Sleeping pills and drugs for hay fever and asthma can cause Alzheimer’s disease by destroying brain cells, according to new research.
The drugs, known as ‘anticholinergics’ , work by blocking the brain chemical acetylcholine which helps transmit electrical impulses between cells.
People with dementia lack the molecule.
Now it has been found how the treatments may exacerbate or trigger the devastating condition which affects 850,000 Britons – a breakthrough that could lead to a treatment.
The medications, which are also prescribed for asthma and depression, have been linked to raising the risk of Alzheimer’s disease for years but the reason has remained a mystery.
Professor Marco Prado, of the University of Western Ontario, said: “There have been several epidemiological studies showing people who use these drugs for a long period of time increase their risk of developing dementia. So the question we asked is ‘why?'”
The researchers said long term use of the allergy drugs lead to an increased risk of developing dementia because their blocking of the neurotransmitter results in changes in the brain.
In the study published in Cerebral Cortex mice genetically engineered to lack acetylcholine, mimicking the action of the drugs in the brain, developed Alzheimer’s like symptoms.
Explained Prof Prado: “We hope by understanding what is happening in the brain due to the loss of acetylcholine, we might be able to find new ways to decrease Alzheimer’s pathology.”
The researchers focused called messenger RNA, a molecule that carries programme ‘instructions’ from genes to protein making machinery in the cell.
They found blocking acetylcholine changed about 10 per cent of this vital bit of DNA in a region of the brain responsible for memory.
Several of the changes they uncovered in the brains of the mutant mice were similar to those observed in Alzheimer’s disease.
Prof Prado said: “We demonstrated in order to keep neurons healthy you need acetylcholine.
“So if acetylcholine actions are suppressed, brain cells respond by drastically changing their messenger RNAs and when they age, they show signs of pathology that have many of the hallmarks of Alzheimer’s disease.”
Importantly, by targeting one of the messenger RNA pathways they uncovered, the researchers improved the condition of the mutant mice.
The study published in Cerebral Cortex used human tissue samples to validate the findings and mouse models to show not only the physical damage but also behavioural and memory changes.
Long term suppression of acetylcholine caused brain cells to die and, as a consequence, decreased memory in the ageing mice.
Added co author Ben Kolisnyk, a PhD candidate: “When the mutant mice were old, memory tasks they mastered at young age were almost impossible for them, whereas normal mice still performed well.”
The researchers hope their findings will have an impact on reducing the burden of dementia by providing new ways to reverse the loss of acetylcholine.
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