Brain-derived neurotrophic factor (BDNF) is a protein implicated in the stress response, long-term memory, Alzheimer’s disease, and psychiatric disorders such as bipolar disorder, depression, and schizophrenia. Brain-derived neurotrophic factor (BDNF) is a neurotrophin essential for neuronal development and survival, synaptic plasticity, and cognitive function. Dysregulation of BDNF signaling is involved in several neurodegenerative disorders, including Alzheimer’s disease. Alteration of metal ion homeostasis is observed both in normal aging and in many neurodegenerative diseases. Interestingly, there is a significant overlap between brain areas characterized by metal ion dyshomeostasis and those where BDNF exerts its biological activity. Therefore, it is reasonable to speculate that metal ions, especially zinc, can modulate the activity of BDNF. BDNF is active in the hippocampus, cortex, cerebellum, and basal forebrain – areas involved in learning, long term memory, and executive function. Most importantly, it plays a role in neuroplasticity, the ability of the brain to reorganize and remodel itself. Neuroplasticity is impaired in depression and other mental disorders; however, exercise increases BDNF and may be responsible for improvements in cognition and mood.
BDNF is a central nervous system growth factor protein coded for by a gene of the same name. The BDNF gene is expressed in the greatest quantity in the dorsal vagal complex and the dorsal motor nucleus of the vagus—both housed in the hypothalamus. A new theory has suggested that infections may migrate via the vagus nerve and perpetuate ME/CFS symptoms. If correct, this theory may also encompass BDNF gene activity in these key vagal areas in the brain. In the body, BDNF is found primarily in serum, plasma, and platelets. It is also produced by immune cells such as lymphocytes and macrophages. To a lesser extent it circulates in cerebral spinal fluid.
BDNF acts like fertilizer for neurons—prompting sprouting of new neuronal connections in a process known as neural plasticity. Suppression of BDNF has been found to lead to neuronal atrophy within the hippocampus—a key area for memory formation and implicated in depression. Higher levels throughout life are associated with a reduced risk of age-related cognitive decline from oxidative stress. In some studies, when the stress response is exaggerated at the HPA axis, there appears to be a reduction in BDNF, which shows up as impaired cognition and increased stress as measured by plasma neurotransmitters. One study reintroduced the bacterial species B. longum which normalized BDNF levels and reduced markers of stress. The mechanism is believed to be mediated by the vagus nerve, which directly links the gut to the brain—a gut-brain axis. As mentioned above, the densest concentration of BDNF genes is found in vagus nerve nuclei in the hypothalamus, further supporting that bacterial species can migrate or perpetuate their effects via this important cranial nerve.
Ways to Increase BDNF: