Team:UCL/Background

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                <p class="major_title">RESEARCH</p>
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<p class="major_title">RELATED NEUROSCIENCE</p>
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<p class="minor_title">Alzheimer's Disease</p>
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Dementia is an age related neurodegenerative condition, characterised by failure of recent memory and intellectual functions (attention, language, visual-spatial orientation, abstract thinking, judgement), and tends to progress steadily. These changes are due to the mounting dysfunction and death of brain cells, called neurons, that are responsible for the storage and computation of information. Late stages of the disease often see patients bedridden, mute and incontinent. Although some drugs can temporarily improve memory, pharmaceutical research, through enlightening, has been clinically unsuccessful.  At present there are no treatments that can halt, let alone revert, the inexorable progression of dementia. </p>
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Alzheimer’s disease is the most common of the dementias, afflicting 5-10% of the US population over 45, and 2% of the population in industrialised countries (Mattson 2004). It is
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predicted that its incidence will rocket up threefold 50 years from now (http://www.alz.org).
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It is mainly ‘late-onset’, arising after the age of 60, though rarer early onset types exist. Because there are other forms of dementia and other means of memory impairment, AD can only be verified post-mortem by examining the deceased’s brain. </p>
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<p class="minor_title">Neuro-genetic engineering</p>
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<p class="abstract_text" style="color:#404040;">
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Our project this year blends the fields of synthetic biology and neuroscience. We aim to demonstrate that genetic engineering techniques can be applied to the central nervous system, in order to rectify abnormalities in, for example, the brain on a cellular and/or macromolecular level. Such a novel application of synthetic biology could offer new ways to treat certain brain diseases, such as Alzheimer’s disease, for which modern pharmaceutical treatment is purely symptomatic.<br><br>
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Click the abstracts below to read more.
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<p class="minor_title">Neuropathology</p>
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<a href="https://2013.igem.org/Team:UCL/Background/Alzheimers">
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<p class="abstract_text">There are many vying hypotheses which postulate how Alzheimer’s Disease (AD) may arise. There are many vying hypotheses which postulate how Alzheimer’s Disease (AD) may arise.
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<p class="abstract_title">Alzheimer's Disease</p>
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Alzheimer’s disease is the most prevalent form of dementia. Symptoms include memory loss, mood fluctuations and problems with communication and reasoning. It is a physical, degenerative condition that causes cell death in the brain.
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<p class="citation_text">Links here</p>
 
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<p class="minor_title">Histopathology</p>
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<p class="body_text">Senile plaques are extracellular deposits of an abnormal form of the waste protein β-amyloid (Aβ), which tangle with cell matter in the brain. These plaques are larger than cell bodies (15-25 um in diameter) and mature to become even denser. The tangling of the plaques, however, is not proportional to the amount of amyloid proteins in an area, and so the process by which the tangling and the plaques are created are still as yet unknown. Aβ is cleaved from a larger precursor protein - amyloid precursor protein (APP).
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<p class="abstract_title">Neuropathology</p>
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<p class="abstract_text">There are many hypotheses on the causes for Alzheimer’s disease, though there are three accepted signs in the brain: plaques, tangles and cell death. We focus on the so called ‘Amyloid Hypothesis’.  
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<p class="minor_title">Genetics</p>
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<p class="body_text">Studying the genetics of Alzheimer’s Disease has uncovered key genetic risk factors. Down’s Syndrome is caused by having three copies of  chromosome 21, meaning a duplication of the APP gene. Having an extra copy of the APP gene may increase production of beta-amyloid, triggering the chain of biological events leading to AD. Early onset AD is a component of Down Syndrome, indicating that defects in chromosome 21 can lead to Alzheimer’s independently of Downs syndrome.  
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<p class="abstract_title">Microglia</p>
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<p class="abstract_text">Microglia are the resident, mobile immune cells in the brain, performing many of the same roles as one’s white blood cells. In our project, we try to use microglia as a chassis for our genetic circuit.  
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Latest revision as of 17:33, 19 September 2013

RELATED NEUROSCIENCE

Neuro-genetic engineering

Our project this year blends the fields of synthetic biology and neuroscience. We aim to demonstrate that genetic engineering techniques can be applied to the central nervous system, in order to rectify abnormalities in, for example, the brain on a cellular and/or macromolecular level. Such a novel application of synthetic biology could offer new ways to treat certain brain diseases, such as Alzheimer’s disease, for which modern pharmaceutical treatment is purely symptomatic.

Click the abstracts below to read more.

Alzheimer's Disease

Alzheimer’s disease is the most prevalent form of dementia. Symptoms include memory loss, mood fluctuations and problems with communication and reasoning. It is a physical, degenerative condition that causes cell death in the brain.

Neuropathology

There are many hypotheses on the causes for Alzheimer’s disease, though there are three accepted signs in the brain: plaques, tangles and cell death. We focus on the so called ‘Amyloid Hypothesis’.

Microglia

Microglia are the resident, mobile immune cells in the brain, performing many of the same roles as one’s white blood cells. In our project, we try to use microglia as a chassis for our genetic circuit.

Retrieved from "http://2013.igem.org/Team:UCL/Background"