MIAMI—Molecular imaging detects the pathology that leads to Alzheimer’s disease years before the development of symptoms, which could allow physicians to detect signs of the disease in healthy patients, according to studies presented June 11 at the annual meeting of the Society of Nuclear Medicine and Molecular Imaging (SNMMI).
“Diagnosis of Alzheimer’s disease can now be made when the patient first presents symptoms and still has largely preserved mental function,” said Christopher Rowe, MD, lead investigator for the Australian Imaging, Biomarkers and Lifestyle study of aging (AIBL), in a release. “Previously there was an average delay of three years between consulting a doctor over memory concerns and the diagnosis of Alzheimer’s, as the diagnosis required the presence of dementia. When used as an adjunct to other diagnostic measures, molecular imaging can help lead to earlier diagnosis.”
Rowe shared results of an AIBL study that tracked 194 healthy participants, 92 people with mild cognitive impairment and 70 subjects with Alzheimer’s disease for 36 months after a C-11 PiB (Pittsburgh compound B) PET scan to gauge amyloid burden in the brain. Researchers also assessed episodic memory and hippocampal volume at baseline and follow-up.
At baseline, 98 percent of patients with Alzheimer’s disease, 65 percent of those with mild cognitive impairment and 31 percent of healthy participants were classified at PiB+. At three years, progression from mild cognitive impairment to Alzheimer’s occurred in 66 percent of PiB+ participants and 7 percent of PiB- participants.
Thus, in this study group, widespread amyloid plaque build-up preceded decline in memory and the development of dementia, and those with extensive amyloid burden were at higher risk of cognitive decline.
“The implication is that molecular imaging can help lead to diagnosis of Alzheimer’s disease when the patient has mild symptoms rather than wait until the patient has progressed to dementia,” Rowe said.
Amyloid imaging could provide an opportunity to identify patients on the path to dementia and allow physicians to intervene with preventive treatments as they become available. This prevention model should be more effective than trying to reverse damage after the onset of dementia, said Rowe.
In another study focused on beta amyloid in healthy subjects, 137 adults with normal cognitive function aged 30 to 89 years were imaged using PET with F-18 florbetapir, as well as functional MRI to explore how amyloid build-up affects connections in the default mode and salience networks. Those with increased amyloid burden in these neural networks were prone to impaired cognitive performance.
Finally, a third study assessed C-11 PiB for its ability to detect amyloid plaque in comparison to F-18 FDG in 100 cognitively normal participants from Wisconsin Registry for Alzheimer’s Prevention.
Participants underwent C-11 PiB PET, F-18 FDG PET and comprehensive neuropsychological testing. Studies were independently interpreted by two readers. Inter-reader agreement was higher for PiB than for FDG, the researchers reported in the abstract. Amyloid burden seemed to occur earlier than abnormal metabolism in high-risk participants. Visual ratings classified 15 percent of subjects as possible or probable Alzheimer’s disease pattern on PiB studies compared with 3.5 percent of participants who were rated as possible Alzheimer’s pattern.
Molecular imaging studies could allow physicians to evaluate whether pathological changes associated with Alzheimer’s disease are happening many years before the onset of clinical symptoms, Guofan Xu, MD, PhD, researcher scientist at University of Wisconsin, Madison, said in a release.