Sandbox Reserved 963: Difference between revisions

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You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.


== Function ==
Alzheimer's disease (AD), is the most common form of dementia. It is a chronic neurodegenerative disease that usually develops slowly and get worse over time, becoming severe enough to interfere with daily tasks. The most common early symptom of Alzheimer's is difficulty remembering recently learned information. As the patient with Alzheimer’s disease ages, many symptoms can appear: speaking problems, language problems, mood swings, disorientation, behavioural issues, and loss of motivation.
 
Five medications are currently used to treat the cognitive problems of AD: four are acetylcholinesterase inhibitors (tacrine, rivastigmine, galantamine and donepezil) and the other (memantine) is an NMDA receptor antagonist.[156] The benefit from their use is small.[157][158] No medication has been clearly shown to delay or halt the progression of the disease.
 
Acetylcholinesterase inhibitors such as rivastigmine, tacrine, donepezil and galantamine or, memantine, which is a NMDA receptor antagonist, are used to treat the patients suffering from AD but unfortunately, the benefit from their use is small. It is important to understand that none of these medications stops the disease itself.
 
However, many groups of researchers are seeking a solution to this problem and most of them are currently focused on the activity of a small peptide called Amyloid ß.
 
 
The known cause of this disease is depicted as the presence of the amyloid plaques found in the brains of Alzheimer patients, which are composed of Amyloid ß (Aß).
These are peptides  of 36–43 amino acids, obtained via proteolysis of Amyloid Precursor Protein (APP).
An immunologic approach to the disease is made. Researchers have developped a monoclonal antibody which can bind specifically to the Aß’s epitope.
Alzheimer's disease (AD), is the most common form of dementia. It is a chronic neurodegenerative disease that usually develops slowly and get worse over time, becoming severe enough to interfere with daily tasks. The most common early symptom of Alzheimer's is difficulty remembering recently learned information. As the patient with Alzheimer’s disease ages, many symptoms can appear: speaking problems, language problems, mood swings, disorientation, behavioural issues, and loss of motivation.
 
Five medications are currently used to treat the cognitive problems of AD: four are acetylcholinesterase inhibitors (tacrine, rivastigmine, galantamine and donepezil) and the other (memantine) is an NMDA receptor antagonist.[156] The benefit from their use is small.[157][158] No medication has been clearly shown to delay or halt the progression of the disease.
 
Acetylcholinesterase inhibitors such as rivastigmine, tacrine, donepezil and galantamine or, memantine, which is a NMDA receptor antagonist, are used to treat the patients suffering from AD but unfortunately, the benefit from their use is small. It is important to understand that none of these medications stops the disease itself.
 
However, many groups of researchers are seeking a solution to this problem and most of them are currently focused on the activity of a small peptide called Amyloid ß.
 
 
The known cause of this disease is depicted as the presence of the amyloid plaques found in the brains of Alzheimer patients, which are composed of Amyloid ß (Aß).
These are peptides  of 36–43 amino acids, obtained via proteolysis of Amyloid Precursor Protein (APP).
An immunologic approach to the disease is made. Researchers have developped a monoclonal antibody which can bind specifically to the Aß’s epitope.
 
== Biological Function ==


== Disease ==
== Disease ==

Revision as of 21:28, 29 December 2014

This Sandbox is Reserved from 15/11/2014, through 15/05/2015 for use in the course "Biomolecule" taught by Bruno Kieffer at the Strasbourg University. This reservation includes Sandbox Reserved 951 through Sandbox Reserved 975.
To get started:
  • Click the edit this page tab at the top. Save the page after each step, then edit it again.
  • Click the 3D button (when editing, above the wikitext box) to insert Jmol.
  • show the Scene authoring tools, create a molecular scene, and save it. Copy the green link into the page.
  • Add a description of your scene. Use the buttons above the wikitext box for bold, italics, links, headlines, etc.

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Structure of anti-amyloid-beta Fab WO2 (Form A, P212121)

Caption for this structure

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References