Table 2.

Summary of the various antioxidants studied for Alzheimer’s disease

Disease	Test agent	Primary endpoint	Result/Outcome	Model	Ref
AD	SAM	GST inhibition, presenilin-1 expression	Improvement in neuropathological features	Mouse	152
	Apple juice concentrate	PS-1 expression in ApoE−/− mice	Improved neuroprotection via inhibition of PS-1 expression	Mouse	30
	Curcumin	Binding to Aβ species and brain oxidative damage and plaque formation	Facilitates disaggregation of Aβ and reduction in AD associated neuropathology	Mouse Human	88, 167
	Vitamin E and C	Behavioral performance, lipid peroxidation and glutathione in plasma samples	Decreased TBARS levels and decreased lipid peroxidation susceptibility	Mouse Human	54, 155
	Vitamin E alone or with Vitamin C	Honolulu-Asia Aging Study (dementia and cognitive function)	Protection against vascular dementia and not against AD dementia	Human	98
		Chicago Health and Aging Project (telephone tests of cognitive function)	Vitamin E, and NOT vitamin C, offered modest cognitive benefits in older women	Human	57
		Nurse’s Health Study	Vitamin E, and NOT vitamin C, offered modest cognitive benefits in older women	Human	80, 118
	Vitamin E alone	Honolulu-Asia Aging Study (dementia)	Failure to lower the AD risk	Human	80, 118
		Washington Heights Study	Lack of decreased risk of AD by neither dietary, supplemental, nor total intake of vitamin E	Human	92
		Cache County Study	Lack of decreased risk of AD by vitamin E alone	Human	61, 143
		Prophylactic protection in young versus aged mice	Decreased amyloid deposition and lipid peroxidation in only in mice receiving vitamin E at younger ages and not in later ages	Mouse	150

SAM: S-adenosyl methionine; GST: Glutathione-s-transferase; PS-1: presenilin-1; TBARS: thiobarbituric acid reactive substances; CoQ10: coenzyme Q10.