The study find that the Brain PET/CT acquisition was started 30 ± 5 min after [18F] FDG injection in all subjects. therefore SPM12 [statistical parametric mapping] implemented in MATLAB 2018a is use for the analysis of PET scans in this study. Suspected non-Alzheimer’s pathophysiology (SNAP) describes a clinical entity where older adults with or without subtle cognitive decline show one of the markers of neurodegeneration (e.g. neuronal injury markers).
The Brain PET/CT
Test negative for brain amyloid (Aβ) pathology [i.e. cerebrospinal fluid (CSF) assay and positron emission tomography (PET)] and have not been diagnosed with a specific neurodegenerative disorder The correct identification of SNAP is crucial; since it has been report to affect up to 23% of cognitively healthy adult individuals ; and is characterize by a benign clinical course; with only a minor proportion of patients progressing to mild cognitive impairment (MCI) or clinical AD.
In the era of Aβ imaging; the exclusion of one of the pathological hallmarks of Alzheimer’s disease (AD) is feasible. Because Several radiolabel compounds are develop for the in vivo visualization of the Aβ burden in brain tissue by means of PET. But On one hand; Aβ imaging with PET enables the correct classification of AD and the identification of those patients with MCI that will progress to AD; on the other hand, it represents a suboptimal biomarker in the assessment of dementia severity.
The pathological hallmarks
Interestingly; cognitive decline is only weakly related to change in Aβ burden and; most importantly, Aβ deposition increases slowly from cognitive normality to moderate severity. On the other side; PET with 2-deoxy-2-[18F] fluoroglucose ([18F] FDG) can efficiently demonstrate significant differences in the brain [18F] ;FDG uptake when comparing AD with other types of dementia (e.g. frontotemporal dementia, FTD); in subjects affected by MCI; the pattern is less specific and reflects the neuropsychological profile; but an involvement of the cingulate cortex and hippocampus is usually observe.
Although extensively studied in AD; but less is know about the role of PET imaging in SNAP individuals. To date; most of the studies in SNAP patients have been carry out using amyloid PET tracers; with the main purpose of excluding AD as a cause of cognitive impairment in these subjects. To the best of our knowledge; the [18F] FDG pattern has been evaluate only in one previous study, on a limit number of SNAP subjects.
The aim of the present study was to compare the pattern of the brain [18F] FDG uptake in SNAP, AD, and healthy controls using [18F] FDG PET imaging. CSF amyloid-β1-42 (Aβ1-42) is use as a marker of amyloid and CSF tau is use as a marker of neuronal injury; in order to differentiate AD from SNAP.