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dc.contributor.authorPham, Seanen_US
dc.date.accessioned2016-02-25T14:39:40Z
dc.date.available2016-02-25T14:39:40Z
dc.date.issued2016
dc.identifier.urihttps://hdl.handle.net/2144/14595
dc.description.abstractAlzheimer’s disease results from an accumulation of aggregated amyloid beta peptide into oligomeric forms. Soluble oligomers are neurotoxic species, which are believed to be the pathophysiological cause of Alzheimer’s neurodegeneration. Amyloid β species (Aβ) are formed via normal physiological cleavage of amyloid precursor protein by β and γ secretases. Cleaved isoforms aggregate further to form oligomeric configurations of Αβ peptide. To target toxic soluble Aβ oligomers, monoclonal antibodies have been synthesized. Experimental analysis demonstrates the ability of these antibodies to recognize synthetic and endogenous oligomers. In transgenic mice designed to overexpress oligomeric isoforms of Aβ, the antibodies were able to reduce the cerebral amyloid load with proceeding improvements in cognitive abilities. However, large-scale clinical trials corroborated results indicating diminished amyloid load, but failed to produce observable improvements in clinical outcome in patients with Alzheimer’s disease. Simply put, the removal of amyloidogenic species was insufficient in alleviating the associated neurodegeneration and elicited no improvement in cognitive ability, suggesting that Aβ might not be the responsible pathogen in Alzheimer’s. The successes of antibodies in in vitro and transgenic mice studies suggest the potential of antibodies in the treatment of Alzheimer’s, but the inability of these drugs to produce marked improvements in clinical trials questions the role of amyloid in the pathophysiology of the disease.en_US
dc.language.isoen_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectMolecular biologyen_US
dc.titleExamining the potential of anti-A(beta) antibodies as Alzheimer's therapeuticsen_US
dc.typeThesis/Dissertationen_US
dc.date.updated2016-02-17T20:20:00Z
etd.degree.nameMaster of Scienceen_US
etd.degree.levelmastersen_US
etd.degree.disciplineMedical Sciencesen_US
etd.degree.grantorBoston Universityen_US


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Attribution-NonCommercial-NoDerivatives 4.0 International
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivatives 4.0 International