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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

EV0850

Outcomes are worse in older adults with late-life depression and slow gait speed

OLDER ADULTS WITH LATE LIFE DEPRESSION AND SLOW GAIT SPEED HAVE WORSE OUTCOMES

Late-life depression accompanied by slow gait speed may represent a distinct phenotype characterized by more severe depressive symptoms, poorer cognitive performance, accelerated brain aging, and cortical atrophy in motor regions, without a marked cerebrovascular burden.

The aim was to investigate whether slow gait speed in late-life depression (LLD) represents a distinct phenotype associated with a more severe clinical presentation. The methods included comprehensive psychiatric, neurocognitive, and clinical assessments and a standardized 4-meter walk test in 115 older adults (85 with LLD and 30 with no history of depression) followed at the UCONN Center on Aging clinic; the sample was divided into controls (n = 30), LLD with normal gait speed (n = 64), and LLD with slow gait speed (n = 21). The slow-gait LLD group had greater depression severity (QIDS-16 scores of 12.9, 10.5, and 3.4, respectively; p < 0.001), a higher medical burden (CIRS-G scores of 16.0, 12.4, and 5.7; p < 0.001), and an older mean age (71.1, 66.7, and 70.1; p = 0.007). Cognitive performance was poorer in this group: MoCA scores were 24.0, 24.9, and 26.5 (p = 0.001); verbal fluency scores were 17.5, 20.9, and 22.9 (p < 0.001); Trail B completion times were 124.2, 94.4, and 66.8 seconds (p < 0.001); and Trail A showed p = 0.045. Gait speed was measured at 0.7, 1.1, and 1.0 m/s, and dual-task gait speed at 0.5, 0.8, and 0.8 m/s (p < 0.001 for both); this finding supports the view that gait impairment is mediated by executive function rather than generalized psychomotor slowing. In the imaging subsample (n = 15, 37, and 25), DunedinPACNI, an indicator of the pace of brain aging, was 1.043 (0.480) in slow-gait LLD, 0.272 (0.701) in normal-gait LLD, and 0.548 (0.753) in controls (F = 5.239; p = 0.0076); the cerebrovascular burden indicators ARTS (F = 1.949; p = 0.150) and PWMD (F = 2.855; p = 0.065) did not differ significantly between groups. Cortical atrophy associated with slow gait was most pronounced in the premotor and motor cortices and the parietotemporal region (P < 0.05); parietotemporal atrophy was suggested to be the most meaningful finding because this region is an important cognitive processing hub for higher-order executive functions such as walking. The authors suggest that LLD accompanied by slow gait may represent a distinct phenotype associated with a more severe clinical presentation, and that assessing gait speed in older adults with depression may point to a different disease course and prognosis, or even provide an early indication of a neurodegenerative process; they identify the lack of a slow-gait control group and other contributing factors, such as body mass index, polypharmacy, parkinsonism, and visual impairment, as limitations.

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