New research reveals that dementia care can be instigated before brain cells die, potentially enhancing the benefits and effectiveness of interventional therapies.
The recommendation comes after researchers from the University of Bristol discovered the very earliest symptoms of dementia might be due to abnormal stability in brain cell connections, rather than the death of brain tissue. Therefore, therapeutic interventions may be applied before brain tissues die.
In the collaborative study, researchers from Bristol’s School of Physiology, Pharmacology and Neuroscience, and the pharmaceutical company Eli Lilly and Company, studied the behavior of nerve synapses.
The synapses are connections between brain cells that help transmit information between the cells. Researchers used a rodent model to study human frontotemporal dementia over the course of the disease progression.
Using cutting-edge microscopy techniques, investigators were able to image inside the brains of rodents and found that, even before the disease causes synapses and neurons start to die off, the synaptic connections already display unusual properties.
In normal brains, a small percentage of the synapses are constantly added and lost as the brain learns new skills or makes new memories. However, in brains with dementia these percentages were quite different.
In a brain with established dementia, the team found some synapses were very unstable while others were almost frozen. This imbalance in synapse stability was linked to changes in the way neurons were activated while the brain was working.
Their findings, published in Cell Reports, reveal that, while dementia is closely linked to the death of neurons in the brain, it is the connections between these neurons and their synapses that are impaired in earlier stages of the condition.
The study highlights that the very earliest symptoms of dementia might be due to this abnormal synapse stability rather than the death of brain tissue, which comes after.
“The need for new treatments for dementia has never been greater, but our ability to make effective new drugs has been hampered by the fact that we don’t yet fully understand the causes of this debilitating group of diseases,” explains Dr. Mike Ashby, the lead author of the study.
“Because neurons are so closely dependent on their synaptic partners, it is possible that the changes in synapse stability could be actually part of the reason that neurons begin to die. If this is true, then it points towards new therapeutic strategies based on treating these very early abnormalities in synaptic behavior.”
Dr. Mike O’Neill, Head of Molecular Pathology at Lilly Research Laboratories, said the experiment was one of the most comprehensive longitudinal assessments of the detailed mechanisms of synapse dysfunction. And, the new analysis technique allowed the dataset to be analyzed in a rapid and effective way.
Dr. Rosa Sancho, Head of Research at Alzheimer’s Research UK, summarized the investigation:
“This new study adds weight to the growing body of evidence suggesting that synapses become disconnected before nerve cells themselves die. By using sophisticated microscopes, the Bristol team has gained valuable new insight into the stability of synapses and how this affects communication between nerve cells.
“Researchers the world over are hunting for ways to tackle the diseases that cause dementia and protect nerve cells from damaging disease processes. As well as improving our understanding of how synapses are affected in dementia, these interesting findings will help inform future research into drugs that could help keep nerve cells healthy for longer.”
Source: University of Bristol/EurekAlert