AI Article Synopsis
- Researchers are exploring the link between neuroinflammation and ALS, with a focus on neurotoxic factors like lipocalin-2 (LCN2) that may cause neuronal death.
- The study measured LCN2 levels in ALS patients' brain tissue and plasma, revealing increased LCN2 alongside various variants associated with the disease.
- LCN2 was found to induce cell death and inflammation in lab tests, but using an anti-LCN2 antibody showed potential to counteract these harmful effects.
Article Abstract
Background: The exact mechanisms underlying neuroinflammation and how they contribute to amyotrophic lateral sclerosis (ALS) pathogenesis remain unclear. One possibility is the secretion of neurotoxic factors, such as lipocalin-2 (LCN2), that lead to neuronal death.
Methods: LCN2 levels were measured in human postmortem tissue using Western blot, quantitative real time polymerase chain reaction, and immunofluorescence, and in plasma by enzyme-linked immunosorbent assay. SH-SY5Y cells were used to test the pro-inflammatory effects of LCN2.
Results: LCN2 is increased in ALS postmortem motor cortex, spinal cord, and plasma. Furthermore, we identified several LCN2 variants in ALS patients that may contribute to disease pathogenesis. Lastly, while LCN2 treatment caused cell death and increased pro-inflammatory markers, treatment with an anti-LCN2 antibody prevented these responses in vitro.
Conclusions: LCN2 upregulation in ALS postmortem samples and plasma may be an upstream event for triggering neuroinflammation and neuronal death.
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| http://dx.doi.org/10.1002/mus.26911 | DOI Listing |
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