A research team led by Professor Mi Hee Lim from the Department of Biological Sciences has reported a small molecule, DAPPD, that is able to improve cognitive function in mouse models with Alzheimer’s disease. The mechanisms in which DAPPD improves cognitive function show potential as treatment for neurodegenerative diseases. The first author was Professor Min Hee Park from Kyungpook National University Alzheimer’s Disease Research Institute and the results of the research were published in the November 4 edition of the Proceedings of the National Academy of Sciences of the United States of America.
Alzheimer’s disease is a type of dementia that results in neuron degeneration in the brain and reduced cognitive function, commonly manifested in the form of memory impairment. A widely accepted signal closely associated with the progression of Alzheimer’s is an increased level of amyloid-beta peptides. Furthermore, glial cells play a vital role in neurological function, as nerve cells and in the neuroinflammatory response. Recent theories on Alzheimer’s suggest that the neuroinflammatory response caused by the interaction of amyloid-beta peptides and glial cells play a key role in the expression of the disease.
As glial cells have multiple roles in the body, they are able to express multiple activity states: a phagocytic state (digestion of other cells) and an inflammatory state. In order to test the ability of DAPPD to restore cognitive function, Professor Park’s team injected the small molecule into the Alzheimer’s mouse models daily, and measured levels of amyloid-beta peptides in the brain. The research results show that the compound reduced amyloid-beta peptide levels and converted the microglial cells from an inflammatory state, as seen in Alzheimer’s, to a phagocytic state.
Professor Lim commented, “This research has shown that it is possible to cure Alzheimer’s by restoring phagocytic activity to microglial cells. DAPPD will spur the development of treatments for a variety of neurodegenerative diseases.”