Cognitive reserve in Parkinson's disease without dementia: β-amyloid and metabolic assessment.


Journal

Movement disorders clinical practice
ISSN: 2330-1619
Titre abrégé: Mov Disord Clin Pract
Pays: United States
ID NLM: 101630279

Informations de publication

Date de publication:
03 Jan 2024
Historique:
revised: 14 11 2023
received: 31 01 2023
accepted: 09 12 2023
medline: 4 1 2024
pubmed: 4 1 2024
entrez: 3 1 2024
Statut: aheadofprint

Résumé

Cognitive reserve (CR) is the mismatch between preserved cognition and neuropathological damage. Amyloidopathy in Parkinson's disease (PD) could be associated with faster progression to dementia, but the putative protective effect of CR is unknown. To evaluate the effect of CR on β-amyloid burden and brain metabolism in non-demented PD subjects. Participants with PD (n= 53) underwent a clinical evaluation, [18F]-Fluorodeoxyglucose and [18F]-Flutemetamol PET-MRs, and were classified according to CR. The metabolic pattern of 16 controls was compared to PD subjects'. The PD subjects showed hypometabolism mainly in the bilateral posterior cortex. Superior-CR subjects (n= 22) exhibited better cognitive performance, increased amyloid burden, and higher metabolism in several right hemisphere areas compared to low-medium-CR subjects (n= 31). Higher CR in non-demented PD is associated with better cognitive performance, which might reduce vulnerability to the effect of β-amyloid. Whether superior CR leads to protection against metabolic deterioration, and predominantly right hemisphere involvement, deserves further exploration This article is protected by copyright. All rights reserved.

Sections du résumé

BACKGROUND BACKGROUND
Cognitive reserve (CR) is the mismatch between preserved cognition and neuropathological damage. Amyloidopathy in Parkinson's disease (PD) could be associated with faster progression to dementia, but the putative protective effect of CR is unknown.
OBJECTIVES OBJECTIVE
To evaluate the effect of CR on β-amyloid burden and brain metabolism in non-demented PD subjects.
METHODS METHODS
Participants with PD (n= 53) underwent a clinical evaluation, [18F]-Fluorodeoxyglucose and [18F]-Flutemetamol PET-MRs, and were classified according to CR. The metabolic pattern of 16 controls was compared to PD subjects'.
RESULTS RESULTS
The PD subjects showed hypometabolism mainly in the bilateral posterior cortex. Superior-CR subjects (n= 22) exhibited better cognitive performance, increased amyloid burden, and higher metabolism in several right hemisphere areas compared to low-medium-CR subjects (n= 31).
CONCLUSIONS CONCLUSIONS
Higher CR in non-demented PD is associated with better cognitive performance, which might reduce vulnerability to the effect of β-amyloid. Whether superior CR leads to protection against metabolic deterioration, and predominantly right hemisphere involvement, deserves further exploration This article is protected by copyright. All rights reserved.

Identifiants

pubmed: 38169114
doi: 10.1002/mdc3.13967
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

This article is protected by copyright. All rights reserved.

Auteurs

Beatriz Fernández-Rodríguez (B)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
PhD Program in Neuroscience, Autonoma de Madrid University-Cajal Institute, Madrid, Spain, 28029.

Rafael Rodríguez-Rojas (R)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
Network Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED), Instituto Carlos III, Madrid, Spain.

Pasqualina Guida (P)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
PhD Program in Neuroscience, Autonoma de Madrid University-Cajal Institute, Madrid, Spain, 28029.

Santiago Angulo-Díaz-Parreño (S)

CEMBIO, Centro de Excelencia en Metabolómica y Bioanálisis, Facultad de Farmacia, Universidad San Pablo CEU, Madrid, Spain.
Departamento de Matemática Aplicada y Estadística, Universidad San Pablo CEU, Madrid, Spain.

Clara Trompeta (C)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
PhD Program in Health Sciences, University of Alcala de Henares, Alcalá de Henares, Madrid, Spain, 28054.

David Mata-Marín (D)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
PhD Program in Neuroscience, Autonoma de Madrid University-Cajal Institute, Madrid, Spain, 28029.

Ignacio Obeso (I)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
Network Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED), Instituto Carlos III, Madrid, Spain.

Lydia Vela (L)

Hospital Universitario Fundación Alcorcón, Alcorcón, Madrid, Spain.

Isabel Plaza de Las Heras (I)

Nuclear Medicine Department, Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.

José A Obeso (JA)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
Network Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED), Instituto Carlos III, Madrid, Spain.

Carmen Gasca-Salas (C)

HM CINAC (Centro Integral de Neurociencias Abarca Campal), Hospital Universitario HM Puerta del Sur, HM Hospitales, Madrid, Spain.
University CEU-San Pablo, Madrid, Spain.

Classifications MeSH