Scientists Found That Nose-Picking Is Strangely Linked to Alzheimer’s Disease

Researchers at Griffith University in Australia published findings in February 2022 establishing that Chlamydia pneumoniae, a common respiratory bacterium, can travel from the nasal cavity into the mouse brain via the olfactory nerve in as little as 72 hours.

The study, published on February 17, 2022 in Scientific Reports, also found that nasal tissue damage, the kind that can result from nose picking, increased bacterial infection rates in the peripheral nerves and olfactory bulb. Brain cells exposed to the bacterium responded by depositing amyloid-beta protein, a compound associated with Alzheimer’s disease pathology.

The findings are specific to mice. No equivalent human trial has been completed. The research team, led by neuroscientist Professor James St John, head of the Clem Jones Centre for Neurobiology and Stem Cell Research at Griffith University, has stated that a human study is planned but not yet conducted.

A Common Respiratory Bug Takes a Shortcut to the Brain

The Griffith team intranasally inoculated adult female BALB/c mice with C. pneumoniae at a concentration of 1 × 10⁶ inclusion-forming units per animal. Mice were sacrificed at 1, 3, 7, and 28 days after inoculation. Tissue samples from the olfactory mucosa, olfactory bulb, trigeminal nerve, and brain were analyzed for viable bacteria using immunohistochemistry and organ load assays.

According to the Scientific Reports paper, infectious C. pneumoniae was isolated from all four tissue types, including brain tissue beyond the olfactory bulb, at both the 3-day and 7-day time points. Blood PCR tests at 2, 3, and 4 days post-inoculation showed no detectable bacterial DNA in the bloodstream, indicating the olfactory and trigeminal nerve routes, rather than systemic circulation, were the primary invasion paths.

Amyloid-beta deposits were detected adjacent to C. pneumoniae inclusions in the olfactory nerve at 3 and 7 days post-inoculation, and in the glomerular layer of the olfactory bulb at 7 and 28 days. The deposits did not appear in adjacent tissue regions where bacterial inclusions were absent. The researchers were unable to quantify differences in amyloid-beta levels between time points due to the sporadic distribution of inclusions across tissue sections.

A secondary experiment used a methimazole-induced injury model to damage the nasal epithelium before inoculation. Epithelial injury produced a statistically significant increase in bacterial load in the olfactory mucosa and olfactory bulb compared with non-injured mice. However, the paper states that epithelial injury did not produce a significant difference in bacterial load in the brain itself, beyond the olfactory bulb.

This Bacterium Has Been Found in 80 Percent of Alzheimer’s Brains

C. pneumoniae is a gram-negative intracellular bacterium responsible for an estimated 5 to 20 percent of community-acquired pneumonia cases. Its potential connection to Alzheimer’s disease has been documented since the late 1990s. A 1998 study published in Medical Microbiology and Immunology identified C. pneumoniae DNA in 90 percent of post-mortem brain samples from patients with late-onset dementia, compared with 5 percent in age-matched controls. A subsequent analysis found C. pneumoniae DNA in 80 percent of dementia-affected brains versus 11 percent of control brains.

The Griffith study is the first to demonstrate a direct nasal-to-brain infection pathway for C. pneumoniae within a short timeframe, and to show associated amyloid-beta accumulation occurring within days rather than months. Earlier mouse studies had detected amyloid-beta deposition only after one to four months post-inoculation.

The research also tested whether C. pneumoniae could infect and survive in four types of glial cells: olfactory ensheathing cells, trigeminal Schwann cells, astrocytes, and microglia. All four cell types supported bacterial infection, though at significantly lower yields than the HEp-2 control cell line (p ≤ 0.001, one-way ANOVA with Tukey’s post-hoc test). This finding matters because the ability to survive inside glial cells is considered a key mechanism by which bacteria can transit along cranial nerves into the central nervous system.

Gene expression analysis using a 770-gene NanoString Alzheimer’s disease panel found that 514 Alzheimer’s-related genes were upregulated in infected mouse brains at 7 days post-inoculation, compared with 232 at 28 days. The duration of infection produced distinct gene expression clustering, with 43 percent of total variance between the two time points explained by the first principal component.

The Mouse Result Is Clear. The Human Question Is Not.

Several methodological limits apply to these results. The study used wild-type mice, not transgenic Alzheimer’s disease mouse models, which means the amyloid-beta responses observed reflect normal immune reactions to bacterial infection rather than disease-model amplification. Whether those responses persist, resolve, or escalate over longer timeframes was not tested.

The causal role of amyloid-beta in Alzheimer’s disease also remains a matter of scientific debate. Amyloid-beta is an antimicrobial peptide released by neural cells in response to infection. Its accumulation in Alzheimer’s brains may reflect a chronic immune response rather than a primary disease driver. The Griffith study does not resolve this question and does not claim to.

The nose-picking connection, while plausible given the epithelial injury findings, is the weakest link in the chain. The methimazole injury model used in mice produces chemical degeneration of nasal tissue. That is not the same as the mechanical damage caused by nose picking in humans, and the paper does not directly test nose-picking behavior.

“We’re the first to show that Chlamydia pneumoniae can go directly up the nose and into the brain where it can set off pathologies that look like Alzheimer’s disease,” Professor St John told Griffith University media when the study was published on October 28, 2022. “We saw this happen in a mouse model, and the evidence is potentially scary for humans as well.”

St John also noted: “If you damage the lining of the nose, you can increase how many bacteria can go up into your brain.”