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New study finds that controlling brain inflammation could slow progression of Alzheimer’s

Scientists have discovered a link between brain inflammation and the progress of Alzheimer's.

New study finds that controlling brain inflammation could slow progression of Alzheimer’s

A new study has discovered a link between inhibiting brain inflammation and slowing the onset of Alzheimer’s in mice.

The findings are exciting for the researchers who have said the results could help revolutionise development of new treatment methods and preventative measures – when it came to a number of neurodegenerative diseases.

The University of Southampton-led study found that blocking a receptor in the brain that was responsible for the regulation of immune cells, could protect against the degenerative changes of Alzheimer’s.

The latest study is building upon evidence that points to inflammation in the brain being responsible for spurring development of the disease – as opposed to being just a result of it.

By reducing the inflammation, the progression of the disease could be inhibited.

Whilst there is currently no cure for Alzheimer’s, the research team is hoping their findings will lead to an overhaul of possible treatments.

The researchers began by analysing tissue samples from healthy brains alongside those with Alzheimer’s. The immune cells, known as microglia, were then counted and samples suggested a higher concentration of cells present in the Alzheimer’s affected tissue.

Following initial findings, the team wanted to discover whether blocking the receptors responsible for regulating the microglia (CSF1R) could improve cognitive skills.

The mice were given oral doses of the inhibitor and found that it prevented an increase in microglia levels as the disease progressed.

Whilst initial stages have only been conducted in studies with mice, the findings open up a new pathway for Alzheimer’s research.

“While this basic science research provides strong evidence, the challenge will now be to develop medicines for people with dementia,” Mark Dallas, a neuroscientist at Reading University who was not involved in the research, told Ian Sample at The Guardian.

“Too often, this has been the stumbling block in turning observations in the laboratory into a workable therapy. Excitingly, it does however highlight new avenues for researchers to exploit and strengthens the case for targeting other cell types within the brain in the fight against Alzheimer’s.”

 

 

 

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