http://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&feed=atom&action=historyTeam:UCL/Project/Developments - Revision history2024-03-29T05:56:41ZRevision history for this page on the wikiMediaWiki 1.16.5http://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=316071&oldid=prevKckiew at 03:21, 5 October 20132013-10-05T03:21:25Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div><p class="major_title">OTHER CIRCUIT COMPONENTS</p></div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div><p class="major_title">OTHER CIRCUIT COMPONENTS</p></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div><p class="minor_title">Avoiding Inflammation And Supporting Neurons</p></div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div><p class="minor_title">Avoiding Inflammation And Supporting Neurons</p></div></td></tr>
</table>Kckiewhttp://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=316062&oldid=prevKckiew at 03:21, 5 October 20132013-10-05T03:21:04Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div><p class="minor_title">Avoiding Inflammation And Supporting Neurons</p></div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div><p class="minor_title">Avoiding Inflammation And Supporting Neurons</p></div></td></tr>
</table>Kckiewhttp://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=316052&oldid=prevKckiew at 03:20, 5 October 20132013-10-05T03:20:37Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>This means that our systems can create proteins in situ to improve the <a href="https://2013.igem.org/Team:UCL/Background/Alzheimers" target="_blank">Alzheimer’s disease (AD)</a> state. However, amyloid proteases such as <a href="https://2013.igem.org/Team:UCL/Project/Degradation" target="_blank">MMP-9</a> would only have a positive impact on the pathology if the <a href="https://2013.igem.org/Team:UCL/Background/Microglia" target="_blank">'Amyloid Hypothesis'</a> is correct, and there is some evidence to suggest that it may not be.</div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>This means that our systems can create proteins in situ to improve the <a href="https://2013.igem.org/Team:UCL/Background/Alzheimers" target="_blank">Alzheimer’s disease (AD)</a> state. However, amyloid proteases such as <a href="https://2013.igem.org/Team:UCL/Project/Degradation" target="_blank">MMP-9</a> would only have a positive impact on the pathology if the <a href="https://2013.igem.org/Team:UCL/Background/Microglia" target="_blank">'Amyloid Hypothesis'</a> is correct, and there is some evidence to suggest that it may not be.</div></td></tr>
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</table>Kckiewhttp://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=316039&oldid=prevKckiew at 03:20, 5 October 20132013-10-05T03:20:23Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>This means that our systems can create proteins in situ to improve the <a href="https://2013.igem.org/Team:UCL/Background/Alzheimers" target="_blank">Alzheimer’s disease (AD)</a> state. However, amyloid proteases such as <a href="https://2013.igem.org/Team:UCL/Project/Degradation" target="_blank">MMP-9</a> would only have a positive impact on the pathology if the <a href="https://2013.igem.org/Team:UCL/Background/Microglia" target="_blank">'Amyloid Hypothesis'</a> is correct, and there is some evidence to suggest that it may not be.</div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>This means that our systems can create proteins in situ to improve the <a href="https://2013.igem.org/Team:UCL/Background/Alzheimers" target="_blank">Alzheimer’s disease (AD)</a> state. However, amyloid proteases such as <a href="https://2013.igem.org/Team:UCL/Project/Degradation" target="_blank">MMP-9</a> would only have a positive impact on the pathology if the <a href="https://2013.igem.org/Team:UCL/Background/Microglia" target="_blank">'Amyloid Hypothesis'</a> is correct, and there is some evidence to suggest that it may not be.</div></td></tr>
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</table>Kckiewhttp://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=316035&oldid=prevKckiew at 03:20, 5 October 20132013-10-05T03:20:12Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>This means that our systems can create proteins in situ to improve the <a href="https://2013.igem.org/Team:UCL/Background/Alzheimers" target="_blank">Alzheimer’s disease (AD)</a> state. However, amyloid proteases such as <a href="https://2013.igem.org/Team:UCL/Project/Degradation" target="_blank">MMP-9</a> would only have a positive impact on the pathology if the <a href="https://2013.igem.org/Team:UCL/Background/Microglia" target="_blank">'Amyloid Hypothesis'</a> is correct, and there is some evidence to suggest that it may not be.</div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>This means that our systems can create proteins in situ to improve the <a href="https://2013.igem.org/Team:UCL/Background/Alzheimers" target="_blank">Alzheimer’s disease (AD)</a> state. However, amyloid proteases such as <a href="https://2013.igem.org/Team:UCL/Project/Degradation" target="_blank">MMP-9</a> would only have a positive impact on the pathology if the <a href="https://2013.igem.org/Team:UCL/Background/Microglia" target="_blank">'Amyloid Hypothesis'</a> is correct, and there is some evidence to suggest that it may not be.</div></td></tr>
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</table>Kckiewhttp://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=315992&oldid=prevKckiew at 03:18, 5 October 20132013-10-05T03:18:44Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>It is thought that AD may be exacerbated into a neurodegenerative condition by the action of microglia themselves, the custodians of the brain. They can inflame the plaque area, and this damages neurons. Therefore, we propose producing a de-activating agent, such as vasoactive intestinal peptide (VIP), BioBrick with an <a href="https://2013.igem.org/Team:UCL/Project/Detection" target="_blank">oxidative stress promoter</a>. This means that our genetically engineered microglia (GEM) would activate when it detects a plaque and move towards that plaque.</div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>It is thought that AD may be exacerbated into a neurodegenerative condition by the action of microglia themselves, the custodians of the brain. They can inflame the plaque area, and this damages neurons. Therefore, we propose producing a de-activating agent, such as vasoactive intestinal peptide (VIP), BioBrick with an <a href="https://2013.igem.org/Team:UCL/Project/Detection" target="_blank">oxidative stress promoter</a>. This means that our genetically engineered microglia (GEM) would activate when it detects a plaque and move towards that plaque.</div></td></tr>
