A key molecule, which is responsible for triggering the chemical processes in our brain linked to our formation of memories was identified by scientists.
The findings have revealed a new target for therapeutic interventions to reverse the devastating effects of memory loss.
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Led by scientists at the University of Bristol, the research aimed to better understand the mechanisms that enable people to form memories by studying the molecular changes in the hippocampus - the part of the brain involved in learning.
The communication is initiated through a chemical process that is triggered by calcium entering brain cells and activating a key enzyme called 'Ca2+ responsive kinase' [CaMKII].
Once this protein is activated by calcium, it triggers a switch in its own activity enabling it to remain active even after the calcium has gone. This special ability of CaMKII to maintain its own activity has been termed 'the molecular memory switch.
The research team comprising of scientists from the University's School of Physiology and Pharmacology, conducted experiments using the common fruit fly [Drosophila] to analyse and identify the molecular mechanisms behind this switch.
Using advanced molecular genetic techniques that allowed the scientists to temporarily inhibit the flies' memory, the team were able to identify a gene called CASK as the synaptic molecule regulating this memory switch.
The team found that by localising the function of the key molecules CASK and CaMKII to the flies' equivalent brain area to the human hippocampus, the flies lacking these genes showed disrupted memory formation.
In repeat memory tests those lacking these key genes were shown to have no ability to remember at three hours (mid-term memory) and 24 hours (long-term memory) although their initial learning or short-term memory wasn't affected.
Finally, they introduced a copy of the human CASK gene - it is 80 per cent identical to the fly CASK gene - into the genome of a fly that completely lacked its own CASK gene and was therefore not usually able to remember. The researchers found that flies which had a copy of the human CASK gene could remember like a normal wildtype fly.
The study has been published in the journal Frontiers in Neural Circuits.
Source: ANI
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Once this protein is activated by calcium, it triggers a switch in its own activity enabling it to remain active even after the calcium has gone. This special ability of CaMKII to maintain its own activity has been termed 'the molecular memory switch.
The research team comprising of scientists from the University's School of Physiology and Pharmacology, conducted experiments using the common fruit fly [Drosophila] to analyse and identify the molecular mechanisms behind this switch.
Using advanced molecular genetic techniques that allowed the scientists to temporarily inhibit the flies' memory, the team were able to identify a gene called CASK as the synaptic molecule regulating this memory switch.
The team found that by localising the function of the key molecules CASK and CaMKII to the flies' equivalent brain area to the human hippocampus, the flies lacking these genes showed disrupted memory formation.
In repeat memory tests those lacking these key genes were shown to have no ability to remember at three hours (mid-term memory) and 24 hours (long-term memory) although their initial learning or short-term memory wasn't affected.
Finally, they introduced a copy of the human CASK gene - it is 80 per cent identical to the fly CASK gene - into the genome of a fly that completely lacked its own CASK gene and was therefore not usually able to remember. The researchers found that flies which had a copy of the human CASK gene could remember like a normal wildtype fly.
The study has been published in the journal Frontiers in Neural Circuits.
Source: ANI
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