What is the role of PET scanning in the diagnosis of Alzheimer disease?

Updated: Apr 12, 2018
  • Author: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS; Chief Editor: L Gill Naul, MD  more...
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PET scanning is a powerful imaging technique that enables in vivo examination of brain functions. It allows for noninvasive quantification of cerebral blood flow, metabolism, and receptor binding. PET scanning helps in understanding the disease's pathogenesis, making the correct diagnosis, and monitoring the disease's progression and response to treatment. [54, 55, 31]

PET scanning involves the introduction of a radioactive tracer into the human body, usually with an intravenous injection. A tracer is essentially a biologic compound of interest that is labeled with a positron-emitting isotope, such as carbon-11 (11C), fluorine-18 (18F), or oxygen-15 (15O). These isotopes are used because they have relatively short half-lives (from minutes to 17</ref> [56, 57, 58, 59, 60, 61, 62, 63, 64]  Fifty radiopharmaceuticals for the in vivo imaging of amyloid burden and other tracers are being developed for the assessment of tauopathies and inflammatory processes, which may underlie the onset of the amyloid cascade. [31]

The 2 most common physiologic process measurements performed using PET scanning are glucose with [18F] FDG and cerebral blood flow using water. [41]

FDG-PET has been used extensively to study Alzheimer disease, and it is evolving into an effective tool for early diagnosis and for differentiation of Alzheimer disease from other types of dementia. FDG-PET has been used to detect persons at risk for Alzheimer disease even before the onset of symptoms. [65]

Patients with Alzheimer disease have characteristic temporoparietal glucose hypometabolism, the degree of which is correlated with the severity of dementia. [66] (Temporal and parietal glucose hypometabolism is widely seen on PET images in patients with Alzheimer disease.) With disease progression, frontal involvement may be evident. Glucose hypometabolism in Alzheimer disease is likely to be caused by a combination of neuronal cell loss and decreased synaptic activity. [67]

In control subjects, entorhinal cortex hypometabolism on FDG-PET has predictive value in the progression of dementia to MCI or even to Alzheimer disease. [68, 69] The identification of asymptomatic individuals at risk will have an enormous role in the treatment strategy for Alzheimer disease. [56] Individuals at high risk for Alzheimer disease (asymptomatic carriers of the APOE*E4 allele) exhibit a pattern of glucose hypometabolism similar to that of patients with Alzheimer disease. After a mean follow-up of 2 years, the cortical metabolic abnormality continues to decline despite preservation of cognitive performance. [70, 69]

Teipel et al found that time to conversion from MCI to Alzheimer disease was best predicted by increased AV45-PET signal in posterior medial and lateral cortical regions, decreased FDG-PET signal in medial temporal and temporobasal regions, and reduced gray matter volume in medial, basal, and lateral temporal regions. [71]

In patients with Alzheimer disease, PET performed with ligand PK11195 labeled with 11C, or (R)-[11C] PK11195, showed increased binding in the entorhinal, temporoparietal, and cingulate cortices. This finding corresponded to the postmortem distribution of Alzheimer disease pathology. [72]

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