Sandbox 160: Difference between revisions

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==Relations to Medicine==

Strong structural analysis and in depth studies of parasitic protozoans has allowed the determination of conservation and differences between the parasite and human forms of GAPDH. ''Trypanosoma cruzi'', a protozoan parasite is responsible for causing Chagas' disease in approximately 16-18 million people from southern and central America<ref name="ref 7">PMID:9580189 </ref>. This parasite is responsible for causing up to 45,000 deaths per year and can cause severe complications such as neurological disorders and chronic cardiopathy<ref name="ref 7"/>. Although there are preexisting drugs on the market that do show some effectiveness, they are all known to cause severe side effects which defeats the purpose of their production.

Strong structural analysis and in depth studies of parasitic protozoans has allowed the determination of conservation and differences between the parasite and human forms of GAPDH. ''Trypanosoma cruzi'', a protozoan parasite is responsible for causing Chagas' disease in approximately 16-18 million people from southern and central America<ref name="ref 7">PMID:9580189 </ref>. This parasite is responsible for causing up to 45,000 deaths per year and can cause severe complications such as neurological disorders and chronic cardiopathy<ref name="ref 7"/>. Although there are preexisting drugs on the market that do show some effectiveness, they are all known to cause severe side effects which defeats the purpose of their production. The role of Glyceraldehyde 3-Phosphate Dehydrogenase in this case is that it has been found that the bloodstream forms of the related protozoan ''T. brucei''are shown to lack a functional tricarboxylic acid cycle and thus its ultimate ATP source must come from glycolysis<ref name="ref 7"/>. It is this finding that has intrigued scientists to find solutions to the diseases caused by these protozoans. At the moment the most relevant target is the binding site of the adenosine ring of the NAD+ cofactor. It has been studied in great detail and its differences from the human form have been well recorded to allow the outcome of a possible solution<ref name="ref 7"/>.

Sandbox 160: Difference between revisions

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Revision as of 05:33, 1 April 2010 view source Satvir Gill (talk \| contribs) 60 edits No edit summary ← Older edit		Revision as of 05:44, 1 April 2010 view source Satvir Gill (talk \| contribs) 60 edits No edit summary Newer edit →
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	==Relations to Medicine==		==Relations to Medicine==
	Strong structural analysis and in depth studies of parasitic protozoans has allowed the determination of conservation and differences between the parasite and human forms of GAPDH. ''Trypanosoma cruzi'', a protozoan parasite is responsible for causing Chagas' disease in approximately 16-18 million people from southern and central America<ref name="ref 7">PMID:9580189 </ref>. This parasite is responsible for causing up to 45,000 deaths per year and can cause severe complications such as neurological disorders and chronic cardiopathy<ref name="ref 7"/>. Although there are preexisting drugs on the market that do show some effectiveness, they are all known to cause severe side effects which defeats the purpose of their production.		Strong structural analysis and in depth studies of parasitic protozoans has allowed the determination of conservation and differences between the parasite and human forms of GAPDH. ''Trypanosoma cruzi'', a protozoan parasite is responsible for causing Chagas' disease in approximately 16-18 million people from southern and central America<ref name="ref 7">PMID:9580189 </ref>. This parasite is responsible for causing up to 45,000 deaths per year and can cause severe complications such as neurological disorders and chronic cardiopathy<ref name="ref 7"/>. Although there are preexisting drugs on the market that do show some effectiveness, they are all known to cause severe side effects which defeats the purpose of their production. The role of Glyceraldehyde 3-Phosphate Dehydrogenase in this case is that it has been found that the bloodstream forms of the related protozoan ''T. brucei''are shown to lack a functional tricarboxylic acid cycle and thus its ultimate ATP source must come from glycolysis<ref name="ref 7"/>. It is this finding that has intrigued scientists to find solutions to the diseases caused by these protozoans. At the moment the most relevant target is the binding site of the adenosine ring of the NAD+ cofactor. It has been studied in great detail and its differences from the human form have been well recorded to allow the outcome of a possible solution<ref name="ref 7"/>.