While it's not a magic solution, this research offers hope: sometimes, the key to addressing complex mental health symptoms might already be sitting in our medical toolkit, waiting to be understood in a new light.
This study aimed to test whether a drug, fampridine, could improve working memory (WM) in healthy adults. Fampridine, typically used for multiple sclerosis, was chosen based on genetic data linking it to WM-related processes. Participants were randomly assigned to either receive fampridine or a placebo in a double-blind, crossover trial, meaning each person served as their own control at different times.
The primary focus was WM performance, measured using a task requiring participants to remember and respond to specific sequences of letters (the "3-back task"). Additional tests assessed reaction times and motor functions. Participants took the medication for 3.5 days, with an 8-82 day washout period between phases to prevent lingering effects.
The results showed no overall improvement in working memory for participants taking fampridine compared to the placebo. However, individuals with lower baseline WM performance improved more under fampridine, suggesting the drug may benefit people with naturally weaker WM. Fampridine also decreased motor thresholds, a sign of increased brain excitability, which may support cognitive functions. Secondary outcomes, like reaction times and other cognitive measures, showed no significant differences.
The study included only 43 young, healthy adults, which limits its applicability to older populations or those with cognitive impairments. The treatment lasted just 3.5 days, so long-term effects remain unknown.
The dosage used was based on its standard approval for multiple sclerosis, which may not be optimal for cognitive benefits. The tightly controlled environment may not reflect real-world conditions. Although genetically guided, the trial excluded promising drugs during its rigorous selection process.
The study highlights fampridine's potential to enhance WM in individuals with low baseline cognitive performance. This finding aligns with prior research showing that cognitive interventions often yield greater benefits for those starting with lower abilities. While the primary hypothesis did not show a universal WM boost, the drug's impact on brain excitability and targeted improvements suggests further exploration is warranted.
Future studies could focus on clinical populations, like individuals with schizophrenia or bipolar disorder, where WM deficits are more pronounced. These findings also emphasize the need for personalized approaches to cognitive therapies based on individual baseline capabilities.
The research was funded by a grant from the Swiss National Science Foundation (SNSF). The funders had no influence on the study's design, data analysis, or results. Two of the lead researchers are co-founders of GeneGuide AG, a company unrelated to this trial. All other authors reported no conflicts of interest.