Revised Temperament and Character Inventory factors predict neuropsychiatric symptoms and aging-related cognitive decline across 25 years

Lucas Ronat; Michael Rönnlund; Rolf Adolfsson; Alexandru Hanganu; Sara Pudas

doi:10.3389/fnagi.2024.1335336

Revised Temperament and Character Inventory factors predict neuropsychiatric symptoms and aging-related cognitive decline across 25 years

Front Aging Neurosci. 2024 Feb 21:16:1335336. doi: 10.3389/fnagi.2024.1335336. eCollection 2024.

Authors

Lucas Ronat^{1

2

3

4}, Michael Rönnlund⁵, Rolf Adolfsson⁶, Alexandru Hanganu^{1

7}, Sara Pudas^{3

4}

Affiliations

¹ Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal, Neuroimaging of Emotions Lab, Montreal, QC, Canada.
² Department of Medicine, Faculty of Medicine, University of Montreal, Montreal, QC, Canada.
³ Department of Medical and Translational Biology, Umeå University, Umeå, Sweden.
⁴ Umeå Center for Functional Brain Imaging, Umeå University, Umeå, Sweden.
⁵ Department of Psychology, Umeå University, Umeå, Sweden.
⁶ Department of Clinical Sciences, Umeå University, Umeå, Sweden.
⁷ Department of Psychology, Faculty of Arts and Sciences, University of Montreal, Montreal, QC, Canada.

Abstract

Introduction: Personality traits and neuropsychiatric symptoms such as neuroticism and depression share genetic overlap and have both been identified as risks factors for development of aging-related neurocognitive decline and Alzheimer's disease (AD). This study aimed to examine revised personality factors derived from the Temperament and Character Inventory, previously shown to be associated with psychiatric disorders, as predictors of neuropsychiatric, cognitive, and brain trajectories of participants from a population-based aging study.

Methods: Mixed-effect linear regression analyses were conducted on data for the full sample (N_max = 1,286), and a healthy subsample not converting to AD-dementia during 25-year follow-up (N_max = 1,145), complemented with Cox proportional regression models to determine risk factors for conversion to clinical AD.

Results: Two personality factors, Closeness to Experience (CE: avoidance of new stimuli, high anxiety, pessimistic anticipation, low reward seeking) and Tendence to Liabilities (TL: inability to change, low autonomy, unaware of the value of their existence) were associated with higher levels of depressive symptoms, stress (CE), sleep disturbance (TL), as well as greater decline in memory, vocabulary and verbal fluency in the full sample. Higher CE was additionally associated with greater memory decline across 25 years in the healthy subsample, and faster right hippocampal volume reduction across 8 years in a neuroimaging subsample (N = 216). Most, but not all, personality-cognition associations persisted after controlling for diabetes, hypertension and cardiovascular disease. Concerning risks for conversion to AD, higher age, and APOE-ε4, but none of the personality measures, were significant predictors.

Conclusion: The results indicate that personality traits associated with psychiatric symptoms predict accelerated age-related neurocognitive declines even in the absence of neurodegenerative disease. The attenuation of some personality effects on cognition after adjustment for health indicators suggests that those effects may be partly mediated by somatic health. Taken together, the results further emphasize the importance of personality traits in neurocognitive aging and underscore the need for an integrative (biopsychosocial) perspective of normal and pathological age-related cognitive decline.

Keywords: Alzheimer’s dementia; MRI; cognitive decline; longitudinal study; neuropsychiatric symptoms; personality.

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. LR’s PhD position was supported by a Medicine Faculty Leadership Scholarship 2022–2023 (University of Montreal), a Biomedical Sciences Program Excellence Scholarship 2022–2023 (University of Montreal), as well as a grant for the end of doctoral studies (BFED 4e ESP A2022) from the Faculty of Graduate and Postdoctoral Studies at the University of Montreal. AH is supported by the Lemaire Foundation, Fonds de Recherche du Québec - Santé, and Parkinson Canada (grant/award number: 2018-00355). The Betula project has been supported by the Bank of Sweden Tercentenary Foundation [grant number 1988-0082:17; J2001-0682]; the Swedish Council for Planning and Coordination of Research [grant numbers D1988-0092, D1989-0115, D1990-0074, D1991-0258, D1992-0143, D1997-0756, D1997-1841, D1999-0739, B1999-474]; the Swedish Council for Research in the Humanities and Social Sciences [grant number F377/1988-2000]; the Swedish Council for Social Research [grant numbers 1988-1990:88-0082, 311/1991-2000]; as well as the Swedish Research Council [grant numbers 345-2003-3883, 315-2004-6977].