Objective
The objective of this study is to compare amyloid β (Aβ) PET positive and negative patients to their neuropsychological profiles. There is a definitive link between Aβ deposits and cognitive disorders such as MCI or Alzheimer’s disease (AD), but does its presence justify the costly imaging tests based on its clinical context?
Background
Amnestic MCI is largely considered prodromal to AD/dementia in a high majority of cases. [1] Many studies have shown a positive correlation between Aβ PET positive individuals and their likelihood to progress to AD. Aβ deposits in the brain are not always a sign of AD or even MCI, and many elderly people live normal lives with elevated levels. The presence of Aβ in the brain should be carefully considered alongside other tests before making a clinical diagnosis of MCI or AD.
Methods
130 subjects from Barrow Neurological Institute (Phoenix, AZ) were included in this study. Amyloid PET report data was pulled from Dignity Health St. Joseph’s Hospital and Medical Center Outpatient Imaging. Amyloid PET scans obtained by using F-18 florbetapir compound and reviewed by an expert radiologist providing a qualitative status of amyloid-beta positive (+) or negative (-). All data was anonymized and categorized into positive amyloid PET, negative amyloid PET, and clinical diagnosis based on neuropsychological profiles.
Results
The demographic data indicated that 38.5% of the 91 patients diagnosed as amnestic MCI were amyloid PET negative while 61.5% were amyloid PET positive. Of the 39 patients diagnosed as Dementia or AD 15.4% were amyloid PET negative and 84.6% were amyloid PET positive. Correlational analysis between diagnosis and neuropsychological variables suggests that some variables correlate well while others do not. There is a significant correlation between diagnosis and dementia rating scale (DRS) r(24) = -.762, between diagnosis and TrailsB Test r(39) = .397, between diagnosis and phonetic fluency r(30) = -.383, between diagnosis and semantic fluency r(29) = -.369, and between diagnosis and the Boston Naming Test (BNT) r(36) = -.312. Comparing the PET positive and PET negative groups there is a marginal significance in the Boston Naming Test (T=1.945, P=.060) suggesting PET positive individuals test lower than PET negative.
Conclusion
Based on all the results of this study, amyloid PET is still a clinical indicator that an individual might be MCI or dementia/AD, but it has its exceptions. A small number of patients diagnosed as dementia/AD had a negative amyloid PET suggesting that beta amyloid plaques are not the only cause of the disease. There is a strong suggestion that amyloid plaques are a major factor in the progression of dementia or AD, however the results from an amyloid PET cannot be directly related to a diagnosis.