When Alzheimer’s disease (AD) recently took the life of a family member and condolences poured in I discovered that almost everyone I know has family or friends who’ve been touched by this devastating disease. In fact, there are currently 50 (1) million people worldwide living with AD and it’s the fifth-leading cause of death (2). However, the actual cause of or treatment to prevent or cure the disease continue to elude us.
Of late, there has been a revival of interest in the gut-brain axis and how neurotoxins from the gastrointestinal (GI) tract microbiome may contribute to progressive age-related neurodegenerative disease development and progression. A recent paper by a team from Lousiana State University (3) provides potential evidence of this. The authors show there is an AD neocortex affinity for lipopolysaccharide (LPS), which is a neurotoxin GI microbiome-derived compound, resulting in selective impairment of transcription of neuron-specific elements known to be required for the maintenance of neuronal cytoarchitecture, synaptic connections and neuron signaling operations.
In addition, their work also shows that when LPS-treated Lonza HGN cells are exposed to LPS the results mimic those noted in the AD neocortex. This is further evidence that primary culture provides a highly useful experimental platform for further study of LPS effects on AD-like processes and their pathogenic consequences.
To learn more about the details of this study, please click here.
Written by Lori
Scientific Support Manager, Lonza Pharma-Bioscience Solutions at Lonza
