Cultures of Streptomyces tendae grown on Actinomyces medium containing clomazone contained less geosmin 48 h after inoculation than untreated controls, suggesting a possible inhibition of reactions prior to sesquiterpenoid biosynthesis. However, exposure to clomazone increased geosmin accumulation in S. tendae cultures grown on Hickey-Tresner medium and in cultures of the fungus Penicillium expansum. Additionally, clomazone increased accumulation of a sesquiterpenoid tentatively identified as a eudesmol in S. tendae, indicating possible point(s) of inhibition subsequent to sesquiterpenoid biosynthesis. Geosmin biosynthesis was induced by transferring cultures of S. tendae inoculated on Actinomyces medium to Hickey-Tresner medium 24 h after inoculation. When harvested at 48 h, geosmin biosynthesis-induced-cultures exposed to clomazone contained more geosmin than untreated controls, indicating that response of a single taxon to clomazone can be rapidly altered by changing medium composition.

Our current therapeutic drugs for Alzheimer's disease are predominantly derived from the alkaloid class of plant phytochemicals. These drugs, such as galantamine and rivastigmine, attenuate the decline in the cholinergic system but, as the alkaloids occupy the most dangerous end of the phytochemical spectrum (indeed they function as feeding deterrents and poisons to other organisms within the plant itself), they are often associated with unpleasant side effects. In addition, these cholinesterase inhibiting alkaloids target only one system in a disorder, which is typified by multifactorial deficits. The present paper will look at the more benign terpene (such as Ginkgo biloba, Ginseng, Melissa officinalis (lemon balm) and Salvia lavandulaefolia (sage)) and phenolic (such as resveratrol) phytochemicals; arguing that they offer a safer alternative and that, as well as demonstrating efficacy in cholinesterase inhibition, these phytochemicals are able to target other salient systems such as cerebral blood flow, free radical scavenging, anti-inflammation, inhibition of amyloid-β neurotoxicity, glucoregulation and interaction with other neurotransmitters (such as γ-aminobutyric acid) and signalling pathways (e.g. via kinase enzymes).