A type of PET scanning may be useful in a non-invasive assessment of the formation of Alzheimer’s disease-related plaques in the brain, according to small study posted online Monday that will appear in the October issue of Archives of Neurology.
Currently, the only reliable way to assess the aggregation of plaques in the brain made of beta-amyloid is through analyzing brain tissue samples obtained during life or autopsy after death, which the authors described as “a major methodological obstacle considering clinical drug trials of early Alzheimer’s disease.”
Ville Leinonen, MD, PhD, of the University of Kuopio in Finland, and colleagues studied 10 patients without severe dementia who had undergone a biopsy of their frontal cortex because they were suspected of having normal-pressure hydrocephalus, an abnormal increase of cerebrospinal fluid in the brain.
In general, 22 to 42 percent of patients with symptoms of normal-pressure hydrocephalus have brain lesions characteristic of Alzheimer’s disease, the researchers said.
Among the participants, the investigators found that six had beta-amyloid plaques in their tissue samples, while four displayed no Alzheimer’s disease–related brain changes. The patients were injected with a marker known as carbon 11–labeled Pittsburgh Compound B ([11C]PiB) and then underwent a 90-minute PET scan.
Leinonen and colleagues said that results of the scan indicated that patients who had beta-amyloid plaques in their brain biopsy specimen displayed a higher uptake of [11C]PiB in certain brain areas as compared with those who did not have such accumulations.
“This study supports the use of [11C]PiB PET in the evaluation of beta-amyloid deposition in, for example, mild cognitive impairment, Alzheimer’s disease or normal-pressure hydrocephalus,” the authors wrote.
“Large and prospective studies are required to verify whether [11C]PiB PET will become a tool in diagnosing Alzheimer’s disease. Another potential use of [11C]PiB would be the quantitative monitoring of beta-amyloid deposits in the brain in subjects under treatment in pharmaceutical trials of early Alzheimer’s disease targeting amyloid accumulation,” they concluded.