Editor's note: Science Scan is a round up of recently publishedbiotechnology-related research.

Monosodium glutamate, (a.k.a. MSG), is a sodium salt of glutamicamino acid. It excites taste buds into heightening the flavor of foods.MSG also causes an acute allergic reaction, Chinese RestaurantSyndrome, in some sensitive people.

Glutamate is one of the brain's main neurotransmitters, but also oneof its neuroexcitatory toxins. It's suspected of complicity in theneuronal apoptosis of Alzheimer's disease.

Aspirin, on the other hand, is a sodium salt of acetylsalicylic acid.This is the familiar pill that people reach for to fight pain, fever andinflammation. Now it looks as if aspirin can fight glutamicneurotoxicity as well.

An article in the current issue of Science, dated Nov. 22, 1996,reports: "Neuroprotection by aspirin and sodium salicylate throughblockade of NF-kB activation." Its first author isneuropharmacologist Mariagrazia Grilli, of Italy's University ofBrescia.

In cultured rat brain cells, Grilli showed that acetylsalicylic acid andsodium salicylate blocked glutamate-induced apoptosis in 83 percentof the cells. "In view of their distinct ability to act not merely as anti-inflammatory compounds," she wrote, "but also as . . . agents againstneurotoxicity, these drugs appear to possess a wider pharmacologicalspectrum than other nonsteroidal anti-inflammatory drugs."

As for the kB neurotranscription factor, Grilli told last week'sNeuroscience meeting, in Washington, that these factors recognizesequences on the amyloid precursor protein, and are "upregulated inresponse to . . . the excitatory amino acid glutamate." She added: Webelieve that these evidences are potentially relevant for understandingthe neuropathology associated with Alzheimer's disease."

New-Found Gene For Most Fanconi'sAnemia Cases Will Speed Diagnosis

Short stature, small head, mental retardation, tiny genitals, crossedeyes _ these are outward signs of a horrendous hereditary malady,Fanconi's anemia (FA). Its victims usually die of leukemia by age 16.

Five gene subtypes _ A, B, C, D, E _ are indicted in FA. The variantthat causes two-thirds of its cases, FA A, has just been cloned. Aconsortium of six centers around the world performed this feat,reported in the November Nature Genetics.

The group located this A subtype in the long arm of humanchromosome A. Two others, C and D, which together account for 19percent of known cases, were previously tracked to chromosomes 9and 3 respectively.

"Cloning of the Fanconi anemia gene," said molecular geneticistArleen Auerbach, at The Rockefeller University in New York, "willhelp develop a quick, accurate diagnostic test for about 65 percent ofFA patients."

Her laboratory at the Rockefeller maintains the international FAregistry, with data on 600 patients in the world. The disease affectsseveral thousand victims worldwide. Auerbach predicts that cloningthe FA subtype A gene "should assist in developing better FAtreatments, even possible therapies to correct the genetic mutations."

Researchers suggest that FA's protean symptoms arise because thegenetic mutations cause heightened sensitivity to agents, such asionizing radiation, that perturb DNA's structure in chromosomes.They compare this effect to a similar susceptibility in a superficiallysimilar disease, ataxia-telangiectasia.

Second Mouse Model Signs OnFor Studying Ataxia-Telangiectasia

A particularly pernicious disease of childhood, with symptoms thatread like a medical dictionary, has just acquired a second mousemodel for elucidating its causes and effects.

A pioneer in generating transgenic mice, Harvard University medicalgeneticist Philip Leder, is the father of this latest murine addition tothe stable of animal models that mimic Ataxia-Telangiectasia's (AT)pathology. An article describing his new surrogate appears in thecurrent Proceedings of the National Academy of Sciences (PNAS),dated Nov. 19, 1996. Its title: "Pleiotropic defects in ataxia-telangiectasia protein-deficient mice."

The first animal to model the disease made its bow last summer in thejournal Cell dated July 12, 1996, headed "Atm-deficient mice: Aparadigm of ataxia-telangiectasia." (See BioWorld Today, July 12,1996, p. 1.) It is the creation of scientists at National Institutes ofHealth's National Center for Human Genome Research (NCHGR).

AT is a rare, fatal, inherited malady that afflicts some 500 youngstersin the U.S. alone. However, its wide spectrum of symptoms makesanimal models indispensable for researching many more commondisorders. These AT scourges range from cerebellar ataxia toimmunodeficiencies to severe respiratory infections to growthretardation to sexual immaturity and male sterility, to prematureaging of hair and skin, to fatal lymphomas. Leder suggests that acutesensitivity to ionizing radiation brings on DNA damage that "is amajor cause of AT."

His mice, and those developed this summer at the NCHGR, alikereproduce this litany of AT morbidity and mortality. n

-- David N. Leff Science Editor

(c) 1997 American Health Consultants. All rights reserved.

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