A new study found that blocking the brain's formation of new immune cells can decrease memory problems which are seen in patients with Alzheimer's disease. The findings strengthen growing evidence that brain inflammation is the main driver of Alzheimer's disease, and can lead to novel treatments.
Researchers from the University of Southampton stopped the brain's production of microglia cells (immune cells) in test mice. The current drugs used in dementia treatment attack the amyloid plaques, which are the protein build-ups in the brain and one of the Alzheimer's disease hallmarks.
The current study proved that attacking the build-up of microglia cells could also stop the disease's progression. The study was published in the Brain journal on Jan. 8.
The research team led by Dr. Diego Gomez-Nicola found an increased rate in the accumulation of microglia cells in the autopsied brains of Alzheimer's patients. In the lab tests, the mice were given a drug that stop the function of the CSF1R, the brain receptor responsible for the surge of microglia cells.
The mice given the drug had less behavioral and memory issues. Communication between nerve cells is compromised in the brains of Alzheimer's patients. The drug used in the study was able to prevent the communication loss in the brains of test mice.
University of Reading's Dr. Mark Dallas commented on the "exciting discovery" and said it could explain why Alzheimer's disease drugs have been unsuccessful so far.
"While this basic science research provides strong evidence, the challenge will now be to develop medicines for people with dementia, so we await the development of clinical treatments with interest," said Dallas, Reading's cellular and molecular neuroscience lecturer who was not involved in the study.
Notably, Alzheimer's Society director Dr. Doug Brown found the findings "encouraging." Brown added that there has been no new dementia drug in over 10 years. The population is fast aging, making the need for a new treatment to prevent and stop the disease's progress more crucial.
Systems Immunity University Research Institute director Paul Morgan from Cardiff University also praised the new research. The results showed a real possibility in targeting the CSFR1 function to halt dementia among patients with early signs of Alzheimer's disease.
At present, there are already drugs capable of targeting CSFR1 function but are used for other medical applications. A new Alzheimer's drug could be achieved far quicker compared to developing an entirely new drug from scratch.
Photo: Vince Alongi | Flickr