They believe their work opens up a new avenue for research on possible treatments for the degenerative brain condition. We have identified a new molecular mechanism which directly contributes to this synapse loss, a discovery we hope could eventually lead to earlier diagnosis of the disease and new treatments. They also showed in mice studies and in the laboratory that NCAM2 was broken down by beta-amyloid, which is the main component of the plaques that build up in the brains of people with the disease. We show that the neural cell adhesion molecule 2 NCAM2 is enriched in synapses in the human hippocampus.
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