Alzheimer’s hope as scientists find a way to stop the build-up of plaques in the brain that are considered to be a tell-tale sign of the cruel disease
- Scientists removed immune cells from the brains of mice with ‘Alzheimer’s’
- Once removed, the animals did not develop the plaques linked to the disease
- Could lead to the development of new drugs that target these immune cells
Scientists claim to have discovered a way to stop the build-up of a toxic protein in the brain that is considered to be a tell-tale sign of Alzheimer’s.
Amyloid β protein has repeatedly been found to clog the brains of patients with the memory-robbing disorder, poisoning and killing crucial cells.
Researchers removed immune cells called microglia from the brains of mice with signs of Alzheimer’s – studies have shown the cells ‘turn on’ genes for the disease.
Once the microglia were removed, the mice did not develop the hallmark amyloid β plaques. The team described the results of their study as ‘striking’.
The researchers at the University of California, Irvine, hope their study will lead to new treatments that ‘affect microglia in targeted ways’.
Scientists blocked the action of cells called microglia, which are found in the central nervous system. When microglia were present (red), they ‘attacked’ harmful amyloid β plaques (green), which are a tell-tale sign of Alzheimer’s. This process ‘switches off’ genes in nerve cells that are required for normal brain functioning, which may trigger Alzheimer’s
Dementia affects 850,000 people in the UK, of which 62 per cent have Alzheimer’s, the most common form of the disease, according to the Alzheimer’s Society.
And in the US, 5.8 million people live with Alzheimer’s, which is set to rise to nearly 14 million by 2050, Alzheimer’s Association statistics show.
Microglia cells are found throughout the brain and spinal cord.
They are thought to be the first line of defence against infections in the central nervous system and ‘swallow’ invading pathogens.
‘However, we hadn’t understood exactly what the microglia are doing and whether they are significant in the initial Alzheimer’s process,’ lead author Dr Kim Green said.
‘We decided to examine this issue by looking at what would happen in their absence.’
The researchers administered a drug that blocks microglia cells from sending out signals that are required for their survival.
Previous studies by the same team have shown blocking this signalling effectively eliminates microglia from the brain.
‘What was striking about these studies is we found that in areas without microglia, plaques didn’t form,’ Dr Green said. ‘However, in places where microglia survived, plaques did develop.
‘You don’t have Alzheimer’s without plaques and we now know microglia are a necessary component in the development of Alzheimer’s.’
Results – published in the journal Nature Communications – also revealed microglia cells recognise amyloid plaques as being harmful and attack them.
This process of attack ‘switches off’ genes in the hippocampus that are required for normal brain functioning.
The hippocampus is an area of the brain that is responsible for forming new memories. It is also involved in learning and emotions.
‘This finding underlines the crucial role of these brain immune cells in the development and progression of Alzheimer’s,’ Dr Green said.
The researchers hope their study will lead to the development of new dementia drugs.
Alzheimer’s is incurable, with existing treatments only being able to temporarily reduce symptoms.
‘We are not proposing to remove all microglia from the brain,’ Dr Green said. ‘What could be possible is devising therapeutics that affect microglia in targeted ways.’
The team also hope their findings will help scientists better understand other brain disorders.
‘These immune cells are involved in every neurological disease and even in brain injury,’ Dr Green said.
‘Removing microglia could enable researchers working in those areas to determine the cells’ role and whether targeting microglia could be a potential treatment.’