PET/MR Imaging: New Frontier in Alzheimer's Disease and Other Dementias

Abstract

Alzheimer's disease (AD) is the most common form of dementia; a progressive neurodegenerative disease that currently lacks an effective treatment option. Early and accurate diagnosis, in addition to quick elimination of differential diagnosis, allows us to provide timely treatments that delay the progression of AD. Imaging plays an important role for the early diagnosis of AD. The newly emerging PET/MR imaging strategies integrate the advantages of PET and MR to diagnose and monitor AD. This review introduces the development of PET/MR imaging systems, technical considerations of PET/MR imaging, special considerations of PET/MR in AD, and the system's potential clinical applications and future perspectives in AD.

Keywords: Alzheimer diseases; PET radiotracers; PET/MR; clinical applications; technical considerations.

Figure 1

Example of simultaneous PET/MRI workflow in dementia. The workflow of PET/MR includes scanning of MR and PET. In the diagram, Dixon VIBE for PET data attenuation correction and other six sequences are shown in turn. MR scans take 40 min, PET takes only 20 min, and MR scans take up most of the process. With permission, from reference 33.

Figure 2

Group differences of functional connectivity based on the seed of right hippocampus in resting state fMRI. The three groups have differences in the medial prefrontal cortex (mPFC), the anterior lobe and the left posterior gyrus (MTG). Comparing with the control group, the functional connectivity of the medial prefrontal cortex and the anterior lobe is enhanced with the right hippocampus in APP/presenilin-1/2 and APOE ε4 carriers. With permission, from reference 39.

Figure 3

¹¹C Pittsburgh compound B (PiB), 18F-fluorodeoxyglucose (FDG) PET, and histopathology in selected patients. Patient 1 had clinical AD with diffuse cortical and striatal PIB, and predominantly temporal regions of the FDG. Post-mortem examination showed amyloid plaques in the temporal cortex. Patient 2 had frontotemporal lobar degeneration [FTLD]–amyotrophic lateral sclerosis [ALS]. The major metabolic loss in frontal lobe is manifested in this patient. Pathological analysis reveals diffuse plaques of early Aβ pathology. Patient 3 had clinical AD and was positive for PiB, but FDG showed decreased frontal lobe metabolism. Autopsy demonstrated AD diagnosis with frequent neuritis and neurofibrillary pathology. With permission, from reference 47.