Towards a Redefinition of Cognitive Frailty.


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: 23 6 2020
medline: 4 6 2021
entrez: 23 6 2020
Statut: ppublish

Résumé

The progressive aging of the population will dramatically increase the burden of dementia related to Alzheimer's disease (AD) and other neurodegenerative disorders in the future. Because of the absence of drugs that can modify the neuropathological substrate of AD, research is focusing on the application of preemptive and disease-modifying strategies in the pre-symptomatic period of the disease. In this perspective, the identification of people with cognitive frailty (CF), i.e., those individuals with higher risk of developing dementia, on solid pathophysiological bases and with clear operational clinical criteria is of paramount importance. This hypothesis paper reviews the current definitions of CF, presents and discusses some of their limitations, and proposes a framework for updating and improving the conceptual and operational definition of the CF construct. The potential for reversibility of CF should be supported by the assessment of amyloid, tau, and neuronal damage biomarkers, especially in younger patients. Physical and cognitive components of frailty should be considered as separate entities, instead of part of a single macro-phenotype. CF should not be limited to the geriatric population, because trajectories of amyloid accumulation are supposed to start earlier than 65 years in AD. Operational criteria are needed to standardize assessment of CF. Based on the limitations of current CF definitions, we propose a revised one according to a multidimensional subtyping. This new definition might help stratifying CF patients for future trials to explore new lifestyle interventions or disease-modifying pharmacological strategies for AD and dementia.

Sections du résumé

BACKGROUND
The progressive aging of the population will dramatically increase the burden of dementia related to Alzheimer's disease (AD) and other neurodegenerative disorders in the future. Because of the absence of drugs that can modify the neuropathological substrate of AD, research is focusing on the application of preemptive and disease-modifying strategies in the pre-symptomatic period of the disease. In this perspective, the identification of people with cognitive frailty (CF), i.e., those individuals with higher risk of developing dementia, on solid pathophysiological bases and with clear operational clinical criteria is of paramount importance.
OBJECTIVE/METHODS
This hypothesis paper reviews the current definitions of CF, presents and discusses some of their limitations, and proposes a framework for updating and improving the conceptual and operational definition of the CF construct.
RESULTS
The potential for reversibility of CF should be supported by the assessment of amyloid, tau, and neuronal damage biomarkers, especially in younger patients. Physical and cognitive components of frailty should be considered as separate entities, instead of part of a single macro-phenotype. CF should not be limited to the geriatric population, because trajectories of amyloid accumulation are supposed to start earlier than 65 years in AD. Operational criteria are needed to standardize assessment of CF.
CONCLUSION
Based on the limitations of current CF definitions, we propose a revised one according to a multidimensional subtyping. This new definition might help stratifying CF patients for future trials to explore new lifestyle interventions or disease-modifying pharmacological strategies for AD and dementia.

Identifiants

pubmed: 32568197
pii: JAD200137
doi: 10.3233/JAD-200137
pmc: PMC7504985
doi:

Substances chimiques

Biomarkers 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

831-843

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Auteurs

Elisa Mantovani (E)

Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.

Chiara Zucchella (C)

Section of Neurology, Department of Neurosciences, Verona University Hospital, Verona, Italy.

Federico Schena (F)

Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.

Maria Grazia Romanelli (MG)

Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.

Massimo Venturelli (M)

Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.
Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA.

Stefano Tamburin (S)

Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.
Section of Neurology, Department of Neurosciences, Verona University Hospital, Verona, Italy.

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