LPS and Health Maintenance

(7) Alzheimer’s Disease and LPS

It has been suggested that LPS lowers the risk of Alzheimer’s disease.

It is estimated that 60–70% of dementia is caused by Alzheimer’s disease. Alzheimer’s disease is characterized by a substance called amyloid β buildup in the brain. Amyloid β is a fibrous insoluble substance that spreads in the brain and affect neurons, which causes dementia symptoms to develop. It is inevitable that amyloid β is produced to some extent with aging; however, microglia, a macrophage in the brain, processes it if the person is healthy. Conversely, in a person with Alzheimer’s disease, the ability of microglia to process amyloid β is believed to be declined. It is therefore expected that LPS, which activates macrophage lineage cells, is useful in preventing Alzheimer’s disease.

When Alzheimer’s disease model mice were given LPS, they had suppressed levels of amyloid β buildup and cognition decline as compared with untreated mice (*1). It was previously reported that LPS injection increased amyloid β levels; however, this is a result of inflammation artificially induced by LPS injected into a blood vessel or the abdominal cavity, which is different from the action of orally ingested LPS.

(*1) Oral administration of Pantoea agglomerans-derived lipopolysaccharide prevents metabolic dysfunction and Alzheimer’s disease-related memory loss in senescence-accelerated prone 8 (SAMP8) mice fed a high fat diet, PLOS ONE, https://doi.org/10.1371/journal.pone.0198493 June 1, 2018