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Topics: Health, World News, Science
Lucy Devine
Scientists are constantly investigating and conducting research into Alzheimer's disease and dementia, how the disease progresses and what we can do to reduce the risk.
Alzheimer's Society explains that two out of three people living in the UK with dementia have Alzheimer's disease, which damages a person's brain as it progresses.
Alzheimer's starts many years before symptoms begin and gradually impacts memory and the ability to carry out everyday tasks.
Above the age of 65, a person's risk of the disease doubles every five years.
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Now, scientists think they may have found an important factor about how the disease progresses.
Researchers at Heidelberg University in Germany have uncovered a 'switch' that leads to cognitive decline.
They looked specifically at the NMDA receptor and the TRPM4 ion channel, which work to maintain cognitive function and immune cell function.
They found that when TRPM4 specifically interacts with certain receptors in the brain, a 'death complex' takes place which damages and kills nerve cells.
A statement reads: "The protein-protein complex, known from previous studies, consists of the NMDA receptor and the TRPM4 ion channel. NMDA receptors, which take part in signal transmission between nerve cells, are found on the surface of the cells and are present both in the synapses and outside these contact points between nerve cells. They are activated by a biochemical messenger, the neurotransmitter glutamate.
"While the activation of synaptic NMDA receptors in the brain is critical for the survival of nerve cells as well as the preservation of cognitive abilities, TRPM4 gives the extrasynaptic NMDA receptors toxic properties. Together they build a 'death complex' that can lead to damage as well as the death of nerve cells."
The research found that the complex is more prevalent in mice with Alzheimer's than those without.
The team also discovered a compound that can prevent the neurons from dying and can break apart the 'death complex' which ultimately slows down progression of the disease.
Researchers at the university also hope the treatment can be used for amyotrophic lateral sclerosis (ALS), however, more work needs to be done to make the treatment a reality.
“The previous results are quite promising in the preclinical context, but comprehensive pharmacological development, toxicological experiments, and clinical studies are needed to realize a possible application in humans,” said neurobiologist Prof. Dr Hilmar Bading of Heidelberg University.