Forskningsartikler

Abstract:

This study investigates the relationships between subjective age, intrinsic capacity, functional ability and health among Norwegians aged 60 years and older. The Norwegian Survey of Health and Ageing (NORSE) is a population-based, cross-sectional study of home-dwelling individuals aged 60-96 years in the former county of Oppland. Age- and sex-adjusted regression models were used to investigate the gap between subjective and chronological age and this gap’s association with self-reported and objectively measured intrinsic capacity (covering all six sub domains defined by WHO), health, and functional ability among 817 NORSE participants. The results show most participants felt younger than their chronological age (86.5%), while relatively few felt the same as their chronological age (8.3%) or older (5.2%). The mean subjective age was 13.8 years lower than mean chronological age. Participants with urinal incontinence, poor vision, or poor hearing felt 3.1 [95% confidence interval (CI) (0.6, 5.5)], 2.9 [95% CI (0.2, 5.6)], and 2.9 [95% CI (0.3, 5.5)] years older, respectively, than participants without those conditions, whereas none of the following factors-anxiety, depression, chronic disease, Short Physical Performance Battery score, grip strength, cognition, or frailty-significantly had an impact on the gap. In line with prior research, this study finds that feeling considerably younger than one’s chronological age is common at older ages. However, those with poor hearing, poor vision, and urinal incontinence felt less young compared to those not having these conditions. These relationships may exert undesirable effects on vitality and autonomy, which are considered key factors of intrinsic capacity and healthy ageing.

Ellen Melbye Langballe, Vegard Skirbekk, Bjørn Heine Strand

ABSTRACT
Introduction: Half of patients with limited stage small cell lung cancer (LS SCLC) are >70 years, but account for <20% of participants in most trials. Comorbidities, reduced organ- and physical function might lead to more treatment toxicity and population-based studies indicate that fewer older than younger LS SCLC patients receive standard chemoradiotherapy, although there is limited evidence for such a policy.
Methods: We compared baseline characteristics, comorbidity, survival, treatment completion, toxicity, health related quality of life (HRQoL) and treatment outcomes between patients >70 and <70 years in an open label randomized phase II trial comparing twice-daily thoracic radiotherapy (TRT) of 45 Gy in 30 fractions with 60 Gy in 40 fractions in LS SCLC. All patients received concurrent platinum/etoposide chemotherapy.
Results: 170 patients who were >18 years and had performance status (PS) 0-2 were randomized. Of these, 53 patients (60 Gy:25, 45 Gy:28) were >70 years and 117 (60 Gy:64, 45 Gy:53) were younger. There were no significant differences in baseline characteristics, treatment completion rates, toxicity, or response rates across age groups. HRQoL mean scores was similar during year one, but older patients reported more decline on functional scales than younger patients during year two. OS was significantly shorter for older patients while there was no significant difference in PFS or TTP.
Conclusion: Patients >70 years tolerated concurrent twice daily chemoradiotherapy and achieved similar disease control as younger patients, indicating that older patients should receive the same treatment as younger patients.

Kristin Toftaker Killingberg, Bjørn Henning Grønberg, Marit Slaaen, Øyvind Kirkevold, Tarje Onsøien Halvorsen

Summary

Despite evidence suggesting that insomnia is associated with the risk of dementia and cognitive dysfunction, studies have shown mixed results. Dementia has a long prodromal phase, and studies with long follow-up are required to avoid reverse causality. In our 11-year follow-up study, we assessed whether probable insomnia disorder (PID) based on diagnostic criteria, and insomnia symptoms were associated with risk of all-cause dementia, Alzheimer’s disease (AD) and cognition, measured with the Montreal Cognitive Assessment scale. We also examined if Apolipoprotein E genotype modified any associations with dementia through interaction. We analysed data from 7492 participants in the Norwegian Trøndelag Health Study. PID was not associated with all-cause dementia (odds ratio = 1.03, 95% confidence interval = 0.74–1.43), AD (odds ratio = 1.07, 95% confidence interval = 0.71–1.60) or Montreal Cognitive Assessment score (regression coefficient = 0.37, 95% confidence interval = −0.06 to 0.80). The insomnia symptom “difficulties maintaining sleep” was associated with a lower risk of all-cause dementia (odds ratio = 0.81, 95% confidence interval = 0.67–0.98), AD (odds ratio = 0.73, 95% confidence interval = 0.57–0.93), and better Montreal Cognitive Assessment score, mean 0.40 units (95% confidence interval = 0.15–0.64). No interaction with Apolipoprotein E genotype was found. PID and insomnia symptoms did not increase the risk of dementia in our study. More research with longer follow-up is needed, and future studies should explore if the associations to dementia risk vary across insomnia subtypes.

Selma Selbæk-Tungevåg, Geir Selbæk, Bjørn Heine Strand, Christian Myrstad, Gill Livingston, Stian Lydersen, Sverre Bergh, Linda Ernstsen

BACKGROUND: The kynurenine pathway (KP) has been identified as a potential mediator linking acute illness to cognitive dysfunction by generating neuroactive metabolites in response to inflammation. Delirium (acute confusion) is a common complication of acute illness and is associated with increased risk of dementia and mortality. However, the molecular mechanisms underlying delirium, particularly in relation to the KP, remain elusive.
METHODS: We undertook a multicenter observational study with 586 hospitalized patients (248 with delirium) and investigated associations between delirium and KP metabolites measured in cerebrospinal fluid (CSF) and serum by targeted metabolomics. We also explored associations between KP metabolites and markers of neuronal damage and 1-year mortality.
RESULTS: In delirium, we found concentrations of the neurotoxic metabolite quinolinic acid in CSF (CSF-QA) (OR 2.26 [1.78, 2.87], P < 0.001) to be increased and also found increases in several other KP metabolites in serum and CSF. In addition, CSF-QA was associated with the neuronal damage marker neurofilament light chain (NfL) (β 0.43, P < 0.001) and was a strong predictor of 1-year mortality (HR 4.35 [2.93, 6.45] for CSF-QA ≥ 100 nmol/L, P < 0.001). The associations between CSF-QA and delirium, neuronal damage, and mortality remained highly significant following adjustment for confounders and multiple comparisons.
CONCLUSION: Our data identified how systemic inflammation, neurotoxicity, and delirium are strongly linked via the KP and should inform future delirium prevention and treatment clinical trials that target enzymes of the KP.

Leiv Otto Watne, Christian Thomas Pollmann, Bjørn Erik Neerland, Else Quist-Paulsen, Nathalie Bodd Halaas, Ane-Victoria Idland, Bjørnar Hassel, Kristi Henjum, Anne-Brita Knapskog, Frede Frihagen, Johan Raeder, Aasmund Godø, Per Magne Ueland, Adrian McCann, Wender Figved, Geir Selbæk, Henrik Zetterberg, Evandro F Fang, Marius Myrstad, Lasse M Giil