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CURRENT SCIENCE REVIEWS by Joe Bruman October 1996 p.1 of 3 Bower H; BMJ 17 Aug 1996:381: UK health authorities want control of alternative medicines adver- tised on the Internet like that in effect for street advertising. While these drugs may have genuine medical value they haven't run the rigorous gantlet of approval, either as prescription or over- counter drugs. Therefore they are marketed as dietary supplements, often by mail order, with claims carefully phrased to avoid government intervention. Products mentioned include DHEA, Melatonin, Shark cartilage, Pycnogenol. Knowlton B et al; Science, 6 Sep 1996:1399-1402: PD patients and amnesiacs were given a gambling-type test where they had to predict an outcome based on cues whose appearance was random in order and variable in accuracy. The amnesiacs learned to predict well, but forgot the training session; PD patients recalled the training well but could not learn to predict. They were at a fairly late stage (H-Y average 2.8) and under various regimes of dopamine-enhancement therapy. Robbins T; Science, 6 Sep 1996: 1263-1264: PD impairs memory (as you always suspected). Declarative memory (of events, facts, and images) resides in the temporal lobes and is unaffected. Non-declarative memory, (the ability to learn habits, skills, or judgement through repeated experience or practice) seems to reside in the caudate and putamen, and is impaired in PD patients. The effect of compensation for the loss or of dopamine-enhancement therapy is still uncertain. Science News, 7 Sep 1996:150 (news item): Conventional wisdom, that memory loss in aging is due to death of cells in the hippocampus (a formation within a ventricle of the temporal lobe) is challenged by more careful counting technique in rat brains. Aged rats, with or without memory impairment, had the same number of hippocampal cells as young ones, suggesting that the cells don't die, but only quit functioning. If that is true, there is hope that various brain diseases may be easier to treat. (In another development, workers found on autopsy that the hippocampus of PD patients was on average 25% smaller than normal. Whether that was a precursor to or a consequence of PD was not determined.) Mercer B; Arch Neur 1996;53:881-884: PROPATH, a health management program for PD patients, consists of a videocassette, a series of pamphlets, and regularly scheduled questionnaires. It helped patients feel better but didn't change their degree of satisfaction with treatment, and most physicians didn't find it helpful. Defebvre L et al; Arch Neur 1996;53:898-903: Either thalamotomy or electrical stimulation of the ventral intermediate nucleus is effective treatment for parkinsonian tremor. Inspired by a single report of reduced gait disturbance in a PD patient with the DBS implant, authors studied 7 others but found no corresponding improvement. CURRENT SCIENCE REVIEWS By Joe Bruman October 1996 p.2 of 3 Hutchinson M, Fazzini E; J Neur N'surg Psych 1996;61:324-325: Although anticholinergics were accepted treatment for PD before the widespread use of levodopa, authors tried tacrine, a drug with the opposite effect, in 7 late-stage patients who also had developed dementia. The dementia (hallucinations) was reduced, and, unexpectedly, gait and rigidity symptoms improved as well. Science News, 21 Sep 1996:180 (news item): Failure of the mammal CNS to repair injury is due to suppression of macrophages, immune cells that are essential to healing elsewhere in the body. Workers speculate that the suppression is an evolved defense against the macrophages, which themselves can cause damage to the complex mammalian CNS. By first exposing the immune cells to a rat's peripheral nerve tissue, and then placing them on its severed optic nerve, researchers were able to stimulate some regeneration, suggesting an eventual breakthrough in treatment of various neurologic disorders. Lancet, 21 Sep 1996:814 (editorial): Review of diverse approaches to spinal cord repair at several laboratories. They aim at persuading replacement neurons not only to grow, but also to connect with the proper target cell, implying a possible clue to future PD therapy. Baron M et al; Ann Neur 1996;40:355-366: Fifteen pallidotomy recipients were followed for a year, showing improvement in all the cardinal PD motor signs as well as reduced drug-induced motor fluctuations and dyskinesias. As currently applied, pallidotomy is highly effective treatment for advanced Parkinson's disease. (Useful reference for insurance claimants) Olanow W; Ann Neur 1996;40:341-343: Reviews history of pallidotomy since its discovery in 1952 and its recent resurgence. Discusses remaining questions such as: who are the best candidates; how do the benefits compare with those of fetal transplants or deep-brain stimulation; how does pallidotomy work. It is paradoxical that dyskinesia and parkinsonian motor symptoms, due to opposing conditions in the subthalamic nucleus, are improved simultaneously by pallidotomy. Ann Neur 1996;40:344-345: Review of transcranial magnetic stimulation as a clinical and research tool. Brief mention of therapeutic use to reduce bradykinesia in PD. Yuen E, Mobley W; Ann Neur 1996;40:346: There are many neurotrophic factors, having different effects on neural development. One hypothesis is that developing neurons compete for a limited supply of NTF emitted by target cells, and the ones that fail to connect die. There is hope that some NTFs may have a therapeutic effect, although there is no example of disease caused by a lack of NTF. Armon C et al; Neur 1996;47:626-635: Valproate, useful against epilepsy, may cause reversible parkin- sonism and cognitive impairment. CURRENT SCIENCE REVIEWS By Joe Bruman October 1996 p.3 of 3 Wilson J et al; Neur 1996;47:718-726: Postmortem studies compared diagnostic value of 5 different neurochemical markers of striatal dopamine nerve terminals, against data from FD PET scans in living PD patients, in the quest for better diagnostic tools. Thal L et al; Neur 1996;47:705-711: Acetyl-L-Carnitine, which I believe has been mentioned as a diet supplement, seems to improve neurotrophin levels, reduce cognitive deficits, and exert a neuroprotective effect, in rats. A double- blind trial in human Alzheimer's patients showed corresponding benefits in early-onset subjects (under 65), but worsened conditions in older ones. Hellenbrand W et al; Neur 1996;47:636-643: Questionnaires about food habits answered by 342 German PD patients and 342 controls showed negative correlation for raw vegetables, potatos, beer, spirits, coffee, but not wine or tea; no significant difference for fruits or cooked vegetables, and positive correlation for sweets, snacks, and raw meat. Hellenbrand W et al; Neur 1996;47:644-650: In the same study, responses about specific nutrients showed inverse correlation for beta-carotene, ascorbic acid and niacin, no difference for tocopherol, protein, or fat, and positive correlation for monosaccharide and polysaccharide intake. Waterhouse A et al: Lancet, 21 Sep 1996:834: Chocolate and red wine are potent antioxidants, and when combined may be both pleasant and good for you. Authors happen to be in the Department of Viticulture and Enology, UC Davis, California. Cheers, Joe J. R. Bruman (818) 789-3694 3527 Cody Road Sherman Oaks CA 91403