Further Evidence of GFAP as a Useful Marker is Offered in New Study by NIOSH, Partner Researchers
January 6, 2005
Contact: Fred Blosser (202) 401-3749
New findings from a study by the National Institute for Occupational Safety and Health (NIOSH) and the Pacific Health Research Institute provide further evidence that a protein in the human brain, glial fibrillary acidic protein (GFAP), can serve as a valuable marker to identify types of brain damage associated with dementia that might not be identified through traditional histopathology.
The findings are published in the Journal of Alzheimer’s Disease, Vol. 6, No. 6. An abstract is available online at www.j-alz.com/issues/6/vol6-6.htmlexternal icon. The study is part of NIOSH’s program of ongoing health-effects research, including work on the development and use of new biomarkers to advance the prevention of work-related neurological disorders.
The prevalence of dementia among the elderly is of growing concern in the U.S. Multiple forms of dementia exist. However, there often is no clear way to distinguish among the various forms. The causes of dementia are also multiple and complex, and in many cases cannot be confirmed until a neuropathological examination is conducted during autopsy.
When such an examination is performed, it often infers the cause of dementia from the presence of specific neuroanatomical markers such as Lewy bodies in the case of Parkinson’s-related dementia, or neurofibrillary plaques and tangles in the case of Alzheimer’s disease. This approach can be limited by:
- The lack of unique neuropathological markers for the various types of dementia,
- The co-expression of existing markers, or
- The lack of markers in some individuals who show clear signs of dementia, or even the presence of these markers in the brains of individuals who did not show any signs of dementia.
NIOSH researchers and their partners have been investigating the question of whether various occupational exposures are associated with a risk of neurological disease, using a study population of Japanese-American men who were born between 1900 and 1919. In this study, levels of GFAP, a sensitive marker of neural damage, were measured in brain tissue samples of deceased men who had been diagnosed with dementia, and of deceased men who had not been diagnosed with dementia. This protein, produced by a type of glial cell thought to support neurons in the brain, has been shown to increase in regions of neural damage, regardless of the cause of the damage. Thus, it is a non-specific yet sensitive marker of neural damage.
The investigators found increased levels of GFAP in several brain regions among individuals diagnosed with Alzheimer’s disease, vascular mediated dementia, and mixed dementia, compared with individuals not diagnosed with those disorders. Further, the researchers showed that higher GFAP levels were associated with a lower performance on a test of cognitive function. This association remained significant even when specific neuropathological markers of dementia were accounted for.