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Cognitive Decline / Depressive Disorder, Treatment Resistant / Late Life Depression · Phase 2 Trial
ClinicalTrials.gov · August 6, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is a completed Phase 2 trial registry record testing carbidopa/levodopa versus placebo in late-life depression, hypothesized to work via dopaminergic enhancement of processing speed, mobility, and motivation. No trial results have been posted to the registry, so efficacy, safety, and cognitive or motor outcomes remain unreported.
Phase 2, Interventional, Randomized, Crossover, Quadruple masking, Treatment purpose. Late Life Depression, Cognitive Decline, Depressive Disorder, Treatment-Resistant, Levodopa, Gait Impairment; age from 60 Years; accepts healthy volunteers. Intervention: L-Dopa First / Placebo Second. Compared with: Placebo First / L-Dopa Second — Placebo Comparator. n = 79. 2 sites: United States.
This is a completed Phase 2 trial registry record testing carbidopa/levodopa versus placebo in late-life depression, hypothesized to work via dopaminergic enhancement of processing speed, mobility, and motivation. No trial results have been posted to the registry, so efficacy, safety, and cognitive or motor outcomes remain unreported.
No results or outcome data posted in registry record; efficacy and safety are unknown. Primary outcomes measured at weeks 3 and 6; longer-term durability and safety not described.
Clinicians should note this trial is complete but unpublished; results must be obtained directly from the investigators or when a manuscript is published. The dopamine hypothesis in late-life depression and its relationship to processing speed, motivation, and mobility is mechanistically plausible but remains unvalidated by this trial's data.
Registry record of a completed Phase 2 interventional trial testing L-DOPA in late-life depression; no results are posted, so efficacy and safety remain unreported.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians should note this trial is complete but unpublished; results must be obtained directly from the investigators or when a manuscript is published. The dopamine hypothesis in late-life depression and its relationship to processing speed, motivation, and mobility is mechanistically plausible but remains unvalidated by this trial's data.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no key findings. That is a gap in the analysis, not a judgement about the study.
Registry record from ClinicalTrials.gov (NCT04469959). This is a study registration, not published results. Lead sponsor: Vanderbilt University Medical Center. Recruitment status: COMPLETED. Phase: PHASE2. Study type: INTERVENTIONAL. Enrollment: 79 participants (ACTUAL). Conditions: Late Life Depression, Cognitive Decline, Depressive Disorder, Treatment-Resistant, Levodopa, Gait Impairment. Interventions: DRUG: L-Dopa; DRUG: Placebo. Primary outcome measures: Change in WAIS-R Digit Symbol Task Score , Baseline, after week 3, and after week 6; Change in Pattern Comparison Test Score , Baseline, after week 3, and after week 6; Change in Letter Comparison Test Score , Baseline, after week 3, and after week 6; Change in NIH EXAMINER Test Score , Baseline, after week 3, and after week 6; Change in Gait pattern , Baseline, after week 3, and after week 6; Change in Effort Expenditure for Rewards Task (EEfRT) , Baseline to after week 3. Brief summary: Late-Life Depression (LLD), or depression in older adults, often presents with motivational deficits, deficits in performance in cognitive domains including processing speed and executive dysfunction, and mobility impairments. This triad of findings implicate dopaminergic dysfunction as a core pathophysiologic feature in depression, and may contribute to cognitive decline and motor disability. Normal aging results in brain-wide dopamine declines, decreased D1/D2 receptor density, and loss of dopamine transporters. Although brain changes associated with depression and aging converge on dopamine circuits, the specific disturbances in LLD and how responsive the system is to modulation remain unclear. In this study, investigators are testing integrative model that aging, in concert with pro-inflammatory shifts, decreases dopamine signaling. These signally changes affects behaviors supported by these circuits, in the context of age-associated cortical atrophy and ischemic microvascular changes, resulting in variable LLD phenotypes. Investigators propose a primary pathway where dopaminergic dysfunction in depressed elders contributes to slowed processing speed and mobility impairments that increase the effort cost associated with voluntary behavior. The central hypothesis of this study is that late-life depression is characterized by dysfunction in the dopamine system and, by enhancing dopamine functioning in the brain. By improving cognitive and motor slowing, administration of carbidopa/levodopa (L-DOPA) will improve depressive symptoms.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.