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dc.contributor.authorKatz, Leven_US
dc.date.accessioned2015-08-04T15:41:43Z
dc.date.available2015-08-04T15:41:43Z
dc.date.issued2013
dc.date.submitted2013
dc.identifier.other
dc.identifier.urihttps://hdl.handle.net/2144/12131
dc.descriptionThesis (M.A.)--Boston Universityen_US
dc.description.abstractIncreasing evidence suggests that much of the neurotoxicity seen in Alzheimer’s disease is due to activation of pro-inflammatory cascades of microglia upon binding to Amyloid-β peptide (Aβ). Such cascade also promotes Aβ production and reduces Aβ clearance leading to increased Aβ accumulation. As these self- damaging processes participate in the progression of Alzheimer’s, research has been aimed at understanding how such activation occurs. Previous studies have shown that different receptors of the innate immune system bind to Aβ and activate distinctive signaling cascades in microglia. One way by which microglia recognize Aβ is through a heterodimer of three cell-surface receptors, Toll Like Receptor 4 (TLR4), Toll Like Receptor 6 (TLR6) and the class B scavenger receptor type II. In this study, we tested the hypothesis that TLR6 deficiency is associated with reduced Aβ accumulation. For this purpose, we quantified fibrillar Aβ deposits (plaques) in the 5xFAD mouse model of Alzheimer’s disease in comparison to 5xFAD mice with partial deficiency in TLR6 at the age of 5 months. Our data show that 5xFAD mice heterozygous for TLR6, exhibit a statistically significant reduction in the total number of plaques and in the surface area covered by such plaques in the cortex. Additional research is needed to confirm these results and provide a mechanistic explanation for these findings.en_US
dc.language.isoen_US
dc.publisherBoston Universityen_US
dc.titleToll-like receptor 6 in Alzheimer's diseaseen_US
dc.typeThesis/Dissertationen_US
etd.degree.nameMaster of Artsen_US
etd.degree.levelmastersen_US
etd.degree.disciplineMedical Sciencesen_US
etd.degree.grantorBoston Universityen_US


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