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In G. lucidum, the chemical structure of the triterpenes is based on lanostane, which is a metabolite of lanosterol, the biosynthesis of which is based on cyclization of squalene (Haralampidis, Trojanowska, and Osbourn 2002). Extraction of triterpenes is usually done by means of methanol, ethanol, acetone, chloroform, ether, or a mixture of these solvents. The extracts can be further purified by various separation methods, including normal and reverse-phase HPLC (Chen et al. 1999; Su et al. 2001). The first triterpenes isolated from G. lucidum are the ganoderic acids A and B, which were identified by Kubota et al. (1982). Since then, more than 100 triterpenes with known chemical compositions and molecular configurations have been reported to occur in G. lucidum. Among them, more than 50 were found to be new and unique to this fungus. The vast majority are ganoderic and lucidenic acids, but other triterpenes such as ganoderals, ganoderiols, and ganodermic acids have also been identified (Nishitoba et al. 1984; Sato et al. 1986; Budavari 1989; Gonzalez et al. 1999; Ma et al. 2002; Akihisa et al. 2007; Zhou et al. 2007; Jiang et al. 2008; Chen et al. 2010). Examples of triterpenes are shown in Figure 9.3.
The DAST-10 is a 10-item self-report instrument that has been condensed from the 28-item DAST. It was copyrighted in 1982 by Harvey Skinner, PhD and the Centre for Addiction and Mental Health, Toronto, Canada.
In the mid-late seventies of the 20th century, reductions in the activity of choline acetyltransferase, the biosynthetic enzyme for acetylcholine, [12-14] as well as in the levels of noradrenaline and the activity of its synthetic enzyme dopamine-ß-hydroxylase [15-17] were described in the cerebral cortex of AD patients. As the human cerebral cortex does not contain cholinergic or noradrenergic neurons, these transmitter deficiencies were correctly attributed to a dysfunction in the ascending cholinergic and noradrenergic innervation of the cortex arising in the basal nucleus of Meynert [18,19] and locus coeruleus, respectively. A corresponding loss of neurons in the NbM was first reported in 1982  and rapidly confirmed by others [9,21-24]. Systematic studies clearly indicated that loss of cholinergic NbM neurons occurs early during the course of AD [25,26] and very unlikely is an event secondary to cortical degeneration . The critical role of cholinergic dysfunction in early AD is clearly documented by the fact that pharmacological inhibition of acetylcholinesterase still is the only treatment available for a modest symptomatic therapy during early stages of the disease. 2b1af7f3a8