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Folate deficiency may exert pro-inflammatory signaling by enhancing the monocytemacrophage system, and the production of the inflammatory mediators, IL1, IL6, TNF, and MCP1, and monocytes were significantly increased when folate deficiency (71)

This collaboration between misfolded proteins characterised as marching separately but striking together creates trafficking deficits that starve distal axonal and synaptic compartments of functional mitochondria, precipitating localised energy failure long before widespread neuronal death [30]

Toxicol Lett 2006

References Diaz-Arrastia R

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