in Alzheimer, being closely related to the decrease of @entity2136 and Trkfl. On these bases, in this work we used a @entity2955 hemi-lesioned @entity35 model, inducing @entity528 , to study the effects of the lesion at three time points from the lesion (1, 2 and 3 weeks), in relevant areas of @entity1726 motor symptoms, such as substantia nigra and globus pallidus and in the area of reward and mood control, the nucleus accumbens. In particular, it was studied: i) the expression of @entity2136 and its downstream signals; ii) the modulation of PPARs levels. The results obtained indicate the possible use of a dual @entity12578 /   antagonist/PPARy agonist to counteract primary and secondary signs of @entity179 . This article is protected by copyright. All rights reserved.
