Potential Therapeutic Targets for PPAR𝜸 after Spinal Cord Injury

Table 1

Summary of effects mediated by PPAR activation in CNS injury or disease models.

Disease/injury model	Known PPAR effects	References
Spinal cord injury	𝛼 locomotor recovery	[15, 16]
	𝛽 myelin sparing
	𝛿 motor neuron sparing
	𝛾 glial activation
	𝛾 proinflammatory cytokines
Experimental allergic encephalomyelitis (model of multiple sclerosis)	𝛾 myelin sparing	[33, 44, 48, 61]
	𝛾 lesion size
	𝛾 inflammatory cell infiltrate
	𝛾 proinflammatory cytokines & chemokines
	𝛾 clinical score (better recovery; lower no. of relapses)
Amyotrophic lateral sclerosis	∼ motor neuron survival	[32]
	𝛾 glial activation
	𝛾 COX-2
	𝛾 iNOS
	𝛾 longevity, delayed disease onset
Parkinson’s disease	𝛾 dopaminergic neuron survival	[43, 46]
	𝛾 gliosis
	𝛾 iNOS
	𝛾 NF𝛾B translocation to the nucleus
	𝛾 I𝛾B
Cerebral ischemia	𝛾 neuron survival in penumbra	[6, 31, 35, 37, 64]
	𝛾 lesion size
	𝛾 COX-2
	𝛾 proinflammatory cytokines
	𝛾 antioxidants
Cerebral hemorrhage	𝛾 catalase	[38]
	𝛾 NF𝛾B
	𝛼 neutrophil infiltration
	𝛽 apoptosis
	𝛾 behavioral dysfunction
Alzheimer's disease	𝛾 gliosis	[7, 45, 65, 66]
	𝜅 COX-2 & iNOS
	𝜅 proinflammatory cytokines
	𝛼 A1-42+ amyloid plaques
	𝛾-secretase mRNA
	𝛾 monocyte differentiation into macrophages