Researchers have discovered a pathway that prevents buildup of β-amyloid protein associated with Alzheimer’s disease. The findings were made by scientists at St. Jude Children’s Research Hospital and reported today in Cell.
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The pathway is called LC3-associated endocytosis or LANDO and was found in microglial cells. However, there is evidence that LANDO is a fundamental process that functions in cells throughout the body.
Scientists have known for some time that microglia cells take up β-amyloid proteins; discovery of the LANDO pathway gives some insight into what happens after that.
In the current study, it was revealed that LANDO acts as an operator in clearance of β-amyloid proteins by microglia. Once the β-amyloid is disposed of, LANDO is key to recycling of the Aβ receptors. Mice lacking the LANDO pathway had a buildup of pro-inflammatory cytokine production and increased levels of neurotoxic β-amyloid.
Several proteins are required for LANDO functioning—Rubicon, Beclin 1, ATG5 and ATG7—known for their roles in a related cell pathway to recycle unneeded cell components. These proteins are known to decline with age.
In addition to its protective role in neurodegenerative disease, the researchers note the inhibiting pathway may boost effectiveness of cancer immunotherapy based on some preliminary data. They are hopeful that these findings will offer treatment targets for Alzheimer’s and other diseases.
Image: Confocal image depicting activated astrocytes surrounding amyloid plaques. Image provided by Wikimedia Commons via the Attribution-Share Alike 4.0 International license.