The pathological accumulation of different peptides is the common base of many neurodegenerative processes, such as Alzheimer's disease (AD). AD is characterized by amyloid deposits which may cause alterations in neurotransmission, activation of inflammatory mechanisms, neuronal death and cerebral atrophy. Diagnosis in vivo is challenging as the criteria rely mainly on clinical manifestations, which become evident only in a late stage of the disease. While AD can currently be definitively confirmed by postmortem histopathologic examination, in vivo imaging may improve the clinician's ability to identify AD at the earliest stage. In this regard, the detection of cerebral amyloid plaques with positron emission tomography (PET) is likely to improve diagnosis and allow for a prompt start of an effective therapy. Many PET imaging probes for AD-specific pathological modifications have been developed and proved effective in detecting amyloid deposits in vivo. We here review the current knowledge on PET imaging in the detection of amyloid deposits and their application in the diagnosis of AD.
F-FDG PET/CT showed high diagnostic performance in the evaluation of BMI in pediatric HL. Thus, BMB should be ideally reserved for patients presenting with doubtful F-FDG PET/CT findings for BMI.
Positron emission tomography (PET) with 18F-Fluorodeoxyglucose (18F-FDG) plays an outstanding role in the diagnostic work-up of dementia. Amyloid PET imaging is a complementary imaging technique for the early detection of Alzheimer disease (AD). β-amyloid precursor protein (APP), Presenilin-1 (PSEN1) and Presenilin-2 (PSEN2) are the 3 main causative genes responsible for autosomal dominant early-onset Alzheimer disease (EOAD). This is the first report of 18F-Florbetapir amyloid imaging findings in a 35-year-old male patient with EOAD carrying the G378E mutation in PSEN1 gene. Brain computed tomography (CT) and magnetic resonance imaging scans showed remarkable cerebral atrophy with dilatation of the cerebrospinal fluid spaces; furthermore, a 18F-Florbetapir PET/CT scan demonstrated also widespread remarkable accumulation of the amyloid tracer in the cerebral cortex, with reduction of the normal contrast between white and gray matter and flattening of the external cortical margins. Furthermore, PET/CT showed intense 18F-florbetapir uptake in the striatum and in the thalamus bilaterally. Our case supports the usefulness of amyloid PET imaging in the diagnostic work-up of EOAD.
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