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dc.contributor.author Son, Gowoon -
dc.contributor.author Steinbusch, Hendrik Wilhelm Maria -
dc.contributor.author López‐Iglesias, Carmen -
dc.contributor.author Moon, Cheil -
dc.contributor.author Jahanshahi, Ali -
dc.date.accessioned 2021-11-22T11:30:05Z -
dc.date.available 2021-11-22T11:30:05Z -
dc.date.created 2021-10-28 -
dc.date.issued 2022-03 -
dc.identifier.issn 1015-6305 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/15834 -
dc.description.abstract Alzheimer's disease (AD) is the most prevalent form of dementia. Key AD symptoms include memory and cognitive decline; however, comorbid symptoms such as depression and sensory-perceptual dysfunction are often reported. Among these, a deterioration of olfactory sensation is observed in approximately 90% of AD patients. However, the precise pathophysiological basis underlying olfactory deficits because of AD remains elusive. The olfactory glomeruli in the olfactory bulb (OB) receive sensory information in the olfactory processing pathway. Maintaining the structural and functional integrity of the olfactory glomerulus is critical to olfactory signalling. Herein, we conducted an in-depth histopathological assessment to reveal detailed structural alterations in the olfactory glomeruli in AD patients. Fresh frozen post-mortem OB specimens obtained from six AD patients and seven healthy age-matched individuals were examined. We used combined immunohistochemistry and stereology to assess the gross morphology and histological alterations, such as those in the expression of Aβ protein, microglia, and neurotransmitters in the OB. Electron microscopy was employed to study the ultrastructural features in the glomeruli. Significant accumulation of Aβ, morphologic damage, altered neurotransmitter levels, and microgliosis in the olfactory glomeruli of AD patients suggests that glomerular damage could affect olfactory function. Moreover, greater neurodegeneration was observed in the ventral olfactory glomeruli of AD patients. The synaptic ultrastructure revealed distorted postsynaptic densities and a decline in presynaptic vesicles in AD specimens. These findings show that the primary olfactory pathway is affected by the pathogenesis of AD, and may provide clues to identifying the mechanism involved in olfactory dysfunction in AD. © 2021 The Authors. Brain Pathology published by John Wiley & Sons Ltd on behalf of International Society of Neuropathology. -
dc.language English -
dc.publisher John Wiley and Sons Inc -
dc.title Severe histomorphological alterations in post‐mortem olfactory glomeruli in Alzheimer’s disease -
dc.type Article -
dc.identifier.doi 10.1111/bpa.13033 -
dc.identifier.wosid 000711455800001 -
dc.identifier.scopusid 2-s2.0-85118213526 -
dc.identifier.bibliographicCitation Brain Pathology, v.32, no.2 -
dc.description.isOpenAccess TRUE -
dc.subject.keywordAuthor Alzheimer&apos -
dc.subject.keywordAuthor s disease -
dc.subject.keywordAuthor morphology -
dc.subject.keywordAuthor olfactory bulb -
dc.subject.keywordAuthor post-mortem histology -
dc.subject.keywordAuthor ultrastructure -
dc.subject.keywordPlus TYROSINE-HYDROXYLASE EXPRESSION -
dc.subject.keywordPlus TAU PATHOLOGY -
dc.subject.keywordPlus AMYLOID-BETA -
dc.subject.keywordPlus MICROGLIA -
dc.subject.keywordPlus BULB -
dc.subject.keywordPlus BRAIN -
dc.subject.keywordPlus ULTRASTRUCTURE -
dc.subject.keywordPlus ORGANIZATION -
dc.subject.keywordPlus DEPRESSION -
dc.subject.keywordPlus MOUSE -
dc.citation.number 2 -
dc.citation.title Brain Pathology -
dc.citation.volume 32 -
dc.description.journalRegisteredClass scie -
dc.description.journalRegisteredClass scopus -
dc.relation.journalResearchArea Neurosciences & Neurology; Pathology -
dc.relation.journalWebOfScienceCategory Clinical Neurology; Neurosciences; Pathology -
dc.type.docType Article -
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Appears in Collections:
Department of Brain Sciences Laboratory of Chemical Senses 1. Journal Articles

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