Fibre diffraction of hair can provide a screening test for Alzheimer's disease: a human and animal model study.

BACKGROUND: Studies of molecular changes in hair as possible biomarkers for specific cancers revealed an additional molecular change in the diffraction patterns of some persons aged over 75. This change was found to correlate with the presence of Alzheimer's disease (AD). To confirm this correlation and its relation to the presence of a human APP mutation, known to definitely cause AD, hairs were examined from AD patients, pregnant women known to have an increase in plasma beta amyloid and transgenic mice carrying a mutated human APP gene. Patients were clinically examined by an experienced physician who recorded the patient's history and completed physical and neurological examinations. Hair samples were held taut and centred in the beam. The diffraction patterns were collected on Fuji-Bas Imaging plates and analysed using standard programs. MATERIAL/METHODS: A fan-shaped set of spot-like reflections was observed in the equatorial diffraction patterns from the hair of all AD patients and all third trimester pregnant women. Combined fibre diffraction of hair and histopathologic examination of brains from transgenic mice carrying a mutated human APP gene confirmed that these changes are related to the mutated human APP genes and the formation of beta amyloid plaques. RESULTS: Here we show results that fibre diffraction analysis would provide a non-invasive, accurate bio-marker for Alzheimer's disease. Our results are consistent with the hypothesis that this marker is related to the presence of mutated human APP genes and indicate that the structural change precedes the significant development of plaques. CONCLUSIONS: Here we show results that fibre diffraction analysis would provide a non-invasive, accurate bio-marker for Alzheimer's disease. Our results are consistent with the hypothesis that this marker is related to the presence of mutated human APP genes and indicate that the structural change precedes the significant development of plaques.

Isolation and growth of a cytopathic agent from multiple sclerosis brain tissue.

Although many studies support a role for viruses in multiple sclerosis (MS) etiopathology, no specific agent has been consistently associated with significant numbers of MS patients without concomitant detection in non-MS controls. Previous studies have shown the presence of viral-like structures in MS plaques, although the specificity of these structures for MS has been questioned. The present study describes the use of polyclonal antisera against feline and human brain-derived cytopathic agents and immunoaffinity chromatography to purify and partially characterize possible virus-like structures from MS brain tissue. Chromatography eluates from 4 MS brains contained pleomorphic particles up to 350 nm in diameter and tubular/filamentous-like structures approximately 10-18 nm in thickness. Inoculation of primary rat glial cell cultures with chromatography eluates from MS brain tissue resulted in a reproducible pattern of cytopathic effects in the form of multinucleation in cells identified immunocytochemically as oligodendrocytes. Antisera raised against the feline and MS-derived cytopathic agents were used to successfully immunolabel infected oligodendrocyte-like cells and syncytia and to detect a 66,000 M(r) protein on Western blots of inoculated cultures or concentrated MS brain eluates. Similar structures, cytopathic effects (CPE) and protein expression were not observed in eluates from 5 control brains or in cultures inoculated with control brain eluates. These studies demonstrate that cytopathic, virus-like structures can be isolated from MS brain tissue using antisera raised against a cytopathic agent rescued from demyelinating brain lesions in cats. The identity of this agent and its possible role in MS aetio-pathology remains unknown.