Despite current knowledge of Alzheimer’s disease (AD) neuropathology, the origin of sporadic forms of the disease is unknown. Systemic inflammation has been postulated as a factor, although the particular mechanisms through which inflammatory processes influence the development and spread of Alzheimer’s disease remain unknown.

Allergy is a chronic inflammatory condition that affects more than 20% of the world’s population, yet little is known about how allergic diseases impair brain processes. This analysis was aimed to see if the expression of AD-related proteins and inflammatory markers in the brain is affected by chronic peripheral inflammation caused by allergies.

Persistent and repeatable eosinophilia in the bronchoalveolar lavage (BAL) fluid of allergic animals proved the validity of the chronic allergy strategy. In addition, allergic mice had higher amounts of both immunoglobulin (Ig) G and immunoglobulin (Ig) E in their brains, with a wide range.

Allergies were also known to increase tau protein phosphorylation in the brain. The current findings support the idea that allergy-induced chronic peripheral inflammation alters the inflammatory status of the brain and influences the phosphorylation of an AD-related protein, implying that allergy may be another factor to consider in the development and progression of neurodegenerative disorders like Alzheimer’s disease.

In mice, an OVA exposure was demonstrated to increase c-fos expression in the brain and improve anxiety-related behaviors, suggesting that allergies influence brain activity. In addition, there is proof that allergies are connected to the release of pro-inflammatory cytokines in the brain. After exposure to polluted air particles, increased levels of the cytokines IL-1 and tumor necrosis factor (TNF)- were found in the brains of OVA-sensitized OVA-sensitized mice.