A new study has found that older people with higher amounts of a key protein from the gene called brain-derived neurotrophic factor, or BDNF in their brains have slower decline in their memory and cognitive skills compared to people with lower amounts of protein from the gene.
People tend to experience decline in physical skills as they age. Although the physical decline is obvious, the brain also has a tendency to slow down.
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However, it is not certain that cognitive decline will occur in all older adults. When it does occur, the speed of decline may vary from person to person. Significant impairment can be seen in some individuals, while others may show virtually no change at all.
The reasons behind these neurological differences are mystery to scientists. Since ageing is a multifaceted process and the brain is a complex organ, clues to the causal factors of mental decline with age are difficult to connect.
Dr.Aron S. Buchman and colleagues at the Rush University Medical Center in Chicago, IL, aimed to explore the involvement of BDNF in age-based cognitive decline.
BDNF is a growth factor that encourages the growth of new neurons and synapses, and supports existing neurons. It can be found extensively in both the brain and the peripheral nervous system. Many studies have shown that it is crucial in various important operations, including the maintenance of long-term memories.
Much of the nervous system in mammals is arranged before birth, but parts of the brain retain the ability to grow new neurons in a process called neurogenesis. BDNF is one of the major participants in this creation of new brain substance.
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The role of BDNF in memory and the protection and development of neurons make it a key candidate for examinations into the cognitive decline seen in many ageing brains.
Rats born without the ability to create BDNF die soon after birth because of neural abnormalities. However, if BDNF is injected into the lateral ventricle of an adult rat, new neurons grow in the striatum, septum, thalamus and hypothalamus.
For the study, researchers recruited 535 people with an average age of 81. These participants were part of the Rush Memory and Aging Project and the Religious Orders Study. They were followed until death, for an average of six years. The participants took yearly tests of their thinking and memory skills, and after death, a neurologist reviewed their records and determined whether they had dementia, some memory and thinking problems called mild cognitive impairment or no thinking and memory problems. Autopsies were conducted on their brains after death, and levels of the gene that codes for BDNF in the brain were measured.
The rate of cognitive decline was about 50% slower for those in the highest 10% of protein from BDNF gene expression compared to the lowest 10%. The effect of plaques and tangles – 2 hallmarks of Alzheimer’s disease –reduced cognitive decline in people with high levels of BDNF. Cognitive decline was about 40% slower for people with the highest amount of protein from BDNF gene expression compared to those with the lowest amount.
On average, thinking and memory skills declined by about 0.10 units per year on the tests. Higher levels of protein from BDNF gene expression reduced the effect of plaques and tangles in the brain on cognitive decline by 0.02 units per year.
The researchers found that the plaques and tangles in the brain accounted for 27% of the variation in cognitive decline, demographics accounted for 3% and BDNF accounted for 2%.
Plaques and tangles can be found in the brains of people with Alzheimer’s. Scientists believe that the plaques and tangles negatively impact cognitive function. The study revealed that the effect of these markers on cognitive decline was reduced by 40% for individuals with the highest levels of BDNF.
Dr. Buchman said:
"This relationship was strongest among the people with the most signs of Alzheimer's disease pathology in their brains.
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."
Buchman noted that the study does not prove that BDNF is the cause of a slower rate of cognitive decline; further work is needed to determine if activities which increase brain BDNF gene expression levels protect or slow the rate of cognitive decline in old age.
The study was published in the online issue of Neurology, the medical journal of the American Academy of Neurology.
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