Oxidant/Antioxidant Imbalance in Alzheimer’s Disease: Therapeutic and Diagnostic Prospects

Table 1

Impaired oxidative stress defense mechanisms in the brain and peripheral blood in AD.

GSH ↓, GSSG ↑, GSH/GSSG ↓ [135, 136]	GSH ↓, GSSG ↓↑ [186, 202–204]
GR activity ↓, GPX activity ↓, GST activity ↓ [135, 137]	GR activity ↓ [188]; GPX protein ↑, GCL protein ↑ [203, 206]
SOD activity ↓↑ [135, 136]	SOD mRNA ↑, SOD activity ↓ [58, 188, 209]
Thx protein ↓, ThxR protein ↑ [139]	Thx protein ↑, ThxR protein ↑ [186, 207]
HO-1 protein ↑ [143, 144]	HO-1 protein ↑, HO-1 activity ↑ [186, 207]
Nrf-2 in nucleus ↓ [141]	P-Nrf2 ↑ [209]
Cat activity ↓↑ [135, 136]	Total antioxidant status ↓ [216]
MsrA mRNA ↓ [138]	SIRT-1 protein ↑ [186, 207]
	HSP60 protein ↑, HSP70 protein ↑ [186, 207]
	UCP1 protein ↓ [207]
	Vitamin E ↓ [204, 217]
	Selenium ↓ [218]

The table summarizes the changes in the oxidative stress defense mechanisms reported in the brain and blood from MCI and/or AD patients relative to healthy controls; the corresponding references are given; arrows indicate direction of changes in protein levels or activities, described in detail in the text. AD: Alzheimer’s disease; MCI: mild cognitive impairment; Cat: catalyse, GCL: glutamylcysteine ligase; GSH: reduced glutathione; GSSG: oxidized glutathione; GPx: glutathione peroxidase; GR: glutathione reductase; GST: glutathione S-transferase; HO-1: heme oxygenase 1; Hsp: heat shock protein; MsrA: methionine sulfoxide reductase A; Nrf-2: nuclear factor (erythroid-derived 2)-like 2; SIRT-1: sirtuin 1; SOD: superoxide dismutase; Thx: thioredoxin; ThxR: thioredoxin reductase; UCP1: uncoupling protein 1.