Improving memory through neuron growth

So far most of the research into memory has focused on a region called the hippocampus. This focus on the hippocampus as the brain’s learning and memory center was inspired by investigations into the patient Henry Molaison (H.M.), who lost several memory functions following a surgical removal of his hippocampus as a way to treat epilepsy.

Within the hippocampus several cellular and molecular processes have been identified as key components of learning and memory. For example, hippocampal neurons adopt structural changes that include the formation of dendritic spines. These dendritic spines can strengthen communication between different neurons, and this strengthened communication is believed to be critical for establishing the neural circuits that encode a piece of memory.

In addition to changes within a single neuron, the hippocampus also has other forms of structural plasticity that occur on a whole cell level. Adult neurogenesis, the process that describes the birth of adult newborn neurons derived from neural stem cells, has been shown to occur in the hippocampus of various mammals, including humans and rodents. Given that the brain needs to adapt to a constantly changing environment, it is reasonable to expect that a continuous production of neurons throughout life provides the brain with the plasticity that it needs in order to perform such a strenuous task.

Based on the belief that adult neurogenesis provides structural plasticity for the brain, it has been hypothesized that adult neurogenesis has a role in memory functions. Inhibition of neurogenesis has been shown to disrupt hippocampus-dependent memory tasks in rats. Based on this finding, one might expect that increasing neurogenesis would improve memory.

To test the hypothesis that more neurogenesis confers improvements in memory, Harvard Medical School’s Amar Sahay and his colleagues genetically engineered mice to have increased hippocampal neurogenesis by preventing cell death in neural stem cells. As expected, stimulation of neurogenesis improved a type of memory function called pattern separation, which allows similar information to be more segregated. Other forms of memory, such as spatial memory, were not affected by increases in neurogenesis. These results suggest that neurogenesis is involved in some, but not all, types of memory and that boosting neurogenesis might be an effective therapeutic strategy for improving certain forms of memory dysfunction in disorders such as Alzheimer’s.

Other works have suggested the opposite. Rather than serving to promote memory, increased neurogenesis can lead to the loss of memories. Based on previous studies that show an increase in hippocampal neurogenesis following exercise, Katherine Akers and colleagues at the Hospital for Sick Children in Toronto subjected mice to exercise in a wheel and then tested their memories in an association task. Interestingly, mice with increased neurogenesis from exercise performed worse on the memory task, leading the authors to conclude that neurogenesis can affect the forgetting of memories.

Ultimately the question of whether boosting neurogenesis can enhance memory functions is still up for debate based on contradicting data in the field. The presence of contradicting studies could be explained by the fact that not all experimental conditions are consistent across the studies. For example, Sahay’s study employed a genetic method to boost neurogenesis whereas Akers’ study utilized exercise, which can cause not only alterations in neurogenesis but also other physiological changes throughout the body. In the end, I believe the answer is “yes” for certain types of memory and “no” for other types.