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CURRENT SCIENCE REVIEWS by Joe Bruman November 1996 p.1 of 2 Ed. Note: Just as in warfare, the front-line trenches of science research may not be so inspiring as the lofty councils of the Big Guns. The samples below are far removed from any immediate improve- ment in the condition of us PWP. Nevertheless, they represent the indispensable foundation of major advances to come. And who knows which future Nobel laureate lurks among these authors? JRB Nirenberg M et al; J Neurosci 1996;16:4135-4145: Authors used electron microscopy and sophisticated labeling to identify dopamine storage sites within the neurons of the substantia nigra and the ventral tegmental area, of rats. Konradi C et al; J Neurosci 1996;16:4231-4239: Amphetamine, cocaine, and dopamine all induce expression of both immediate early genes (IEGs) and neuropeptide genes in rat striatum. The NMDA (glutamate) receptor antagonist MK-801 inhibits it. Backman C et al; J Neurosci 1996;16:5437-5442: While beneficial against certain brain disorders, nerve growth factor (NGF) won't pass the blood-brain-barrier. To avoid the need for stereotactic emplacement, authors linked NGF with OX-26, an anti-transferrin receptor antibody, and the conjugate did cross the BBB. It helped spatial learning in impaired rats but disrupted the learning ability of unimpaired rats. Maher P, Davis J; J Neurosci 1996;16:6394-6401: Toxicity of glutamate, an important neurotransmitter of the basal ganglia, is inhibited by an enzyme distinct from MAO. (Blocking NMDA, one form of glutamate, has shown benefits in PD like those of pallidotomy, without need for the actual surgery. JRB) Rick I et al; J Neurosci 1996;16:6433-6442: Neural Growth Factor and Neurotrophin-3, present in early stages of embryonic brain development, help to guide the differentiation of primitive neurons into specific functional types. Surmeier D et al; J Neurosci 1996;16:6579-6591: Authors used sophisticated mRNA analysis to locate the development of different dopamine receptors in embryonic neurons. Delbanco T et al; JAMA; 9 Oct 1996;1171; One-year follow-up of a dentist's report of his PD (see CSR for April 1996). Among the usual symptoms, his most worrisome problem is speech impediment. Time; 21 Oct 1996:92 (America's Pharmaceutical Research Companies): A full-page ad hyping drug therapy for mental illness hints that "Schizophrenia and psychosis can result when the brain has abnormal dopamine levels" along with an (800) number for a free booklet on mental illness. The booklet turns out to be a puff for some two dozen drug giants, with no info at all about dopamine and only vague generalities about anything else. Now you know part of the reason why your prescription drugs cost so much. CURRENT SCIENCE REVIEWS By Joe Bruman November 1996 p. 2 of 2 Swerdlow R et al; Ann Neur 1996;40:663-671: The mitochondrial electron transport enzyme NADH:ubiquitin oxido- reductase (complex I), encoded by both nuclear and mitochondrial DNA, is defective in PD. To study the its role, authors analyzed cultured platelets from PD patients and controls, concluding that the complex I defect in PD appears to be genetic. Goto S et al; Neur 1996;47:1032-1036: Authors studied neuron connections from the putamen to the globus pallidus and the substantia nigra, in autopsied tissue of six patients who had striato-nigral degeneration, a close relative of PD. They conclude that defects in those pathways may be responsible for the parkinsonism of SND. Whitehead A et al; J Neur N'surg Psych 1996;61:347-351: The e4 form of apolipoprotein E, an enzyme abundant in the brain, is associated with Alzheimer's, and the close relation between AD and PD prompted a study of 215 early-onset PD patients (with and without dementia) and 212 healthy controls. Authors found no connection with either the dementia or the progression of PD. Starkstein S et al; N Neur N'surg Psych 1996;61:381-387: Authors gave a battery of neuropsychological and neuropsychiatric tests to 33 patients with probable AD and 33 with PD and dementia. PD patients had higher incidence of major depression and greater impairment of visual reasoning, but less anosognosia (unconcern) and disinhibition, than the AD patients. Dyck P; Lancet, 19 October 1996:1044-1045: Defect in nerve growth factor (NGF) is associated with sensorimotor effects of diabetes, and trial replenishment (doesn't say just how) seems to provide some relief of symptoms, beyond that of glycemic control. Author suggests therefore that Phase II or Phase III trials may be warranted. J. R. Bruman (818) 789-3694 3527 Cody Road Sherman Oaks CA 91403