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CSF and FDG‐PET study of the AD continuum: Biochemical and imaging features of two different mechanisms of neurodegeneration
Author(s) -
De Lucia Vincenzo,
Bonomi Chiara Giuseppina,
Motta Caterina,
Assogna Martina,
Scaricamazza Eugenia,
Martorana Alessandro,
Koch Giacomo
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.042117
Subject(s) - neurodegeneration , medicine , neuropsychology , positron emission tomography , amyloidosis , disease , neuroscience , pathology , psychology , cognition
Background Alzheimer's Disease (AD) is a biological and clinical continuum which diagnosis necessarily passes through the analysis of CSF and/or imaging biomarkers. Presence of amyloidosis introduces the concept of AD continuum while the presence of either CSF tau pathology or 18FDG‐PET imaging introduce to the concept of neurodegeneration. However isolated amyloidosis, which is part of the AD continuum often presents with positive 18FDG‐PET although CSF tau levels remain within the range. Here we aimed to investigate the neuropsychological, CSF and 18FDG PET biomarkers of the AD continuum in order to better understand the usefulness of the NIA‐A criteria in terms of diagnosis and prognosis of the disease. Method We evaluated 101 patients suffering from amnestic and mild cognitive impairment from March 2018 to January 2019 in our Memory Clinic at the Policlinico Tor Vergata, Rome. Patients underwent neuropsychological assessment, ApoE genotyping, 18FDG PET and lumbar puncture to evaluate CSF biomarkers (Aβ‐42, t‐Tau, p‐Tau) for diagnostic purposes. We classified all patients following the NIA‐A criteria. Result Individuals with AD continuum despite the absence of tau pathology in CSF show images of neurodegeneration. Their pattern remain however different from those suffering from AD, having reduced or even absent involvement of the frontal lobes in 18FDG PET studies. Similar results were not obtained in neuropsychological assessment . Frontal lobe hypometabolism and executive function impairment in A+T+ subjects were associated with CSF t‐Tau and p‐Tau increase. 18FDG PET neurodegeneration and Tau degeneration refers to different mechanisms of cell damage, whereas CSF lactate doesn’t correlate with 18FDG PET hypometabolism. Conclusion AD continuum is characterized by different pattern of CSF and imaging biomarkers. Neurodegenerative mechanisms related to amyloidosis differ qualitatively and quantitatively from those associated to tau pathology and the presence or the absence of ε4 polymorphism. These features represent an important step forward in our understanding of AD pathophysiology.