article: Aluminium adjuvant linked to gulf war illness induces motor neuron deat

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Aluminum adjuvant linked to gulf war illness induces motor neuron

death in mice.

Neuromolecular Medicine

February 2007, Volume 9, Issue 1

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Petrik MS, Wong MC, Tabata RC, Garry RF, Shaw CA.

Department of Ophthalmology and Program in Neuroscience, University

of British Columbia, Vancouver, British Columbia, Canada.

Gulf War illness (GWI) affects a significant percentage of veterans

of the 1991 conflict, but its origin remains unknown. Associated

with some cases of GWI are increased incidences of amyotrophic

lateral sclerosis and other neurological disorders. Whereas many

environmental factors have been linked to GWI, the role of the

anthrax vaccine has come under increasing scrutiny. Among the

vaccine's potentially toxic components are the adjuvants aluminum

hydroxide and squalene.

To examine whether these compounds might contribute to neuronal

deficits associated with GWI, an animal model for examining the

potential neurological impact of aluminum hydroxide, squalene, or

aluminum hydroxide combined with squalene was developed. Young, male

colony CD-1 mice were injected with the adjuvants at doses

equivalent to those given to US military service personnel. All mice

were subjected to a battery of motor and cognitive- behaviora l

tests over a 6-mo period postinjections.

Following sacrifice, central nervous system tissues were examined

using immunohistochemistr y for evidence of inflammation and cell

death. Behavioral testing showed motor deficits in the aluminum

treatment group that expressed as a progressive decrease in strength

measured by the wire-mesh hang test (final deficit at 24 wk; about

50%). Significant cognitive deficits in water-maze learning were

observed in the combined aluminum and squalene group (4.3 errors per

trial) compared with the controls (0.2 errors per trial) after 20

wk.

Apoptotic neurons were identified in aluminum- injected animals that

showed significantly increased activated caspase-3 labeling in

lumbar spinal cord (255%) and primary motor cortex (192%) compared

with the controls. Aluminum-treated groups also showed significant

motor neuron loss (35%) and increased numbers of astrocytes (350%)

in the lumbar spinal cord.

The findings suggest a possible role for the aluminum adjuvant in

some neurological features associated with GWI and possibly an

additional role for the combination of adjuvants.

Neuromolecular Med. 2007; 9(1); 83-100.