• Medicina · May 2024

    Mediator Role of Frailty and Biological Deficits in Dementia Prognosis-Retrospective Cohort Study.

    • Kübra Işık, Burak Mete, Fatma Tanrıöver, Hakan Demirhindi, and Esra Doğan Mete.
    • Department of Neurology, Şanlıurfa Suruç State Hospital, Şanlıurfa 63800, Turkey.
    • Medicina (Kaunas). 2024 May 30; 60 (6).

    AbstractBackground and Objectives: Dementia is increasing worldwide. This study aimed to examine the impact of comorbidity burden and frailty on dementia prognosis in patients with dementia. Materials and Methods: This retrospective cohort study was conducted with 47 patients with dementia who were followed for up to two years. The Modified Charlson Comorbidity Index (MCCI), Mini-Mental State Examination (MMSE-E), and Edmonton Fragility Scale were used besides laboratory and clinical findings. Results: The mean age of the 47 patients was 78.77 ± 12.44 years. During the follow-up period, MMSE-E scores were observed to improve in 50% of the patients. Initial MMSE-E scores were found to be lowest in men and patients with coronary artery disease or depression, while final MMSE-E scores were observed to be lowest in patients with depression and low vitamin B12 or vitamin D levels. The rates of decrease in MMSE-E scores in non-, moderately and severely frail patients were 21.4%, 55.6%, and 70.6%, respectively. There was a moderate negative correlation between MMSE-E scores and both comorbidity burden and frailty scores. The mediation analysis revealed that frailty was a complete mediator, and that comorbidity burden led to an increase in frailty and a decrease in MMSE-E scores. During the follow-up period, patients with moderate frailty, hypertension, diabetes mellitus, alcohol and tobacco use, low B12 levels, or hypothyroidism showed an increased risk of decrease in cognitive functions. Conclusions: There was a significant association between dementia prognosis and both frailty and biological deficits. We recommend the adoption of a syndemic approach in the follow-up of dementia, as we believe that the prevention of frailty and associated biological deficits will contribute to slowing dementia's clinical course.

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