Plants and the central nervous system. One-day symposium at the 135th British Pharmaceutical Conference

Professor PG Jenner (King’s College London) discussed how plant toxins can provide clues to the causes of neurodegenerative diseases. In his view, plant toxins are being “extremely useful” in understanding neurodegenerative diseases. He said, “If we can isolate the toxins from plants like star thistle, then we will have another major advance in our understanding of neurodegenerative diseases”.

Dr Jackie Hunter (SmithKline Beecham, Essex) outlined the following ways in which natural products (from both plants and animals) can be of benefit in the design of therapeutics for CNS disorders.

• By directly acting as the therapeutic entity, e.g. melatonin.
• Provision of novel chemical leads through screening of natural products, e.g. marine organisms, plants and fungi, bacteria.
• Provision of tools for dissecting out pathways and mechanisms, e.g. venoms from sea snails and spiders have provided tools for the dissection of calcium and potassium channel pharmacology.
• Provision of ethnopharmacological leads to new indications or new approaches, e.g. the observation that capsaicin extracted from chilli peppers had analgesic properties.

Leads from ancient herbals

Professor Elaine Perry (Newcastle General Hospital) explained how her group has been using leads from ancient herbals in efforts to develop therapeutic agents for eg Alzheimer’s disease. The memory-enhancing effects of plants such as rosemary and sage were mentioned in herbals as early as the 16th century, yet such plants (with the exception of Ginkgo biloba) have not been widely investigated in the context of current models of Alzheimer’s disease, she said.

Professor Perry described some of her group’s experimental work with plant extracts with a long history of traditional use for memory improvement. Professor Perry now plans to set up randomised controlled trials to investigate the effects of sage extract in Alzheimer’s disease.

Hypericum update

Dr B Vitiello (National Institute of Mental Health, Maryland, US) presented an overview of evidence for the antidepressant activity of Hypericum perforatum (St John’s wort). He described recent work that has proposed that it is hyperforin and not hypericin that is the most active compound.

In order to address some of the limitations in previous trials of hypericum extracts, the National Institute of Mental Health and the Office of Alternative and Complementary Medicine at the US National Institutes of Health are sponsoring a randomised, double-blind trial involving over 300 patients with major depressive disorder. Participants will receive either a well-characterised hypericum extract, a standard selective serotonin reuptake inhibitor, or placebo, over an 8-week treatment period. After this time, responders will be blindly continued on study medication for a further four months. “This trial is intended to provide a definitive answer to the question of the possible value of Hypericum perforatum extracts for patients suffering from depression”, Dr Vitiello said.

Scientific basis for valerian

Dr Houghton (King’s College London) gave a comprehensive overview of valerian and the scientific basis for its reputed sedative activity.

Dr Houghton summarised the clinical evidence for valerian, saying that controlled trials had shown improvements in REM sleep, but that in some studies, improvements were seen only after 4 to 8 weeks’ treatment. In vivo models had also provided evidence to support the sedative activity of valerian; in vitro studies had shown that V.officinalis extract displaces GABA from receptors in rat cerebral cortex synaptosomes.

Dr Houghton went on to discuss some of the modern concerns about valerian: its active constituents are still not fully known; how valerian preparations should be standardised is still not clear; there may be potential for valerian to interact with conventional medicines with CNS effects, leading to, eg potentiation of tranquillising/sedative effects or reduction of antidepressant effects; cytotoxicity of valepotriate constituents (although this has not been shown in vivo).