N-acetylaspartate is an axon-specific marker of mature white matter in vivo: a biochemical and immunohistochemical study on the rat optic nerve.

Axonal pathology is a major cause of neurological disability in multiple sclerosis. Axonal transection begins at disease onset but remains clinically silent because of compensatory brain mechanisms. Noninvasive surrogate markers for axonal injury are therefore essential to monitor cumulative disease burden in vivo. The neuronal compound N-acetylaspartate, as measured by magnetic resonance spectroscopy, is currently the best and most specific noninvasive marker of axonal pathology in multiple sclerosis. The possibility has been raised, however, that N-acetylaspartate is expressed also by oligodendroglial lineage cells. In order to investigate N-acetylaspartate specificity for white matter axons, transected rat optic nerves were analyzed by high-performance liquid chromatography and immunohistochemistry. In transected adult nerves, N-acetylaspartate and N-acetyl aspartylglutamate decreased in concordance with axonal degeneration and were undetectable 24 days posttransection. Nonproliferating oligodendrocyte progenitor cells, oligodendrocytes, and myelin were abundant in these axon-free nerves. At 24 days posttransection, N-acetylaspartate was increased (42%; p = 0.02) in nontransected contralateral nerves. After transection at postnatal day 4, total N-acetylaspartate decreased by 80% (P14; p = 0.002) and 94% (P20; p = 0.003). In these developing axon-free nerves, 25 to 33% of oligodendrocyte progenitor cells were proliferating. These data validate magnetic resonance spectroscopy measurements of N-acetylaspartate as an axon-specific monitor of central nervous system white matter in vivo. In addition, the results indicate that neuronal adaptation can increase N-acetylaspartate levels, and that 5 to 20% of the N-acetylaspartate in developing white matter is synthesized by proliferating oligodendrocyte progenitor cells.     

COMMUNITY PARTICIPATION OR COMMUNITY MANIPULATION? A CASE STUDY OF THE ILLAWARRA CANCER APPEAL-A-THON

Fashion parades, balls, raffles, and weekly deductions from thousands of workers' pay packets were integral to success of the Cancer Appeal-a-thon in the Illawarra region. In 1986–87 the Illawarra community was induced to contribute $1.5 million in order to purchase a linear accelerator for the Wollongong Hospital. The community agreed that a radiotherapy machine was the number one health service priority for the region. Or did it? Application of Alford's structural interests framework to this case-study reveals how failure to examine power relations between medical monopolizers, health care rationalizers and community participants results in an inability to recognise that alternative community needs — for cancer prevention, domiciliary care, or alternative therapies — might be unarticulated or unobservable, and in an inability to ask whether the community may be mistaken about, or unaware of, its own health needs. Specifically, the paper argues that, ‘community needs’ are easily manipulated or distorted by powerful interest groups and that the political context within which community needs are recognized, articulated and mobilized is the most important issue for community participation in the health policy-making process.