New research offers hope for Alzheimer’s disease cure by opening a new window into the link between synapse loss and and the onset of the neurodegenerative disease.
As Alzheimer’s disease sets in, symptoms associated with the cognitive-impairing disease aren’t too obvious. During the early stages, some patients may not exhibit any symptoms at all. In turn, this leads to a rapid advancement of Alzheimer’s disease and makes prevention all the more difficult.
However, if regular tests are conducted, neurologists are able to spot some changes occurring in the brains of those affected. Among them, synapse loss predicts the onset of this form of dementia and offers the possibility of early intervention. While there is no cure for Alzheimer’s disease just yet, new research offers hope for Alzheimer’s disease cure by targeting the degradation of cell connections in the brain.
The research team coming from the University of New South Wales (UNSW), Australia has published the study in the Nature Communications journal. Lead researcher Doctor Vladimir Sytnyk with the School of Biotechnology and Biomolecular Sciences of the UNSW explained that synapse loss translated in the loss of brain neurons’ connection is the first visible sign of Alzheimer’s disease onset. Synapses play a crucial role for memory forming and learning, as well as for all other brain functions.
As synapse loss happens even before nerve cells die, it’s hard to detect the onset of Alzheimer’s disease and the early stages marked by mild cognitive impairment. To further understand the role of synapses and synapse loss, the research team looked at NCAM2 – neural cell adhesion molecule 2. This protein is responsible along with other molecules in the same family for connecting synapse membranes. Thus, synaptic connections are maintained between neurons in the brain.
After conducting a study on brain tissue collected from people both suffering from Alzheimer’s disease and who hadn’t been diagnosed with the neurodegenerative disease, the research team found that for the former group, the synaptic levels of NCAM2 were low in the hippocampus. The hippocampus marks the region of the brain where memories are formed. At the same time it is the region of the brain most affected by Alzheimer’s disease and where most of the toxic changes occur.
Another study conducted on mice revealed that the levels of NCAM2 were significantly lowered by other proteins known as beta-amyloids. These are the clumps building up in the brain and often observed with those who suffer from Alzheimer’s disease.
Targeting this connection and working to improve it and maintain it safe could lead to a cure for Alzheimer’s in the near future. The research has the potential to save millions of lives as it is estimated that by 2050, 14 million U.S. adults will be affected by Alzheimer’s disease.
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