Brain-derived neurotrophic factor and Alzheimer's disease
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Abstract
Alzheimer’s disease (AD) is associated with a decrease in brain-derived neurotrophic factor (BDNF) mRNA expression in the hippocampus, the parietal cortex, the entorhinal cortex, the hilus and temporal cortex. The expression of catalytic TrkB is found to be decreased in the basal forebrain, and the frontal and temporal cortex. A substantial body of work has shown that BDNF can prevent death of several types of injured CNS neurons, including those from the basal forebrain, hippocampus and cortex. Therefore, BDNF could help to prevent neuronal death in AD. Genetic studies have shown a polymorphism of the gene coding for BDNF that correlated with sporadic, late-onset AD, suggesting that genetic variation in the gene coding for BDNF might be associated with increased risk of AD. BDNF has been reported to modify neuronal structure and function by modifying spine turnover and dendritic arbours of cortical neurons. In the hippocampus, BDNF is an important mediator of long-term potentiation (LTP), a long-lasting increase in synaptic strength. Central local administration of exogenous BDNF might be beneficial for the treatment of AD, in order to stop or delay the progression of neuronal loss and cognitive consequences. Since decreased BDNF is related to both AD and depression, BDNF could be a bridge between AD and depression.
참고문헌 (55)
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