Table 1.

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

Disease/injury model	Known PPARγ effects	References
Spinal cord injury	↑locomotor recovery	[15, 16]
	↑myelin sparing
	↑motor neuron sparing
	↓glial activation
	↓proinflammatory cytokines
Experimental allergic encephalomyelitis (model of multiple sclerosis)	↑myelin sparing	[33, 44, 48, 61]
	↓lesion size
	↓inflammatory cell infiltrate
	↓proinflammatory cytokines & chemokines
	↓clinical score (better recovery; lower no. of relapses)
Amyotrophic lateral sclerosis	↑motor neuron survival	[32]
	↓glial activation
	↓ COX-2
	↓ iNOS
	↑longevity, delayed disease onset
Parkinson's disease	↑dopaminergic neuron survival	[43, 46]
	↓gliosis
	↓ iNOS
	↓ NFκB translocation to the nucleus
	↑ IκBα
Cerebral ischemia	↑neuron survival in penumbra	[6, 31, 35, 37, 64]
	↓ lesion size
	↓COX-2
	↓ proinflammatory cytokines
	↑ antioxidants
Cerebral hemorrhage	↑ catalase	[38]
	↓NFκB
	↓ neutrophil infiltration
	↓ apoptosis
	↓ behavioral dysfunction
Alzheimer's disease	↓gliosis	[7, 45, 65, 66]
	↓COX-2 & iNOS
	↓proinflammatory cytokines
	↓Aβ1-42+ amyloid plaques
	↓β-secretase mRNA
	↓monocyte differentiation into macrophages