Researchers from the University of Seville, the Seville Biomedicine Institute and Lund University (Sweden) have been able to describe how the body responds to a component present in the brain in Alzheimer's patients. This discovery opens new pharmacological possibilities for the control of brain inflammation and its harmful effects.
Specifically, the researchers have revealed the fundamental role that the protein Galectin-3 plays in the regulation of immune response associated with the peptide Amyloid beta, which is responsible for the amyloid and senile plaques that are present in the brains of Alzheimer's sufferers. For that reason, they have analyzed both post-mortem samples from patients diagnosed with Alzheimer's and samples from transgenic rats that emulate the disease. In both cases, they have shown that the microglia that are activated (set of cells that measure immune response in the brain) show high levels of galectin-3.
The researchers have carried out genetic studies that show that certain mutations of the gene of Galectin-3 are associated with a higher risk of suffering from Alzheimer's. In their work, they have shown how the activated microglia release galectin-3 in response to the fibrous form of the Amyloid beta peptide, so playing an essential regulatory role in the activation of the microglia.
The researchers have shown that transgenic rats with Alzheimer's that have been genetically modified so that they are not able to synthesize galectin-3 demonstrate diminished inflammatory response and preserved cognitive response. The researchers have shown for the first time that Galectin-3 has the capacity to join to the microglial receptor TREM2, which has recently been shown to play an important role in the pathology of Alzheimer's given that the appearance of certain mutations associated with this gene significantly increase the risk of suffering the illness.
Boza-Serrano, A. et al. (2019) Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer's disease. Acta Neuropathologica. doi.org/10.1007/s00401-019-02013-z