Master Thesis Project Collaboration Wanted

Syed Umair bin Akhtar
Linkoping University, SE
Degree & Study program
Master in Biomedicine
GPA: 60.0
Infectious disease (Endotoxins and pyrogenation)
1: For Alzheimer Disease: We know the brain is made up of neurons and these are interconnected with the vast network these connections knowns as synapses which involve in the transmission of information from one neuron to another neuron. Alzheimer disease was first described by the German psychiatrist Alois Alzheimer in 1907.During the histopathological examination of his patient Auguste. D suffered from dementia, he found two types of lesions in his patient brain. Senile Plaque and neurofibrillary tangles. In Alzheimer's disease, we know that there are two types of lesions Senile plaques composed of beta-amyloid protein and neurofibrillary tangles composed of Tau proteins. o n the surface of neurons there is a large protein APP (Amyloid precursor protein) normally APP is sectioned by an enzyme called beta secretase on the surface of neurons which forms Amyloid beta. Amyloid beta is then cleared in the body in the Alzheimer disease there is an imbalance that Amyloid beta is no longer regulated and is found in the two greater quantity this protein then accumulate and join together in the form of fibers and for Senile plaques. However, in the case of neurofibrillary tangles when neurons communicate with each other signal goes from the synapse to the neuronal cell body knowns as soma these signals actually passes through the skeletal of the neurons composed of microtubules these microtubules are stabilized through the Tau proteins in Alzheimer's disease tau proteins become defective and detached from the microtubules thus skeletal of the neurons become dissociate and no longer maintain defective tau protein then form assemble and form filaments without skeletal neurons degenerate and connection between the neurons are lost. The abnormal accumulation of the Tau and neurons form tangles called Neurofibrillary tangles and eventually causes the death of the neurons. These two lesions spread throughout the brain as we know that two lesion is necessary to developed Alzheimer's disease. Before the appearance of the senile plaque, there is the formation of the smaller amyloid plaque called amyloid beta oligomer appear to be toxic for the neurons they disturbed the communication between the neurons as they stick on the synapses. It is studied that the appearance of the Amyloid oligomers(initially) and Amyloid beta proteins are responsible for the dissociation of the Tau protein from the microtubules and leads to the development of the Alzheimer's disease symptoms. The relationship between the Amyloid beta protein and the Tau proteins is still not understood. What is the exact sequence of molecular mechanisms leading to the development of dementia, what is the role of the genetics and the environmental risk factor in the appearance of the disease? 2: For Cluster Regularly Interspaced Short Palindromic Repeats (CRISPR): As research continues to make progress into how diseases work and the genes that are associated with these diseases, a question of how the genes are involved springs up. This can be investigated by so-called functional genetic tests, in which you can, for example, activate cells that you have somehow manipulated and see if there is any difference between the cells you have manipulated and the ones you have not. This would allow you to distinguish between genes that are important and those that are not. One type of these manipulation methods you can use is clustered regularly interspaced short palindromic repeats (CRISPR), which allows you to guide a protein to any gene sequence and knock it out, effectively stopping it from working as a template for protein production. However, this approach is not always possible, as it can be unpredictable and might affect other genes than the one you are trying to target, an effect called off-target activity. Another approach is CRISPR activation (CRISPRa) or CRISPR interference (CRISPRi), where you utilize a mutated version of the protein used in ordinary CRISPR; this protein cannot knock out genes. To this protein, you can fuse a transcriptional activator or inhibitor, which can increase or decrease the activity of a gene. In the research, we can sight to test the use of one CRISPR (called VP64) and two CRISPRi (one called dCas9 and one KRAB) systems. We can find the VP64 as a reliable way to increase expression of a gene, and that KRAB decreases expression of genes in some of the cases. As CRISPR methods for determining the function of a gene, something that could help us understand the function of genes in normal development and in diseases, such as cancer.

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