A study by a team from the University of Chicago has shown that the key role isn't solely played by vascular damage or oxygen deprivation, as previously thought, but also by a direct biological connection between the lungs and the brain. Nicotine, it turns out, triggers a chain of signals that disrupts neuronal function.
Scientists have been studying smoking and dementia risk in detail since a 2011 study found that heavy smoking in midlife was associated with a more than 100% increased risk of dementia, Alzheimer's disease, and vascular dementia more than two decades later. Now, scientists have discovered that this link is explained by a previously unexplored signaling pathway: from the lungs to the brain via pulmonary neuroendocrine cells.
"When exposed to nicotine, these cells release exosomes that disrupt the iron balance in neurons, causing symptoms often seen in patients with dementia," the authors explained. Now, understanding these mechanisms, scientists have a new target for developing treatments to prevent smoking-related neuronal damage. However, a challenging research phase lies ahead, as the target cells constitute less than 1% of all lung cells.
Previously, other studies have shown that smoking increases the risk of obesity and suppresses immune system function for years.
