Neurogenesis refers to the process of developing new nerve cells from multipotent neural stem cells, and it is essential during embryonic and infant brain development. While it also occurs throughout adulthood, it is restricted to specific parts of the brain as we age. These areas include the ventricular-subventricular zone (V-SVZ) and the subgranular zone (SGZ) of the dentate gyrus, a hippocampal structure important for episodic memory formation. Episodic memories are long-term memories characterized by conscious recollection of past events and experiences.
As we learn from experiences throughout life, our brains are predominantly developing through the formation of new synaptic connections rather than increasing in number of neurons. In healthy brains, old connections are also pruned over time to ensure proper brain functioning if they are no longer necessary. However, the number of neurons becomes pertinent when we take neurodegenerative conditions such as Alzheimer’s and dementia into consideration, wherein abnormally configured beta amyloid proteins accumulate in the brain. This forms sticky plaques which are thought to contribute to brain atrophy by disrupting synaptic transmission, eventually eliciting cell death. In simpler terms, conditions that involve neuronal cell death highlight the importance of processes that increase the number of neuronal cells. Thus, studying adulthood neurogenesis in brain areas related to memory in order to see what promotes this proliferation may provide insight into how we can maximize brain and memory maintenance.
Some studies done on mice suggest that exercise, and particularly aerobic exercise results in the incorporation of new neurons into hippocampal pathways. A molecule called brain derived neurotrophic factor, or BDNF, plays an integral role in this process. As exercise duration and intensity increase, so does BDNF concentration. Periodic moderate exercise over prolonged periods of time was determined to be optimal for increasing neurogenesis (Liu, 2018).
Since exercise and neurogenesis appear to promote brain health, one would assume they protect against episodic memory deterioration as well. However, the opposite is true: neurogenesis also plays a key role in forgetting, and studies involving infantile amnesia showcase this interesting phenomenon. Contrary to Sigmund Freud’s reasoning that we have repressed early childhood memories because they are unacceptable or traumatic, one study posits that the formation of new neuronal cells during infancy is the reason why most of us can’t remember anything from that period of our lives. In the study, both adult and infant mice were trained and then tested to assess the maintenance of their memory. Under baseline conditions, the infants appeared to retain the memory of the training experience for a short time, but that memory was not maintained over a longer duration, as opposed to the adult mice which had no problems with their recall. However, when the adult mice were provided with exercise wheels, increased neurogenesis created weaker, shorter-lasting memories of the training experience (Ackers, 2014).
A group of infant mice were then treated with a drug called temozolomide (TMZ) which is known to prevent neurogenesis by preventing mitotic cell division. Surely enough, blocking neurogenesis in the infant mice resulted in stronger memories, essentially undermining infantile amnesia. Like humans, when mice are born they are unable to remember anything without such a treatment. However, there are similar rodent species that are precocial, meaning they are born more developed. Thus, for instance, when guinea pigs were tested, there was no difference between memory maintenance in adults and infants, as both groups had already completed most of their neurogenesis. Also as expected, exercise decreased their memory maintenance and induced infantile amnesia by promoting neurogenesis. This converging evidence therefore suggests that neurogenesis can also play a role in forgetting under certain conditions. The fact that neurogenesis may be involved in both remembering and forgetting processes may seem counterintuitive, but it does link neurogenesis to infantile amnesia, despite its long-standing association with memory promotion (Ackers, 2014).
References
Akers, K. G., Martinez-Canabal, A., Restivo, L., Yiu, A. P., De Cristofaro, A., Hsiang, H.-L. (L., et al. (2014). Hippocampal neurogenesis regulates forgetting during adulthood and infancy. Science, 344(6184), 598–602. doi:10.1126/science.1248903
Josselyn, S. A., & Frankland, P. W. (2012). Infantile amnesia: A neurogenic hypothesis. Learning & Memory, 19(9), 423–433. doi:10.1101/lm.021311.110
Liu, P. Z., & Nusslock, R. (2018). Exercise-mediated neurogenesis in the hippocampus via BDNF. Frontiers in Neuroscience, 12(7). doi:10.3389/fnins.2018.00052
