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Neuroinflammation in Huntington’s disease - effects of fractalkine on microglia in a mouse model R6/2 of Huntington’s disease

Adusumalli, Ravi (2013) MOBM29 20131
Degree Projects in Molecular Biology
Abstract
Popular science summary:


Huntington’s disease (HD) is a rare disease but more commonly found in ethnic populations belonging to Europe and North America than in those of Asian or African ancestry. This disease causes loss of neurons in different areas of the brain, that gives rise to different behavioural changes and psychological disturbances including involuntary movements and depression. The statistical prevalence of HD is reported to be 5-10 per 100,000 in the caucasian population. Microglial (one of the brain immune cell) induced inflammation of cells in the brain is considered to be one of the reasons behind progression of HD. Receptors for a signalling protein, fractalkine, are majorly expressed on microglia and it is believed... (More)
Popular science summary:


Huntington’s disease (HD) is a rare disease but more commonly found in ethnic populations belonging to Europe and North America than in those of Asian or African ancestry. This disease causes loss of neurons in different areas of the brain, that gives rise to different behavioural changes and psychological disturbances including involuntary movements and depression. The statistical prevalence of HD is reported to be 5-10 per 100,000 in the caucasian population. Microglial (one of the brain immune cell) induced inflammation of cells in the brain is considered to be one of the reasons behind progression of HD. Receptors for a signalling protein, fractalkine, are majorly expressed on microglia and it is believed that fractalkine receptor signalling plays a major role in neurodegeneration (cell loss within the brain) in the case of HD patients. Hence, in the present study, alterations were made in the fractalkine-receptor DNA sequence to study the impact on adult neurons in brain regions of a mouse model of HD.

Studies were performed using an antibody which stains Huntington protein aggregation in the cell body and nucleus. The staining has produced convincing results and distinctly stained inclusions in cell and nucleus, confirming the onset of HD. The protein aggregation is observed in an HD mice model while there is no protein aggregation in wild type mice. Quantification of neurogenesis (generation of new brain cells) was done using specific stains and it is observed that there is decreased neurogenesis in HD mice compared to wild type mice. Also, the amount of neurogenesis observed is greater in specific areas of the brain in wild type mice.

The purpose of this study was to understand the neurogenesis in wild type mice and HD mice and to gain a better understanding of disease progression in HD. This could therefore help to develop new therapeutic drugs to treat neurodegenerative diseases.

Supervisor:Prof.Jia Yi Li
Master´s Degree Project – Neurobiology, 30 credits
Department of Biology, Lund University
Neural Plasticity and Repair
Experimental Medical Science, BMC A10,
Lund University (Less)
Please use this url to cite or link to this publication:
author
Adusumalli, Ravi
supervisor
organization
course
MOBM29 20131
year
type
H2 - Master's Degree (Two Years)
subject
language
English
id
4332189
date added to LUP
2014-02-26 14:01:36
date last changed
2014-02-26 14:01:36
@misc{4332189,
  abstract     = {Popular science summary:


Huntington’s disease (HD) is a rare disease but more commonly found in ethnic populations belonging to Europe and North America than in those of Asian or African ancestry. This disease causes loss of neurons in different areas of the brain, that gives rise to different behavioural changes and psychological disturbances including involuntary movements and depression. The statistical prevalence of HD is reported to be 5-10 per 100,000 in the caucasian population. Microglial (one of the brain immune cell) induced inflammation of cells in the brain is considered to be one of the reasons behind progression of HD. Receptors for a signalling protein, fractalkine, are majorly expressed on microglia and it is believed that fractalkine receptor signalling plays a major role in neurodegeneration (cell loss within the brain) in the case of HD patients. Hence, in the present study, alterations were made in the fractalkine-receptor DNA sequence to study the impact on adult neurons in brain regions of a mouse model of HD.

Studies were performed using an antibody which stains Huntington protein aggregation in the cell body and nucleus. The staining has produced convincing results and distinctly stained inclusions in cell and nucleus, confirming the onset of HD. The protein aggregation is observed in an HD mice model while there is no protein aggregation in wild type mice. Quantification of neurogenesis (generation of new brain cells) was done using specific stains and it is observed that there is decreased neurogenesis in HD mice compared to wild type mice. Also, the amount of neurogenesis observed is greater in specific areas of the brain in wild type mice.

The purpose of this study was to understand the neurogenesis in wild type mice and HD mice and to gain a better understanding of disease progression in HD. This could therefore help to develop new therapeutic drugs to treat neurodegenerative diseases.

Supervisor:Prof.Jia Yi Li
Master´s Degree Project – Neurobiology, 30 credits
Department of Biology, Lund University
Neural Plasticity and Repair
Experimental Medical Science, BMC A10,
Lund University},
  author       = {Adusumalli, Ravi},
  language     = {eng},
  note         = {Student Paper},
  title        = {Neuroinflammation in Huntington’s disease - effects of fractalkine on microglia in a mouse model R6/2 of Huntington’s disease},
  year         = {2013},
}