Individual Brain Metabolic Signatures in Corticobasal Syndrome.


Journal

Journal of Alzheimer's disease : JAD
ISSN: 1875-8908
Titre abrégé: J Alzheimers Dis
Pays: Netherlands
ID NLM: 9814863

Informations de publication

Date de publication:
2020
Historique:
pubmed: 17 6 2020
medline: 8 5 2021
entrez: 16 6 2020
Statut: ppublish

Résumé

Corticobasal syndrome (CBS) is the usual clinical presentation of patients with corticobasal degeneration pathology. Nevertheless, there are CBS individuals with postmortem neuropathology typical of Alzheimer's disease (AD). In this study, we aim to detect FDG-PET metabolic signatures at the single-subject level in a CBS sample, also evaluated with cerebrospinal fluid (CSF) markers for AD pathology. 21 patients (68.9±6.4 years; MMSE score = 21.7±6.3) fulfilling current criteria for CBS were enrolled. All underwent a clinical-neuropsychological assessment and an instrumental evaluation for biomarkers of neurodegeneration, amyloid and tau pathology (i.e., FDG-PET imaging and CSF Aβ42 and tau levels) at close intervals. CBS subjects were classified according to the presence or absence of CSF markers of AD pathology (i.e., low Aβ42 and high phosphorylated tau levels). Optimized voxel-based SPM procedures provided FDG-PET metabolic patterns at the single-subject and group levels. Eight CBS had an AD-like CSF profile (CBS-AD), while thirteen were negative (CBS-noAD). The two subgroups did not differ in demographic characteristics or global cognitive impairment. FDG-PET SPM t-maps identified different metabolic signatures. Namely, all CBS-AD patients showed the typical AD-like hypometabolic pattern involving posterior cingulate cortex, precuneus and temporo-parietal cortex, whereas CBS-noAD cases showed bilateral hypometabolism in fronto-insular cortex and basal ganglia that is typical of the frontotemporal lobar degeneration spectrum. These results strongly suggest the inclusion of FDG-PET imaging in the diagnostic algorithm of individuals with CBS clinical phenotype in order to early identify functional metabolic signatures due to different neuropathological substrates, thus improving the diagnostic accuracy.

Sections du résumé

BACKGROUND
Corticobasal syndrome (CBS) is the usual clinical presentation of patients with corticobasal degeneration pathology. Nevertheless, there are CBS individuals with postmortem neuropathology typical of Alzheimer's disease (AD).
OBJECTIVE
In this study, we aim to detect FDG-PET metabolic signatures at the single-subject level in a CBS sample, also evaluated with cerebrospinal fluid (CSF) markers for AD pathology.
METHODS
21 patients (68.9±6.4 years; MMSE score = 21.7±6.3) fulfilling current criteria for CBS were enrolled. All underwent a clinical-neuropsychological assessment and an instrumental evaluation for biomarkers of neurodegeneration, amyloid and tau pathology (i.e., FDG-PET imaging and CSF Aβ42 and tau levels) at close intervals. CBS subjects were classified according to the presence or absence of CSF markers of AD pathology (i.e., low Aβ42 and high phosphorylated tau levels). Optimized voxel-based SPM procedures provided FDG-PET metabolic patterns at the single-subject and group levels.
RESULTS
Eight CBS had an AD-like CSF profile (CBS-AD), while thirteen were negative (CBS-noAD). The two subgroups did not differ in demographic characteristics or global cognitive impairment. FDG-PET SPM t-maps identified different metabolic signatures. Namely, all CBS-AD patients showed the typical AD-like hypometabolic pattern involving posterior cingulate cortex, precuneus and temporo-parietal cortex, whereas CBS-noAD cases showed bilateral hypometabolism in fronto-insular cortex and basal ganglia that is typical of the frontotemporal lobar degeneration spectrum.
DISCUSSION
These results strongly suggest the inclusion of FDG-PET imaging in the diagnostic algorithm of individuals with CBS clinical phenotype in order to early identify functional metabolic signatures due to different neuropathological substrates, thus improving the diagnostic accuracy.

Identifiants

pubmed: 32538847
pii: JAD200153
doi: 10.3233/JAD-200153
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

517-528

Auteurs

Chiara Cerami (C)

Dipartimento di Scienze Umane e della Vita, Scuola Universitaria di Studi Superiori IUSS Pavia, Pavia, Italy.
IRCCS Mondino Foundation, Pavia, Italy.

Alessandra Dodich (A)

CeRiN, Centre for Mind/Brain Sciences, University of Trento, Rovereto, Italy.

Sandro Iannaccone (S)

Neurorehabilitation Unit, San Raffaele Hospital, Milan, Italy.

Giuseppe Magnani (G)

Department of Neurology, San Raffaele Hospital, Milan, Italy.

Alessandra Marcone (A)

Neurorehabilitation Unit, San Raffaele Hospital, Milan, Italy.

Priscilla Guglielmo (P)

Nuclear Medicine Unit, San Raffaele Hospital, Milan, Italy.

Giovanna Vanoli (G)

Nuclear Medicine Unit, San Raffaele Hospital, Milan, Italy.

Stefano F Cappa (SF)

Dipartimento di Scienze Umane e della Vita, Scuola Universitaria di Studi Superiori IUSS Pavia, Pavia, Italy.
IRCCS Mondino Foundation, Pavia, Italy.

Daniela Perani (D)

Nuclear Medicine Unit, San Raffaele Hospital, Milan, Italy.
Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.
Vita-Salute San Raffaele University, Milan, Italy.

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