The human auditory cortex in Alzheimer’s disease: A characterisation of tau and amyloid-beta in the primary and secondary auditory cortex

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dc.contributor.advisor Thorne,, P en
dc.contributor.advisor Waldvogel, H en
dc.contributor.advisor Faull, R en
dc.contributor.author Gill Singh, Navdip en
dc.date.accessioned 2019-01-14T21:27:30Z en
dc.date.issued 2018 en
dc.identifier.uri http://hdl.handle.net/2292/45096 en
dc.description Full Text is available to authenticated members of The University of Auckland only. en
dc.description.abstract Alzheimer's disease (AD), a progressive neurodegenerative disorder, is the most prevalent cause of dementia. Since the discovery of the histopathological hallmarks, amyloid-β (Aβ)and hyperphosphorylated Tau, the components of plaques and neurofibrillary tangles (NFTs) respectively, significant progress has elucidated their molecular mechanisms. However, little is known about the cause of AD, with no cure in sight. Hearing loss was recently indicated as the largest modifiable risk factor in the development of dementia (Livingston et al., 2017). Interestingly, patients with AD exhibit signs of central auditory dysfunction (CAD), like deficits to speech and language. Studies have similarly implicated an increased risk of AD in individuals with CAD (Gates et al., 2011; Lin et al., 2011). Previous reports have characterised the presence of NFTs and Aβ plaques within the primary and secondary regions of the human auditory cortex (AC), with a distribution pattern tilted to the secondary regions. However, no studies have examined whether these findings are lateralized to a hemisphere. This study investigated 6 AD and 6 age-matched normal brains for Aβ and Tau within the primary and secondary AC in both hemispheres. Immunohistochemical techniques were utilised to qualitatively assess the laminar distribution for each marker and quantitatively estimate their load in the primary and secondary AC. The findings suggest hyperphosphorylated Tau was deposited similarly within cortical layers I-III & V within the primary and secondary AC, whilst Aβ plaques accumulated to a lesser degree with no predictable pattern. Further, NFTs were shown to lateralise to the left AC. This potentially correlates with deficits to executive tasks like speech and language in patients with AD, and may suggest the left AC is more prone to damage in AD. en
dc.publisher ResearchSpace@Auckland en
dc.relation.ispartof Masters Thesis - University of Auckland en
dc.relation.isreferencedby UoA99265111108702091 en
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. en
dc.rights Restricted Item. Full Text is available to authenticated members of The University of Auckland only. en
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm en
dc.title The human auditory cortex in Alzheimer’s disease: A characterisation of tau and amyloid-beta in the primary and secondary auditory cortex en
dc.type Thesis en
thesis.degree.discipline Audiology en
thesis.degree.grantor The University of Auckland en
thesis.degree.level Masters en
dc.rights.holder Copyright: The author en
pubs.elements-id 759605 en
pubs.record-created-at-source-date 2019-01-15 en


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