Table 2.

The mechanisms of action of single Chinese herbs in the treatment of AD.

Herb	Mechanisms of actions
	(i) Increase in cholinergic neuron function,
	(ii) Protection against the Aβ protein induced oxidative damages (degrading hydrogen peroxide, preventing lipid from oxidation and trapping reactive oxygen species),
G. biloba [20]	(iii) Prevention of Aβ protein induced fibrillogenesis as well as the formation ADDLs,
	(iv) Inhibition of cholesterol-induced overproduction of APP,
	(v) Anti-apoptosis (opposing mitochondria-initiated apoptosis, downgrading caspase-12, upgrading BCL2),
	(vi) Regulation of gene expression
	(i) Protection against the Aβ protein and hydrogen peroxide induced oxidative damages
	(ii) Anti-apoptosis (regulating gene expression: Bcl-2, Bax, P53 and caspase-3),
	(iii) Modulating secretary APP and protein kinase C-α,
Huperzine A [21, 22]	(iv) Protection against hypoxia, ischemia and glutamate induced brain injury and cytotoxiicity,
	(v) Antagonizing effects on NMDA (N-methyl-D-aspartate) receptors,
	(vi) Regulation of the expression and secretion of nerve growth factor and its signaling
Uncaria rhynchophylla [23]	(i) Inhibition of aggregation of Aβ protein,
	(ii) Destabilization of preformed Aβ neurofibrills
	(i) Increase in the uptake of choline in central nervous system,
	(ii) Release of acetylcholine from hippocampus,
Ginseng [19]	(iii) Increase in choline acetyltransferase,
	(iv) Protection against the Aβ protein induced neurotoxic effects,
	(v) Repair of Aβ-damaged neuron networks,
	(vi) Reducing the level of Aβ
Tenuigenin (P. tenuifolta) [24]	(i) Decrease of the secretion of Aβ protein via BACE1 (β-secretase) inhibition
	(i) Alteration of the processing of amyloidal precursor protein,
Berberine (C. rhizoma) [25, 26]	(ii) Decrease of the secretion of Aβ protein,
	(iii) Acetylcholinesterase inhibitory activity
Indirubins [27]	(i) Inhibition of abnormal tau phosphorylation by inhibiting glycogen synthase kinase-3 beta and CDK5/p25