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DOI: 10.14800/ICS.805
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摘要: Systemic and brain-localised inflammations are hallmark features of ageing that further elevated in dementia particularly Alzheimer’s disease (AD). However, although present other chronic diseases co-associated with AD, the potential role inflammation as a causative risk factor for cognitive decline AD may have been overlooked. Peptide-derived forms amyloid precursor protein (APP) beta peptides (Aβ) together intact peptide-derived lactoferrin (Lf), both co-localised deposits eye senile plaques brain. It is proposed their co-incidence supports hypothesis APP Lf exert similar mutually supportive biological roles. There strong evidence base protective host defence during infection its very high affinity to ferric iron representing front line attack against pathogenic microbes binding interactions scavenge virus particles. turn-over involves release exerting anti-inflammatory effects via multiple pathways, ‘self-regulating’ system. We compelling exerts functional signaling molecule innate immune system, can account co-expression AD. The supported by membrane-localisation APP, metal ligand capacities, involvement chemo-attraction cells endothelium cell extracellular matrix. Consistent systemic expression correlated status conditions ageing, lowered treatments regulate inflammation. While over-expression occurs pro-inflammatory than infection, it possible specific presence infection-mediated causes upregulation. If does participate response, then relationship between development onset represents new basis understanding risk. Furthermore, if substantiated, managing longitudinal changes amyloid-mediated pathology, treating inflammation, offer promising targets prevention potentially therapy.