Dr. Aron S. Buchman and his colleagues at the Rush University Medical Center in Chicago, have conducted research to find out what effect brain-derived neurotrophic factor (BDNF) has on cognitive decline associated with advanced age. The results of the study were published in the journal, Neurology.
As the brain ages, cognitive abilities begin to decline and some individuals develop dementias, including Alzheimer’s disease. While researchers are unsure as to why advancing age leads to cognitive decline, the current study suggests that BDNF may have a neuroprotective effect on the brain.
BDNF is responsible for promoting the growth of new neurons and synapses, as well as supporting the health of existing neurons. This growth factor is commonly found in both the brain and peripheral nervous system.
While the mammalian brain is almost completely formed before birth, neurogenesis – the process of creating new neurons – still occurs in specific parts of the nervous system. Previous research has shown that BDNF is vital in the generation of new brain matter, as well as in the retention and maintenance of long-term memory.
Rats who are unable to synthesize BDNF are born with neural abnormalities and are not viable. When exogenous BDNF is injected into the lateral ventricle of a normal, adult rat, neurons begin to grow in the septum, hypothalamus, thalamus and striatum.
In order to test the effects of the growth factor on aging brains, Buchman and his team conducted tests on 535 individuals participating in the Rush Memory and Aging Project and the Religious Orders Study. The average age of the participants was 81 years old, and each was tested on cognitive and mental abilities until their death.
During autopsies on each participant, the levels of the gene that encodes BDNF in the brain were measured. Based on the participant’s scores on the annual mental agility tests, they were rated as having dementia, no cognitive impairment or mild cognitive impairment.
The researchers found that higher levels of BDNF in the brain was positively correlated with prolonged cognitive function. Participants in the top 10 percent for BDNF levels showed a rate of mental decline that was 50 percent slower than those in the bottom 10 percent.
Individuals with Alzheimer’s disease often display plaques in the brain which are thought to be the cause of the decline in brain function. Individuals with the highest levels of BDNF had a 40 percent reduction in cognitive decline despite the presence of the Alzheimer’s disease markers in the brain.
“This relationship was strongest among the people with the most signs of Alzheimer’s disease pathology in their brains,” said Buchman. “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.”