Convergent and Discriminant Validity of Default Mode Network and Limbic Network Perfusion in Amnestic Mild Cognitive Impairment Patients.


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:
2021
Historique:
pubmed: 6 7 2021
medline: 24 11 2021
entrez: 5 7 2021
Statut: ppublish

Résumé

Previous studies reported default mode network (DMN) and limbic network (LIN) brain perfusion deficits in patients with amnestic mild cognitive impairment (aMCI), frequently a prodromal stage of Alzheimer's disease (AD). However, the validity of these measures as AD markers has not yet been tested using MRI arterial spin labeling (ASL). To investigate the convergent and discriminant validity of DMN and LIN perfusion in aMCI. We collected core AD markers (amyloid-β 42 [Aβ42], phosphorylated tau 181 levels in cerebrospinal fluid [CSF]), neurodegenerative (hippocampal volumes and CSF total tau), vascular (white matter hyperintensities), genetic (apolipoprotein E [APOE] status), and cognitive features (memory functioning on Paired Associate Learning test [PAL]) in 14 aMCI patients. Cerebral blood flow (CBF) was extracted from DMN and LIN using ASL and correlated with AD features to assess convergent validity. Discriminant validity was assessed carrying out the same analysis with AD-unrelated features, i.e., somatomotor and visual networks' perfusion, cerebellar volume, and processing speed. Perfusion was reduced in the DMN (F = 5.486, p = 0.039) and LIN (F = 12.678, p = 0.004) in APOE ɛ4 carriers compared to non-carriers. LIN perfusion correlated with CSF Aβ42 levels (r = 0.678, p = 0.022) and memory impairment (PAL, number of errors, r = -0.779, p = 0.002). No significant correlation was detected with tau, neurodegeneration, and vascular features, nor with AD-unrelated features. Our results support the validity of DMN and LIN ASL perfusion as AD markers in aMCI, indicating a significant correlation between CBF and amyloidosis, APOE ɛ4, and memory impairment.

Sections du résumé

BACKGROUND
Previous studies reported default mode network (DMN) and limbic network (LIN) brain perfusion deficits in patients with amnestic mild cognitive impairment (aMCI), frequently a prodromal stage of Alzheimer's disease (AD). However, the validity of these measures as AD markers has not yet been tested using MRI arterial spin labeling (ASL).
OBJECTIVE
To investigate the convergent and discriminant validity of DMN and LIN perfusion in aMCI.
METHODS
We collected core AD markers (amyloid-β 42 [Aβ42], phosphorylated tau 181 levels in cerebrospinal fluid [CSF]), neurodegenerative (hippocampal volumes and CSF total tau), vascular (white matter hyperintensities), genetic (apolipoprotein E [APOE] status), and cognitive features (memory functioning on Paired Associate Learning test [PAL]) in 14 aMCI patients. Cerebral blood flow (CBF) was extracted from DMN and LIN using ASL and correlated with AD features to assess convergent validity. Discriminant validity was assessed carrying out the same analysis with AD-unrelated features, i.e., somatomotor and visual networks' perfusion, cerebellar volume, and processing speed.
RESULTS
Perfusion was reduced in the DMN (F = 5.486, p = 0.039) and LIN (F = 12.678, p = 0.004) in APOE ɛ4 carriers compared to non-carriers. LIN perfusion correlated with CSF Aβ42 levels (r = 0.678, p = 0.022) and memory impairment (PAL, number of errors, r = -0.779, p = 0.002). No significant correlation was detected with tau, neurodegeneration, and vascular features, nor with AD-unrelated features.
CONCLUSION
Our results support the validity of DMN and LIN ASL perfusion as AD markers in aMCI, indicating a significant correlation between CBF and amyloidosis, APOE ɛ4, and memory impairment.

Identifiants

pubmed: 34219733
pii: JAD210531
doi: 10.3233/JAD-210531
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

1797-1808

Auteurs

Giulia Quattrini (G)

Laboratory of Alzheimer's Neuroimaging and Epidemiology (LANE), IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy.
Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.

Moira Marizzoni (M)

Laboratory of Alzheimer's Neuroimaging and Epidemiology (LANE), IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy.
Laboratory of Biological Psychiatry, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy.

Francesca B Pizzini (FB)

Radiology, Department of Diagnostic and Public Health, University of Verona, Verona, Italy.

Ilaria Boscolo Galazzo (IB)

Department of Computer Science, University of Verona, Verona, Italy.

Marco Aiello (M)

IRCCS SDN, Napoli, Italy.

Mira Didic (M)

Aix-Marseille Univ, INSERM, INS, Instit Neurosci des Syst, Marseille, France.
APHM, Timone, Service de Neurologie et Neuropsychologie, Hôpital Timone Adultes, Marseille, France.

Andrea Soricelli (A)

IRCCS SDN, Napoli, Italy.
Department of Sport Sciences, University of Naples Parthenope, Naples, Italy.

Diego Albani (D)

Neuroscience Department, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy.

Melissa Romano (M)

Laboratory of Alzheimer's Neuroimaging and Epidemiology (LANE), IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy.

Olivier Blin (O)

Aix-Marseille Univ, INSERM, INS, Instit Neurosci des Syst, DHUNE, Ap-Hm, Marseille, France.

Gianluigi Forloni (G)

Neuroscience Department, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy.

Xavier Golay (X)

Department of Brain Repair and Rehabilitation, UCL Queen Square Institute of Neurology, London, United Kingdom.

Jorge Jovicich (J)

Center for Mind/Brain Sciences - CIMeC, University of Trento, Rovereto, Italy.

Pradeep J Nathan (PJ)

Department of Psychiatry, University of Cambridge, Cambridge, UK.

Jill C Richardson (JC)

Neurosciences Therapeutic Area, GlaxoSmithKline R&D, Gunnels Wood Road, Stevenage, United Kingdom.

Marco Salvatore (M)

IRCCS SDN, Napoli, Italy.

Giovanni B Frisoni (GB)

Memory Clinic and LANVIE-Laboratory of Neuroimaging of Aging, University Hospitals and University of Geneva, Geneva, Switzerland.

Michela Pievani (M)

Laboratory of Alzheimer's Neuroimaging and Epidemiology (LANE), IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy.

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