Study summary · research use only
β-Amyloid (Aβ) and Human Cathelicidin LL-37: Two Sides of the Same Coin?
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses circulating β-amyloid (Aβ) and human cathelicidin (LL-37) as antimicrobial peptides with roles in innate immune defense and in Alzheimer's disease (AD) pathology. The authors describe Aβ as physiologically beneficial at infection onset, contributing to defense against pathogens, and note that LL-37, upregulated in the brain, binds to Aβ and modulates its aggregation. The review states that Aβ and LL-37 are protective under physiological conditions, but that during chronic infection or dysregulation their interaction becomes toxic and contributes to AD pathology. LL-37 is also described as able to induce neuroinflammation by stimulating human microglia to release inflammatory cytokines such as TNF-α and IL-6, with the authors noting neuroinflammation protects the brain from pathogens but, when prolonged, drives pathological processes underlying AD, Parkinson's disease, and other neurodegenerative disorders.
Abstract
Physiologically produced circulating β-amyloid (Aβ) exerts critical physiological functions. Although Aβ is a key player in Alzheimer's disease (AD), it may initially be beneficial at the onset of infection. As an evolutionary conserved antimicrobial peptide (AMP), Aβ contributes to innate immune defense against pathogens. Host defense peptides such as Aβ and human cathelicidin (LL-37) not only kill pathogens through their antimicrobial activity but also exhibit high affinity for bacterial lipopolysaccharides (LPSs) and membrane receptors. LL-37, which is upregulated in the brain, binds to Aβ, modulating its aggregation; Aβ and LL-37 are protective under physiological conditions, but during chronic infection or dysregulation, their interaction becomes toxic and contributes to AD pathology. Similarly to Aβ, LL-37 can induce neuroinflammation by stimulating human microglia to release inflammatory cytokines, such as TNF-α and IL-6. Neuroinflammation is essential for protecting the brain from pathogens-when prolonged, it drives pathological processes underlying AD, Parkinson's disease (PD), and other neurodegenerative disorders.
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