CSF p-tau181 Increases in Patients with Neuronal Intranuclear Inclusion Disease without Amyloid Burden
CSF p-tau181 Increases in Patients with Neuronal Intranuclear Inclusion Disease without Amyloid Burden
Abstract Background and ObjectivesCSF tau phosphorylated at threonine 181 (p-tau181) is a widely used biomarker for Alzheimer’s disease (AD) and has recently been regarded to reflect amyloid-beta (Aβ) and/or p-tau deposition in the AD brain. Although it is important to know how this biomarker reacts in other neurocognitive diseases, CSF p-tau181 in patients with neuronal intranuclear inclusion disease (NIID) has not been studied. MethodsCSF concentrations of p-tau181, total tau, amyloid-beta 1-42 (Aβ42), monoamine metabolites homovanillic acid (HVA), and 5-hydroxyindole acetic acid (5-HIAA) were compared between 12 patients with NIID, 120 patients with symptomatic AD biologically confirmed based on CSF biomarker profiles, and patients clinically diagnosed with other neurocognitive disorders (dementia with Lewy bodies [DLB], 24; frontotemporal dementia [FTD], 13; progressive supranuclear palsy [PSP], 21; and corticobasal syndrome [CBS], 13). Amyloid PET using Pittsburgh compound B (PiB) was performed in six NIID patients. ResultsCSF p-tau181 concentration was significantly higher in NIID (72.7 ± 24.8 pg/mL) compared to DLB, PSP, and CBS and was comparable between NIID and AD. CSF p-tau181 was above the cutoff value (50.0 pg/mL) in 11 of 12 NIID patients (91.7%). Within these patients, only two patients showed decreased CSF Aβ42, and these patients showed negative or mild local accumulation in PiB PET, respectively. PiB PET scans were negative in the remaining 4 patients tested. CSF HVA and 5-HIAA concentrations were significantly higher in patients with NIID compared to disease controls. DiscussionCSF p-tau181 was increased in patients with NIID without amyloid accumulation. Although the deposition of p-tau has not been reported in NIID brains, molecular mechanism of tau phosphorylation or secretion of p-tau may be altered in NIID.
Higashihara Mana、Kurihara Masanori、Shibukawa Mari、Morimoto Satoru、Saito Yuko、Murayama Shigeo、Kanemaru Kazutomi、Mitsutake Akihiko、Ishiura Hiroyuki、Adachi Kaori、Ihara Ryoko、Nishina Yasushi、Komatsu Hiroki、Hatano Keiko、Matsubara Tomoyasu、Ishii Kenji、Shibata Shota、Sengoku Renpei、Ishibashi Kenji、Ohse Kensuke、Arakawa Akira、Iwata Atsushi、Orita Makoto、Tokumaru Aya Midori
Department of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of GerontologyDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of GerontologyDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of Gerontology||Department of Neurology, Toho University Faculty of MedicineDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of Gerontology||Department of Physiology, Keio University School of MedicineDepartment of Neuropathology (Brain Bank for Aging Research), Tokyo Metropolitan Geriatric Hospital and Institute of GerontologyDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of Gerontology||Department of Neuropathology (Brain Bank for Aging Research), Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology||Brain Bank for Neurodevelopmental, Neurological and Psychiatric Disorders, United Graduate School of Child Development, Osaka UniversityDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of GerontologyDepartment of Neurology, Graduate School of Medicine, the University of TokyoDepartment of Neurology, Graduate School of Medicine, the University of TokyoResearch Initiative Center, Organization for Research Initiative and Promotion, Tottori UniversityDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of GerontologyDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of GerontologyDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of GerontologyDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of GerontologyDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of Gerontology||Department of Neuropathology (Brain Bank for Aging Research), Tokyo Metropolitan Geriatric Hospital and Institute of GerontologyResearch Team for Neuroimaging, Tokyo Metropolitan Institute of GerontologyDepartment of Neurology, Graduate School of Medicine, the University of TokyoDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of Gerontology||Department of Neuropathology (Brain Bank for Aging Research), Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology||Department of Neurology, the Jikei University School of MedicineResearch Team for Neuroimaging, Tokyo Metropolitan Institute of GerontologyIntegrated Research Initiative for Living Well with Dementia, Tokyo Metropolitan Geriatric Hospital and Institution of GerontologyDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of Gerontology||Department of Neuropathology (Brain Bank for Aging Research), Tokyo Metropolitan Geriatric Hospital and Institute of GerontologyDepartment of Neurology, Tokyo Metropolitan Geriatric Hospital and Institution of Gerontology||Integrated Research Initiative for Living Well with Dementia, Tokyo Metropolitan Geriatric Hospital and Institution of GerontologyDepartment of Neuropathology (Brain Bank for Aging Research), Tokyo Metropolitan Geriatric Hospital and Institute of GerontologyDepartment of Diagnostic Radiology, Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology
神经病学、精神病学基础医学医学研究方法
all cognitive disorders/dementiatrinucleotide repeat diseasesCerebrospinal FluidAlzheimer’s diseaseneuronal intranuclear inclusion disease
Higashihara Mana,Kurihara Masanori,Shibukawa Mari,Morimoto Satoru,Saito Yuko,Murayama Shigeo,Kanemaru Kazutomi,Mitsutake Akihiko,Ishiura Hiroyuki,Adachi Kaori,Ihara Ryoko,Nishina Yasushi,Komatsu Hiroki,Hatano Keiko,Matsubara Tomoyasu,Ishii Kenji,Shibata Shota,Sengoku Renpei,Ishibashi Kenji,Ohse Kensuke,Arakawa Akira,Iwata Atsushi,Orita Makoto,Tokumaru Aya Midori.CSF p-tau181 Increases in Patients with Neuronal Intranuclear Inclusion Disease without Amyloid Burden[EB/OL].(2025-03-28)[2025-08-10].https://www.medrxiv.org/content/10.1101/2022.06.09.22275750.点此复制
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