A growing body of research suggests that habitual nose picking could heighten the risk of developing Alzheimer’s disease. The proposed mechanism involves pathways for pathogenic microbes to enter the body through the nasal cavity, potentially triggering inflammatory processes in the brain. Findings attributed to scientists at Western Sydney University and reported in Biomolecules underpin this perspective.
Experts note that touching the nasal mucosa with unclean hands can introduce pathogens that may travel along nerves or through other routes to reach brain tissue. Inflammation in these neural regions can then influence the aggregation of beta-amyloid proteins, a hallmark observed in Alzheimer’s disease. This sequence highlights how everyday actions might intersect with long-term brain health.
Among the infectious agents discussed in the literature are herpesviruses, coronaviruses, Candida albicans fungi, and bacteria responsible for pneumonia. Each of these has the potential to provoke neuroinflammation under certain conditions, particularly when the immune defenses are compromised or when pathogens persist in the nasal cavity for extended periods.
Researchers emphasize that the presence of a pathogen in the nose does not immediately lead to brain involvement. There can be a long latency period—years in some cases—between initial exposure and the appearance of dementia symptoms. This temporal gap underscores the complexity of linking infections directly to cognitive decline, while still recognizing that chronic nasal infections may contribute to neural changes over time.
The review at the heart of these discussions synthesizes more than a century of prior studies on Alzheimer’s disease. One key finding from animal research indicated that nasal infection with certain bacteria could amplify the buildup of toxic proteins in brain tissue, providing a potential clue about how early-life or chronic nasal infections might influence later brain health [Source: Western Sydney University].
Connections drawn between dementia and herpes simplex virus often reference the APOE4 gene, a genetic factor that increases the risk of Alzheimer’s disease in some individuals. Some studies cited by researchers found that a substantial proportion of people who carry APOE4 and develop Alzheimer’s also harbor herpes simplex virus in brain tissue, suggesting a possible interaction between genetics, viral presence, and disease risk. These observations are presented as associations rather than definitive cause-and-effect proofs, highlighting the need for further investigation [Source: Western Sydney University].
In addition to viruses, fungi such as Candida, Malassezia, Cladosporium, and Alternaria have been implicated in triggering inflammatory responses in people with weakened immune systems. The broader implication is that a spectrum of microorganisms might contribute to neuroinflammation under certain health conditions, potentially influencing the trajectory of cognitive aging.
Earlier discussions in this area occasionally referenced a factor reported to triple dementia risk, though contemporary interpretations emphasize a multifactorial view of brain health. The evolving picture suggests that infections may be one of several interacting elements—genetic predisposition, immune status, lifestyle factors, and other health conditions—that collectively shape the likelihood of developing Alzheimer’s disease over time [Source: Western Sydney University].