The association between brain‐derived neurotrophic factor and improved cognition in mild cognitive impairment and Alzheimer's disease patients in an exercise‐primed transcranial‐direct current stimulation study

Abstract

AbstractBackgroundBrain derived neurotrophic factor (BDNF) has been associated with cognitive decline in Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Transcranial direct current stimulation (tDCS), a non‐invasive brain stimulation, has been found to improve cognitive functions in AD/MCI, particularly after priming. While the mechanism of tDCS response remains unclear, BDNF has been proposed to be involved with the beneficial effects of tDCS. However, few studies have investigated the direct relationship between cognition and BDNF in individuals receiving tDCS. With data from an ongoing clinical trial (the EXPRESS study), we examined the relationship between BDNF and changes in cognition before and after intervention in individuals with MCI/mild AD.MethodParticipants completed a 5‐week, blinded, randomized trial investigating the effects of exercise priming on tDCS. The Montreal Cognitive Asssessment (MoCA), to assess global cognition, was administered and blood samples were collected to quantify serum BDNF at baseline and endpoint visits. Baseline BDNF concentrations were log‐transformed prior to analyses. A Pearson’s partial correlation was used to assess the relationship between baseline BDNF and change in MoCA (ΔMoCA) over time across all participants.ResultIn 18 participants (10 males [55.6%], mean [±SD] age 73.9±8.5 years, education 17.1±2.0 years, and baseline MoCA score 21.5 ± 3.5), mean baseline BDNF concentration was 116.0 ± 40.9 (ng/mL). A Pearson’s partial correlation, controlling for age, showed a significant positive correlation between baseline BDNF concentrations and ΔMoCA score over time (rpartial(15) = .517, p = 0.034).ConclusionHigher baseline BDNF levels were correlated with greater improvement in global cognition over time in MCI/mild AD patients. This finding contributes to current literature that suggests BDNF as a therapeutic target in AD treatment. Further analyses upon unblinding will be done to evaluate the predictive capacity of baseline BDNF concentrations on cognitive improvement across treatment groups.