Abstract
An enriched environment is effective in stimulating learning and memory in animal models as well as in humans. Environmental enrichment increases brain-derived neurotrophic factor (BDNF) in aged rats and reduces levels of Alzheimer-related proteins in the blood, including amyloid-β (Aβ) peptides and misfolded toxic forms of tau. To address whether stimulation of curiosity, which is a form of enrichment, may provide a buffer against Alzheimer’s disease (AD), we measured levels of biomarkers associated with AD at baseline and after a 6-week intervention in older adults (>65 years of age) randomized to one of three different intervention conditions. Specifically, in this pilot study, we tested the effectiveness of a traditional, structured learning environment compared to a self-motivated learning environment designed to stimulate curiosity. There were no significant differences from baseline to post-intervention in any of the groups for Aβ42/Aβ40 ratio or t-tau (total-tau) plasma levels. Serum BDNF levels decreased significantly in the control group. Interestingly, individuals who had the lowest serum BDNF levels at baseline experienced significantly higher increases in BDNF over the course of the 6-week intervention compared to individuals with higher serum BDNF levels at baseline. As expected, older individuals had lower MoCA scores. Years of education correlated negatively with Aβ levels, suggesting a protective effect of education on levels of this toxic protein. ECog scores were negatively correlated with BDNF levels, suggesting that better performance on the ECog questionnaire was associated with higher BDNF levels. Collectively, these findings did not suggest that a 6-week cognitive training intervention focused on curiosity resulted in significant alterations in blood biomarkers but showed interesting correlations between cognitive scores and BDNF levels, further supporting the role of this trophic factor in brain health in older adults.
Highlights
Alzheimer’s disease (AD) is the most common cause of dementia, with an estimated 44 million people living with AD or related dementias worldwide (Nichols et al, 2019)
Our group has previously reported a significant increase in serum brain-derived neurotrophic factor (BDNF) levels after a 5-week long computer-based cognitive intervention in healthy older adults that involved 35 min cognitive training sessions 5 days a week
We found that serum BDNF levels stayed stable over the course of 6-weeks in individuals randomized into the traditional group compared to the curiosity group and the sedentary control group, this result was not statistically significant
Summary
Alzheimer’s disease (AD) is the most common cause of dementia, with an estimated 44 million people living with AD or related dementias worldwide (Nichols et al, 2019). The disease is characterized by synaptic dysfunction, neuronal atrophy of forebrain temporal structures, and protein aggregation. Amyloid precursor protein and tau misfold and aggregate into extracellular Aβ plaques and intracellular neurofibrillary tau tangles (Bloom, 2014). Elevated plasma levels of tau are associated with cognitive impairment and brain atrophy and are predictive of future rates of cognitive decline in AD patients (Gómez-Ramos et al, 2006; Zetterberg et al, 2013; Blennow, 2017; Deters et al, 2017). AD is associated with decreased levels of brain-derived neurotrophic factor (BDNF), a protein that is expressed throughout the brain and promotes the survival, growth, differentiation and regeneration of neurons (Nagahara et al, 2009; Bathina and Das, 2015; Miranda et al, 2019)
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