Just like a superhero shield protects its user from harm, lactoferrin acts as a guardian for the brain against Parkinson’s disease. This neurodegenerative condition is caused by the loss of dopaminergic cells, leading to motor dysfunctions. Oxidative stress and malfunctioning glial cells worsen the situation. Fortunately, lactoferrin, a protein commonly found in milk, has been found in brain regions as well. When faced with a mitochondrial toxin called MPTP, lactoferrin steps in and reduces oxidative damage to dopaminergic cells. It does so by preventing the harmful Fenton reaction and increasing surveillance. Amazingly, lactoferrin’s protective effects extend beyond situations of oxidative stress. Scientists are exploring various mechanisms behind its actions, including possible interactions with cellular membranes in dopaminergic cells. Additionally, lactoferrin has a unique ability to interact with receptors in both endothelial cells and dopaminergic cells, making it a promising candidate for delivering therapeutic agents across the blood-brain barrier. Want to know more about how lactoferrin saves the day? Check out the full research article!

Parkinson’s disease (PD) is the second-most common neurodegenerative disease and is largely caused by the death of dopaminergic (DA) cells. Dopamine loss occurs in the substantia nigra pars compacta and leads to dysfunctions in motor functions. Death of DA cells can occur with oxidative stress and dysfunction of glial cells caused by Parkinson-related gene mutations. Lactoferrin (Lf) is a multifunctional glycoprotein that is usually known for its presence in milk, but recent research shows that Lf is also found in the brain regions. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a known mitochondrial toxin that disturbs the mitochondrial electron transport chain (ETC) system and increases the rate of reactive oxygen species. Lf’s high affinity for metals decreases the required iron for the Fenton reaction, reduces the oxidative damage to DA cells caused by MPTP, and increases their surveillance rate. Several studies also investigated Lf’s effect on neurons that are treated with MPTP. The results pointed out that Lf’s protective effect can also be observed without the presence of oxidative stress; thus, several potential mechanisms are currently being researched, starting with a potential HSPG–Lf interaction in the cellular membrane of DA cells. The presence of Lf activity in the brain region also showed that lactoferrin initiates receptor-mediated transcytosis in the blood–brain barrier (BBB) with the existence of lactoferrin receptors in the endothelial cells. The existence of Lf receptors both in endothelial cells and DA cells created the idea of using Lf as a secondary molecule in the transport of therapeutic agents across the BBB, especially in nanoparticle development.

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