Scientists identify vulnerable set of immune cells that lead to Alzheimer’s

Scientists identify vulnerable set of immune cells that lead to Alzheimer’s

A breakthrough has been made in Alzheimer’s research, which pinpoints a set of immune cells in the brain that leaves individuals susceptible to the condition. Scientists from the University of Bonn believe the findings could mean better treatments within five years.

It is inflammation of these cells – known as microglia – that causes clumps of amyloid beta in the brain, research has discovered. This in turn leads to impaired cognitive function, so destroying these vulnerable cells could prevent the onset of Alzheimer’s disease.

Most of the treatments that have been trialled on Alzheimer’s patients in the past have targeted the amyloid plaques in the brain, but have not been effective. The German researchers hope that by tackling the rogue proteins, there might be a better chance of stopping the neurological illness in its tracks.

Some scientists had suspected that inflammation is involved in the development of Alzheimer’s, but until now they didn’t understand the role it plays. The research found that the microglia respond to the inflammation by releasing tiny amounts of a protein called ASC.

They become stuck to the amyloid beta protein and boost its production, causing more damage. Tests showed that by using an ASC-blocking antibody, clumps of amyloid beta didn’t form, which is a major breakthrough.

Professor Heneka, of the University of Bonn, said: “In patients with Alzheimer's disease, deposition of amyloid beta is accompanied by activation of the innate immune system and involves formation of ASC specks in microglia.

“The patho-physiological link between inflammasome responses and amyloid-beta plaque spreading suggests pharmacological targeting of inflammasomes could represent a novel treatment for Alzheimer's disease.”

ASC can be found in an inflammatory pathway known as the NLRP3 inflammasome, so interfering with this could be the answer. The professor believes a safe NLRP3 inhibitor could be developed within five to ten years, entirely transforming the outlook for patients with Alzheimer’s.

In response to the study, Professor Richard Ransohoff, a cell biologist at Harvard Medical School, said that identifying specific chemicals in the formation of plaque is “extremely welcome”. He agreed that the discovery could accelerate the development of new treatments, but knowing exactly where to target will be key.

“Despite this difficulty, which bedevils all pathway directed therapeutics, it is heartening and invigorating to have a newly discovered mechanism to consider in the quest to treat Alzheimer's disease,” Professor Ransohoff added.

Scientists across the globe are working on treatments for Alzheimer’s, as the options at present are very limited and there is no cure. Some 850,000 people are living with dementia in the UK alone and the most common form of the condition is Alzheimer’s. It is a situation that is echoed in many other countries too.

There are a number of drugs that are under development and expected to undergo clinical trials in the coming years, which offer hope for those in the early stages of dementia. The more that the scientific community can learn about the neurological condition, the better chances there are of finding effective treatments.