25/11-15). “
“Alzheimer’s disease (AD), the most common age-related neurodegenerative disorder [1], is characterized by the formation of neurofibrillary tangles in the medial temporal lobe and cortical areas of the brain [2] and senile plaques [3]. The brains of patients with AD show losses of choline acetyltransferase activity or basal forebrain cholinergic neurons, which are correlated with cognitive impairments [4], [5] and [6]. The current mainstay of treatment for cognitive loss associated with AD has been muscarinic Selleck Raf inhibitor or

nicotinic receptor ligands and acetylcholinesterase (AChE) inhibitors [7], drugs which also show unwanted side effects such as diarrhea, nausea, vomiting, muscle cramps, sedation and bradycardia [8]. Ginseng (the root of Panax ginseng Meyer) is frequently used in Asian countries as a traditional medicine. The major components of ginseng are ginsenosides; a diverse

group of steroidal saponins [9] and [10] capable of exerting many beneficial BKM120 manufacturer effects including enhancement of memory and cognitive functions. Acceleration of memory acquisition and improved cognition has been reported with treatment of ginsenosides Rb1 and Rg1 in animal models [11] and [12]. For instance, Rg1 exerted ameliorative effects on scopolamine-induced memory impairment in rats in a radial arm maze task [13], while Rb1 improved Abeta ( [25], [26], [27], [28], [29], [30], [31], [32], [33], [34] and [35]) induced memory dysfunction, axonal hypertrophy, and synaptic loss in a mouse model of AD [14]. Both ginsenosides enhanced cholinergic function [15], conferred neuroprotection [16], and promoted neurite outgrowth in cultured neurons [17]. These Low-density-lipoprotein receptor kinase mechanisms are thought to explain the memory-enhancing activities of these ginsenosides. Rg3, another type of ginsenoside, has also been shown to protect against scopolamine-induced memory deficit in mice [18], [19] and [20]. Scopolamine is an antimuscarinic agent that decreases central cholinergic activity and causes impairment of learning and memory [21]. Moreover, the

neuroprotective effects of Rg3 have also been demonstrated in many studies [15], [22], [23], [24] and [25]. In fact, Rg3 was the most effective ginsenoside in inhibiting N-methyl-d-aspartic-acid-induced neurotoxicity in hippocampal neurons [26]. Rg3 was also observed to produce the most significant reduction of accumulation of the Alzheimer’s amyloid β peptide in a cell-based model system, as well as in a mouse model of AD [27]. Altogether, these studies indicate the potentiality of Rg3 in the treatment of AD. Despite the attractive features of ginsenosides as potential nutraceuticals for AD, their use has been limited for several reasons, including high production cost and poor bioavailability. In particular, the process of extracting pure Rg3 from ginseng is laborious and expensive [28]. Furthermore, conventional manufacturing processes produce only minimal amounts of Rg3.