Researchers by means of two brain-imaging technologies have identified Alzheimer's-like brain changes in normal adults with amyloid plaques.

Definitive diagnosis of Alzheimer's disease requires finding amyloid plaques and neurofibrillary tangles in the brain at autopsy. In recent years it has been possible to detect amyloid in living brains by PET scanning with an imaging agent known as Pittsburgh Compound B (PiB). Plaques have been observed in the brains of apparently healthy individuals, as well as those with dementia, but whether the presence of plaques indicates the early stages of Alzheimer's disease is not yet known.
High-resolution magnetic resonance imaging studies have identified characteristic changes in brain structure thinning of key cortical regions and reduced volume of structures such as the hippocampus in persons with mild cognitive impairment, in individuals known to carry gene mutations that directly cause Alzheimer's disease and in diagnosed Alzheimer's patients. A recent study reported similar brain changes in some cognitively normal elders but did not distinguish those who had amyloid deposits from those who did not.
The current study involved 87 cognitively normal older individuals and 32 patients diagnosed with mild Alzheimer's matched for age, gender and education who had enrolled in the long-term Harvard Aging Brain Study. Participants underwent both high-resolution MR imaging of brain structure and PET scanning with PiB to detect amyloid plaques. The results showed that those cognitively normal individuals who had amyloid plaques also had structural changes similar to but less pronounced than the neurodegenerative changes seen in the symptomatic patients. Structural changes were most evident in areas comprising what is called the default network, which is known to be affected early in the course of Alzheimer's disease.
"If amyloidosis deposits of amyloid plaques in the brains of clinically normal people is associated with Alzheimer's-like neurodegeneration, then amyloidosis itself may signify 'preclinical' AD," say Johnson, an associate professor of Radiology at Harvard Medical School. "We need to learn more about how long it takes a normal person with amyloid to develop AD, whether there are critical 'second hit' factors that convert amyloidosis to Alzheimer's disease, and if there are measures that can halt the process of neurodegeneration."
Source-Eurekalert
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