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Published on: January 22, 2014
by Emily Mullin for Fierce Biotech Research:
For the first time, researchers at the Cleveland Clinic have linked a protein in the brain to critical memory loss associated with amyloid beta in Alzheimer’s patients.
The culprit is neuroligin-1 (NLGN1), which is known to be involved in memory formation. In a new study that appears in Nature Neuroscience, investigators have now linked the protein to amyloid-associated memory loss.
Alzheimer’s disease is characterized by the buildup of amyloid beta plaques in the brain. But it’s still unknown whether these amyloid plaques cause Alzheimer’s or if they’re a byproduct of the disease. Drug research that has used the amyloid theory as a basis for new Alzheimer’s therapies has been riddled with clinical failures.
The accumulation of these amyloid beta proteins induces inflammation in the brain. This inflammation causes certain gene modifications that interrupt the functioning of synapses in the brain, leading to memory loss.
In animal models, Cleveland Clinic researchers found that during this neuroinflammatory process, NLGN1 disrupts the synaptic network in the brain responsible for developing and maintaining memories. Destroying these vital brain connections can cause the type of memory loss seen in Alzheimer’s disease. The finding could provide scientists with a new approach for preventing and treating the devastating and irreversible disease.
Previous research by the Cleveland Clinic team found that a novel compound called MDA7 can potentially stop the neuroinflammatory process that leads to the modification of NLGN1. In an animal model, the compound restored cognition, memory and synaptic plasticity–an important foundation of learning and memory.
Researchers have already completed in vitro studies and preliminary clinical toxicology and pharmacokinetic work and plan to begin a Phase I human study on the safety of this class of compounds in the near future.
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