Imaging Techniques Detect Alzheimer's Disease

Investigators at Washington University (St. Louis, MO, USA) and the University of Pittsburgh (PA, USA) combined sophisticated brain imaging with measurement of beta-amyloid protein fragments in cerebrospinal fluid (CSF). They discovered that greater amounts of beta-amyloid-containing plaques in the brain were associated with lower levels of a specific protein fragment, amyloid-beta 1-42, in CSF. Earlier studies demonstrated that amyloid-beta 1-42 is vital to AD development. The substance is a key component of amyloid plaques in the brain, which are thought to influence cell-to-cell communication and are considered a characteristic of the Alzheimer's brain.

The study, published in the online December 21, 2005, issue of the journal Annals of Neurology, is the first to evaluate the relationship between levels of amyloid plaque deposits in the brain and different forms of beta-amyloid in CSF in living humans.

The research utilized a newly developed imaging tracer for beta-amyloid from investigators at the ADRC at the University of Pittsburgh. The study included 24 individuals aged 48 to 83 years who were cognitively normal or had very mild, mild, or moderate dementia. The researchers utilized positron emission tomography (PET), a brain imaging method, with a tracing substance called Pittsburgh Compound B (PIB), to determine the amount of plaques in the participants' brains. PIB attaches to beta-amyloid-containing plaques in the brain. PIB makes it possible to see on PET images any brain regions with high concentrations of plaques. The scientists also studied samples of study participants' CSF and blood plasma for levels of specific protein fragments, including two forms of beta-amyloid and the protein tau.

The seven participants whose PET scans showed PIB binding--and therefore deposits of beta-amyloid-containing plaques in the brain--had the lowest levels of amyloid-beta 1-42 in their CSF. Those without PIB binding had the highest levels of CSF amyloid-beta 1-42.

Significantly, three of the participants had normal cognitive assessments but had high PIB binding and low CSF amyloid-beta 1-42, suggesting the possibility that this combination of methods may be useful as "antecedent” biomarkers of AD, identifying the presence of AD amyloid deposits before the development of cognitive impairments.





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