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</table>Kckiewhttp://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=315984&oldid=prevKckiew at 03:18, 5 October 20132013-10-05T03:18:21Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>This means that our systems can create proteins in situ to improve the <a href="https://2013.igem.org/Team:UCL/Background/Alzheimers" target="_blank">Alzheimer’s disease (AD)</a> state. However, amyloid proteases such as <a href="https://2013.igem.org/Team:UCL/Project/Degradation" target="_blank">MMP-9</a> would only have a positive impact on the pathology if the <a href="https://2013.igem.org/Team:UCL/Background/Microglia" target="_blank">'Amyloid Hypothesis'</a> is correct, and there is some evidence to suggest that it may not be.</div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>This means that our systems can create proteins in situ to improve the <a href="https://2013.igem.org/Team:UCL/Background/Alzheimers" target="_blank">Alzheimer’s disease (AD)</a> state. However, amyloid proteases such as <a href="https://2013.igem.org/Team:UCL/Project/Degradation" target="_blank">MMP-9</a> would only have a positive impact on the pathology if the <a href="https://2013.igem.org/Team:UCL/Background/Microglia" target="_blank">'Amyloid Hypothesis'</a> is correct, and there is some evidence to suggest that it may not be.</div></td></tr>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>It is thought that AD may be exacerbated into a neurodegenerative condition by the action of microglia themselves, the custodians of the brain. They can inflame the plaque area, and this damages neurons. Therefore, we propose producing a de-activating agent, such as vasoactive intestinal peptide (VIP), BioBrick with an <a href="https://2013.igem.org/Team:UCL/Project/Detection" target="_blank">oxidative stress promoter</a>. This means that our genetically engineered microglia (GEM) would activate when it detects a plaque and move towards that plaque.</div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>It is thought that AD may be exacerbated into a neurodegenerative condition by the action of microglia themselves, the custodians of the brain. They can inflame the plaque area, and this damages neurons. Therefore, we propose producing a de-activating agent, such as vasoactive intestinal peptide (VIP), BioBrick with an <a href="https://2013.igem.org/Team:UCL/Project/Detection" target="_blank">oxidative stress promoter</a>. This means that our genetically engineered microglia (GEM) would activate when it detects a plaque and move towards that plaque.</div></td></tr>
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</table>Kckiewhttp://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=315970&oldid=prevKckiew at 03:17, 5 October 20132013-10-05T03:17:25Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>It is thought that AD may be exacerbated into a neurodegenerative condition by the action of microglia themselves, the custodians of the brain. They can inflame the plaque area, and this damages neurons. Therefore, we propose producing a de-activating agent, such as vasoactive intestinal peptide (VIP), BioBrick with an <a href="https://2013.igem.org/Team:UCL/Project/Detection" target="_blank">oxidative stress promoter</a>. This means that our genetically engineered microglia (GEM) would activate when it detects a plaque and move towards that plaque.</div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div>It is thought that AD may be exacerbated into a neurodegenerative condition by the action of microglia themselves, the custodians of the brain. They can inflame the plaque area, and this damages neurons. Therefore, we propose producing a de-activating agent, such as vasoactive intestinal peptide (VIP), BioBrick with an <a href="https://2013.igem.org/Team:UCL/Project/Detection" target="_blank">oxidative stress promoter</a>. This means that our genetically engineered microglia (GEM) would activate when it detects a plaque and move towards that plaque.</div></td></tr>
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</table>Kckiewhttp://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=315943&oldid=prevKckiew at 03:16, 5 October 20132013-10-05T03:16:30Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div> As a GEM approaches, oxidative stress increases so that once near the plaque the de-activating agent would return the GEM and wild-type microglia surrounding the plaque into their resting state, avoiding neuroinflammation. This would stop them from producing amyloid proteases such as neprilysin. However, our MMP-9 BioBrick can ensure that amyloid degradation continues (the positive action of microglia in AD) without inflammation (the negative action of microglia in AD). </div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div> As a GEM approaches, oxidative stress increases so that once near the plaque the de-activating agent would return the GEM and wild-type microglia surrounding the plaque into their resting state, avoiding neuroinflammation. This would stop them from producing amyloid proteases such as neprilysin. However, our MMP-9 BioBrick can ensure that amyloid degradation continues (the positive action of microglia in AD) without inflammation (the negative action of microglia in AD). </div></td></tr>
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</table>Kckiewhttp://2013.igem.org/wiki/index.php?title=Team:UCL/Project/Developments&diff=315934&oldid=prevKckiew at 03:16, 5 October 20132013-10-05T03:16:15Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div> As a GEM approaches, oxidative stress increases so that once near the plaque the de-activating agent would return the GEM and wild-type microglia surrounding the plaque into their resting state, avoiding neuroinflammation. This would stop them from producing amyloid proteases such as neprilysin. However, our MMP-9 BioBrick can ensure that amyloid degradation continues (the positive action of microglia in AD) without inflammation (the negative action of microglia in AD). </div></td><td class='diff-marker'> </td><td style="background: #eee; color:black; font-size: smaller;"><div> As a GEM approaches, oxidative stress increases so that once near the plaque the de-activating agent would return the GEM and wild-type microglia surrounding the plaque into their resting state, avoiding neuroinflammation. This would stop them from producing amyloid proteases such as neprilysin. However, our MMP-9 BioBrick can ensure that amyloid degradation continues (the positive action of microglia in AD) without inflammation (the negative action of microglia in AD). </div></td></tr>
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</table>Kckiew