A new hypothesis for Parkinson’s disease pathogenesis: GTPase-p38 MAPK signaling and autophagy as convergence points of etiology and genomics

Table 1 Participation of p38 MAPK signaling in ALP

Experimental context	Cell type	p38 MAPK signalling	ALP
Alexander disease	Astrocytes	↑	↑
Inflammatory process in nervous system	BV2 microglial cells	↑	↓
Hypo-osmotic condition	Hepatocytes	↑	↓
Depletion of p38 gene	HEK293 cells	↓	↓
Stimulation of p38 MAPK signaling	Mouse embryonic fibroblasts	↑	↓
Downregulation of p38 in AD	Neurons	↓	↑

The first two columns of the table indicate the model system and the cellular context in which studies are performed; in the last two columns the implication, seen as activation (↑) or suppression (↓), of p38 MAPK signaling and ALP in the disease/ experimental context, is shown

ISSN: 1750-1326