Association of dietary and nutritional factors with cognitive decline, dementia, and depressive symptomatology in older individuals according to a neurogenesis-centred biological susceptibility to brain ageing.
cognitive decline
dementia
diet
hippocampal neurogenesis
late-life depression
older people
Journal
Age and ageing
ISSN: 1468-2834
Titre abrégé: Age Ageing
Pays: England
ID NLM: 0375655
Informations de publication
Date de publication:
11 May 2024
11 May 2024
Historique:
received:
31
01
2024
revised:
15
02
2024
medline:
15
5
2024
pubmed:
15
5
2024
entrez:
15
5
2024
Statut:
ppublish
Résumé
Hippocampal neurogenesis (HN) occurs throughout the life course and is important for memory and mood. Declining with age, HN plays a pivotal role in cognitive decline (CD), dementia, and late-life depression, such that altered HN could represent a neurobiological susceptibility to these conditions. Pertinently, dietary patterns (e.g., Mediterranean diet) and/or individual nutrients (e.g., vitamin D, omega 3) can modify HN, but also modify risk for CD, dementia, and depression. Therefore, the interaction between diet/nutrition and HN may alter risk trajectories for these ageing-related brain conditions. Using a subsample (n = 371) of the Three-City cohort-where older adults provided information on diet and blood biobanking at baseline and were assessed for CD, dementia, and depressive symptomatology across 12 years-we tested for interactions between food consumption, nutrient intake, and nutritional biomarker concentrations and neurogenesis-centred susceptibility status (defined by baseline readouts of hippocampal progenitor cell integrity, cell death, and differentiation) on CD, Alzheimer's disease (AD), vascular and other dementias (VoD), and depressive symptomatology, using multivariable-adjusted logistic regression models. Increased plasma lycopene concentrations (OR [95% CI] = 1.07 [1.01, 1.14]), higher red meat (OR [95% CI] = 1.10 [1.03, 1.19]), and lower poultry consumption (OR [95% CI] = 0.93 [0.87, 0.99]) were associated with an increased risk for AD in individuals with a neurogenesis-centred susceptibility. Increased vitamin D consumption (OR [95% CI] = 1.05 [1.01, 1.11]) and plasma γ-tocopherol concentrations (OR [95% CI] = 1.08 [1.01, 1.18]) were associated with increased risk for VoD and depressive symptomatology, respectively, but only in susceptible individuals. This research highlights an important role for diet/nutrition in modifying dementia and depression risk in individuals with a neurogenesis-centred susceptibility.
Identifiants
pubmed: 38745492
pii: 7668928
doi: 10.1093/ageing/afae042
doi:
Types de publication
Journal Article
Multicenter Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
ii47-ii59Subventions
Organisme : Caisse Nationale pour la Solidarité et l'Autonomie (CNSA)
Organisme : Fondation Plan Alzheimer
ID : FCS 2009-12
Organisme : French National Research Agency COGINUT
ID : ANR-06-PNRA-005
Organisme : Ministry of Research-INSERM Programme "Cohortes et collections de données biologiques"
Organisme : Fondation de France
Organisme : Regional Governments of Aquitaine and Bourgogne
Organisme : Institut de la Longévité
Organisme : Mutuelle Générale de l'Education Nationale
Organisme : Direction Générale de la Santé
Organisme : Caisse Nationale Maladie des Travailleurs Salariés
Organisme : The Fondation pour la Recherche Médicale
Organisme : French National Research Agency (ANR) 'Programme d'Investissement d'Avenir'
Organisme : Urban Mental Health Program of the University of Amsterdam
Organisme : ZonMw
Pays : Netherlands
Organisme : Alzheimer Nederland and the NWO Food & Cognition Program
Organisme : BMWFW
ID : BMWFW-10.420/0009-WF/V/3c/2015
Organisme : ICREA 2018 Academia Award from the Generalitat de Catalunya
Organisme : FEDER Program from EU
ID : 2017SGR1546
Organisme : MINECO
ID : PCIN-2015-229
Organisme : French National Research Agency
ID : ANR-15-HDHL-0002-05
Organisme : Medical Research Council UK
ID : MR/N030087/1
Organisme : JPI-HDHL
Informations de copyright
© The Author(s) 2024. Published by Oxford University Press on behalf of the British Geriatrics Society.