Significant strides have been made in understanding the factors that influence cognitive decline in older adults. Multiple studies have found that the brain-derived neurotrophic factor (BDNF) may play a role in late-life cognitive impairment, particularly in the pathogenesis of Alzheimer’s disease. For example, beta-amyloid, which is increased in Alzheimer’s disease, may interact with BDNF and suppress its expression, resulting in impaired cognition.
In a new study, Aron S. Buchman, MD, Professor, Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, and colleagues found that BDNF gene expression levels can slow cognitive decline in older individuals (Buchman AS, et al. Neurology. 2016;86:735-741).
A total of 535 community-dwelling older adults with or without cognitive impairment underwent annual cognitive assessments and brain autopsy at death. BDNF gene expression was measured to determine its association with cognitive decline (with adjustments for age, sex, and education) and Alzheimer’s disease.
BDNF expression was found to be independently associated with the rate of cognitive decline: higher levels of BDNF gene expression were linked to a slower rate of cognitive decline during an average of 6 years before death.
The association between BDNF expression and cognitive decline was strongest in participants with dementia compared with those with mild cognitive impairment or those without cognitive impairment.
Furthermore, higher BDNF expression reduced the effect of Alzheimer’s disease pathology on the rate of cognitive decline, suggesting that increased levels of BDNF may protect against the effects of Alzheimer’s disease pathology in older adults.
However, the protective effects of BDNF expression were most evident in participants with the highest Alzheimer’s disease pathology, and, therefore, with the lowest BDNF expression.
Dr Buchman and colleagues attribute these findings to the fact that “reserve is most necessary for individuals with more pathology and greater cognitive impairment. Thus, in addition to an association between BDNF expression and the rate of cognitive decline, BDNF expression may also provide reserve, which mitigates the deleterious effects of AD [Alzheimer’s disease] pathology on cognitive decline.”
The investigators contend that previous studies of cognitive reserve are difficult to translate into the clinical setting, because the mechanisms linking education or purpose in life, for example, with cognitive decline are not well-defined.
“Further work is needed to replicate these findings and determine the direction of causality and whether strategies that increase brain BDNF expression might one day be used to protect or slow the rate of cognitive decline in older adults,” Dr Buchman and colleagues concluded.