A new study has revealed that scientists have selectively and safely managed to remove new and old memories from mice.
In the collaborative study, researchers were able to eliminate new and old memories alike by over-expressing a protein, called aCaMKII, critical to brain cell communication just as the memory was recalled.
Alzheimers Disease
Alzheimer''s disease is a progressive neurodegenerative disease affecting memory and thinking and making the person increasingly dependent on others.
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"While memories are great teachers and obviously crucial for survival and adaptation, selectively removing incapacitating memories, such as traumatic war memories or an unwanted fear, could help many people live better lives," said Dr. Joe Z. Tsien, brain scientist and co-director of the Brain and Behavior Discovery Institute at the Medical College of Georgia School of Medicine.
He added: "Our work reveals a molecular mechanism of how that can be done quickly and without doing damage to brain cells."
Already, Tsien had created a mouse that couldn't form memories by eliminating the NMDA receptor, which receives messages from other neurons. He then made "Doogie," a smart mouse in which a subunit of the NMDA receptor is over-expressed.
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Schizophrenia is a mental disorder characterized by symptoms of thought, behavior and social problems.
In the current study, the researchers focussed on downstream cascades of the NMDA receptor to learn more about memory formation, and they closed in on aCaMKII protein in the brain, as it's a major signaling molecule for the NMDA receptor.
He found that when he over-expressed aCaMKII while a memory was being recalled, that single memory was eliminated.
"Learning changes the way cells connect to each other," says Tsien.
To form a memory, the NMDA receptor is activated, which results in the insertion of AMPA receptors into those synapses and subsequent strengthening of the synaptic connections among hundreds of thousands of neurons.
Scientists believe that aCaMKII plays an important role in the insertion of AMPA receptors into synapses during learning and subsequent strengthening of connections between neurons to create a memory.
While previous technology would have taken several days to switch off the protein, the researchers developed a powerful chemical-genetic method that allows him to use a pharmacologic inhibitor to instantly turn aCaMKII off and on in a mouse that he genetically engineered to over express this signaling molecule.
That enabled him to study exactly what happened if he threw off the natural balance during the retrieval stage.
While the ability to rapidly erase a selective memory is exciting, Tsien cautioned that its translation to humans would be difficult at this stage.
A possible strategy for humans would be a drug that mimics the aCaMKII over expression that researchers accomplished through genetic manipulation.
Or, further downstream substrates that aCaMKII acts upon could become possible drug targets.
The study is published on the cover of the recent issue of Neuron.
Source: ANI
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Already, Tsien had created a mouse that couldn't form memories by eliminating the NMDA receptor, which receives messages from other neurons. He then made "Doogie," a smart mouse in which a subunit of the NMDA receptor is over-expressed.
Schizophrenia
Schizophrenia is a mental disorder characterized by symptoms of thought, behavior and social problems.
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In the current study, the researchers focussed on downstream cascades of the NMDA receptor to learn more about memory formation, and they closed in on aCaMKII protein in the brain, as it's a major signaling molecule for the NMDA receptor.
He found that when he over-expressed aCaMKII while a memory was being recalled, that single memory was eliminated.
"Learning changes the way cells connect to each other," says Tsien.
To form a memory, the NMDA receptor is activated, which results in the insertion of AMPA receptors into those synapses and subsequent strengthening of the synaptic connections among hundreds of thousands of neurons.
Scientists believe that aCaMKII plays an important role in the insertion of AMPA receptors into synapses during learning and subsequent strengthening of connections between neurons to create a memory.
While previous technology would have taken several days to switch off the protein, the researchers developed a powerful chemical-genetic method that allows him to use a pharmacologic inhibitor to instantly turn aCaMKII off and on in a mouse that he genetically engineered to over express this signaling molecule.
That enabled him to study exactly what happened if he threw off the natural balance during the retrieval stage.
While the ability to rapidly erase a selective memory is exciting, Tsien cautioned that its translation to humans would be difficult at this stage.
A possible strategy for humans would be a drug that mimics the aCaMKII over expression that researchers accomplished through genetic manipulation.
Or, further downstream substrates that aCaMKII acts upon could become possible drug targets.
The study is published on the cover of the recent issue of Neuron.
Source: ANI
RAS/SK
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Dyslexia is a reading disability that occurs when the brain does not properly recognize and process certain symbols.
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