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Table 1 Summary of the effects of QUIN in comparison with Aβ mediated toxicity

From: Effect of quinolinic acid on human astrocytes morphology and functions: implications in Alzheimer's disease

QUIN toxicity

References

Aβ toxicity

References

• Free radical production via over-activation of NMDA receptor and/or QUIN-Fe2+ complexes and consequent lipid peroxidation and cell death.

(Platenik et al., 2001) (Stone and Perkins, 1981)

• Free radical production via Fenton reaction by metals Cu and Fe and consequent lipid peroxidation and apoptosis.

(Huang et al., 1999) (Varadarajan et al., 2001) (Markesbery and Lovell, 1998) (Tamaoka et al., 2000)

• Excessive PARP activation leading to NAD depletion.

(Maldonado et al., 2007)

• DNA damage by ROS leads to PARP over-activation and NAD depletion.

(Meyer et al., 2006) (Love et al., 1999)

• Activation of astrocytes including release of inflammatory chemokines and astrogliosis.

(Guillemin et al., 2003b) (Dihne et al., 2001) (Hanbury et al., 2002)

• Activation of microglia and other immune cells leading to secretion of inflammatory cytokines and proteins.

• Co-activation of astrocytes by inflammatory factors leading to further release of cytokines and astrogliosis.

Griffin and Mrak, 2002) (Murphy et al., 1998) (Selmaj et al., 1990)

• Inhibition of glutamate uptake leading to excitotoxicity.

(Tavares et al., 2002)

• Aβ can increase extracellular glutamate resulting in NMDA receptor over-activation and excitotoxicity.

(Lafon-Cazal et al., 1993; Keller et al., 1997; Lauderback et al., 2001) (Harris et al., 1995; Harris et al., 1996)

• NMDA receptor activation by QUIN can lead to Aβ production.

(Lesne et al., 2005)

• Aβ can induce IDO in the KP and increase production of QUIN.

(Guillemin et al., 2003a)