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Making room for new memories

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Joe Tsien (Princeton University, Princeton, NJ) and colleagues have suggested that the creation of new neurons in the hippocampus may allow old memories to be wiped clean, thus making way for the new... Tsien found he had a tool for testing the possible link between memory and neurogenesis when he made mice that lacked Presenilin-1 (PS1) in their forebrains... When Tsien put the mice in an enriched environment (with new toys every day), the normal increase in neurogenesis was reduced in mutants relative to that seen in wild-type mice... Next, Tsien changed the order of activities: learning came first, then enrichment, and then testing... The enrichment procedure still increased memory retention... Tsien believes that the interference arises from hippocampal neurogenesis, which helps obliterate the old memories by making random connections to old memory neurons... With less neurogenesis the mutant mouse can retain a memory more successfully in the short term... But this might not work forever. “These animals spend their entire lives in cages,” says Tsien. “The system really never has a chance to process a lot of memories... In a more natural situation you might show a problem. ” Tsien plans to look for such a problem by challenging the mice with multiple, overlapping tasks... If proven, the new theory would have widespread implications... Those searching for memory drugs would now face the fact that the hippocampus, where new memories are first processed, has a far more limited storage capacity than the cortex. “Eventually the hippocampus may run the risk of overloading with memories,” says Tsien... The opposite problem of premature memory obliteration may arise if excessive neurogenesis occurs as a result of either AD or the addition of a neural stem cell transplant. ▪ Reference:

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Neuron proliferation in rich environments (top) is impaired in presenilin mutants (bottom).Tsien/Elsevier
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Making room for new memories
Neuron proliferation in rich environments (top) is impaired in presenilin mutants (bottom).Tsien/Elsevier
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2199315&req=5

uro1: Neuron proliferation in rich environments (top) is impaired in presenilin mutants (bottom).Tsien/Elsevier

View Article: PubMed Central

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

Joe Tsien (Princeton University, Princeton, NJ) and colleagues have suggested that the creation of new neurons in the hippocampus may allow old memories to be wiped clean, thus making way for the new... Tsien found he had a tool for testing the possible link between memory and neurogenesis when he made mice that lacked Presenilin-1 (PS1) in their forebrains... When Tsien put the mice in an enriched environment (with new toys every day), the normal increase in neurogenesis was reduced in mutants relative to that seen in wild-type mice... Next, Tsien changed the order of activities: learning came first, then enrichment, and then testing... The enrichment procedure still increased memory retention... Tsien believes that the interference arises from hippocampal neurogenesis, which helps obliterate the old memories by making random connections to old memory neurons... With less neurogenesis the mutant mouse can retain a memory more successfully in the short term... But this might not work forever. “These animals spend their entire lives in cages,” says Tsien. “The system really never has a chance to process a lot of memories... In a more natural situation you might show a problem. ” Tsien plans to look for such a problem by challenging the mice with multiple, overlapping tasks... If proven, the new theory would have widespread implications... Those searching for memory drugs would now face the fact that the hippocampus, where new memories are first processed, has a far more limited storage capacity than the cortex. “Eventually the hippocampus may run the risk of overloading with memories,” says Tsien... The opposite problem of premature memory obliteration may arise if excessive neurogenesis occurs as a result of either AD or the addition of a neural stem cell transplant. ▪ Reference:

No MeSH data available.