Brain-derived neurotrophic factor may provide a buffer against Alzheimer's disease

Elderly individuals with higher levels of brain-derived neurotrophic factor (BDNF) had a 50% slower rate of cognitive decline than those with the lowest levels of BDNF, according to a study published online January 27, 2016 in the journal Neurology. 

Importantly, researchers concluded that higher BDNF in older adults may act as a "buffer" against the effects of Alzheimer’s disease (AD).

“This relationship was strongest among the people with the most signs of Alzheimer’s disease pathology in their brains,” said study author Aron S. Buchman, MD, Professor of Neurological Sciences at Rush University Medical Center in Chicago, IL. “This suggests that a higher level of protein from BDNF gene expression may provide a buffer, or reserve, for the brain and protect it against the effects of the plaques and tangles that form in the brain as a part of Alzheimer’s disease.”

These findings hold the promise that increasing BDNF in the brain might one day protect against, or slow down, cognitive decline, the researchers predicted.

For this investigation, the researchers analyzed data on 535 older adults (average age of 81 at baseline) from two longitudinal studies with a mean follow-up of 6 years. Participants underwent annual cognitive testing; after death, a neurologist reviewed their data to determine a possible diagnosis of dementia or cognitive impairment.

Postmortem examination revealed their level of Alzheimer’s disease pathology, as well as measures of BDNF gene expression in the brain.

After analyzing the data, researchers determined that rate of cognitive decline was about 50% slower for those with the highest levels of BDNF gene expression compared to those with the lowest levels.

Also, in the people with the highest amount of Alzheimer’s pathology, cognitive decline was about 40% slower for people with the highest levels of BDNF gene expression compared to those with the lowest levels.

“Thus, higher BDNF expression reduced the effect of AD pathology on the rate of cognitive decline,” the authors wrote. “These data suggest that a higher level of brain BDNF expression is associated with slower cognitive decline and may provide reserve against the effects of AD pathology in older adults.”

The researchers acknowledged that these findings show only an association and do not confirm that BDNF is a direct cause of slowed cognitive decline. Further studies will be needed to replicate these findings and to show whether increasing BDNF expression in the brain might protect against cognitive decline in older adults, they noted.