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Spatially distinct neural mechanisms differentially linking tau aggregations, oxidative stress, and neuronal loss to apathic phenotypes in progressive supranuclear palsy

https://repo.qst.go.jp/records/85832
https://repo.qst.go.jp/records/85832
73346ba4-224e-4e48-9396-e9482e0e5f00
Item type 会議発表用資料 / Presentation(1)
公開日 2022-03-31
タイトル
タイトル Spatially distinct neural mechanisms differentially linking tau aggregations, oxidative stress, and neuronal loss to apathic phenotypes in progressive supranuclear palsy
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference object
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Kiwamu, Matsuoka

× Kiwamu, Matsuoka

WEKO 1034413

Kiwamu, Matsuoka

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Kiwamu, Matsuoka

× Kiwamu, Matsuoka

WEKO 1034414

en Kiwamu, Matsuoka

Search repository
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内容記述タイプ Abstract
内容記述 Objectives: Although progressive supranuclear palsy (PSP) patients are known to exhibit apathy frequently, neuropathological processes leading to this phenotype remains elusive. The current study was aimed to examine the involvement of tau aggregations, oxidative stress (OS), and neuronal loss in the apathic manifestation of PSP patients.
Methods: Twenty PSP patients and 23 healthy controls (HCs) were enrolled. We evaluated tau depositions by PET with a specific probe, 18F-PM-PBB3, and brain volumes by MRI. Glutathione (GSH) levels as resilience measures against OS were also quantified by MRS in the anterior and posterior cingulate cortices (ACC and PCC).
Results: Tau pathologies were noted in the subcortical and cortical structures of the patient brains. Among these areas, tau accumulations were positively correlated with apathy scale (AS) in the angular gyrus (AG). Although PSP cases did not show alterations of GSH relative to HCs, GSH levels in PCC but not ACC were correlated with AS and tau depositions in AG. Marked atrophy was observed in the subcortical but not neocortical regions of PSP subjects, while gray matter (GM) volumes of the inferior frontal gyrus (IFG) and ACC were positively correlated with AS but had no relations to PET-detectable tau depositions and GSH. Finally, path analysis highlighted synergistic contributions of PET-detectable tau pathologies and GSH reductions in the posterior brain regions to AS, in parallel with associations of GM volume loss in the anterior brain regions with AS.
Conclusions: Our findings have indicated neural mechanisms underlying apathy in PSP may consist of PET-detectable tau aggregation and OS without marked neuronal loss in the posterior cortex and neuronal loss with neither PET-detectable tau pathologies nor OS in the anterior cortex.
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 The 8th JHBI Talk Series
発表年月日
日付 2022-03-31
日付タイプ Issued
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