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Kunikazu Tanji

Researcher at Hirosaki University

Publications -  152
Citations -  10392

Kunikazu Tanji is an academic researcher from Hirosaki University. The author has contributed to research in topics: Dementia with Lewy bodies & Lewy body. The author has an hindex of 38, co-authored 144 publications receiving 9129 citations.

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Thalamic retrograde degeneration in the congenitally hydrocephalic rat is attributable to apoptotic cell death.

TL;DR: The histopathological findings suggest that the neuronal cell death observed in the thalamus in hydrocephalic HTX rats is retrograde degeneration due to extensive damage of axons in the cerebral white matter and that theThalamic retrogrades degeneration is attributable to apoptotic cell death.
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α-Synuclein pathology in the cranial and spinal nerves in Lewy body disease.

TL;DR: Investigation of the cranial and spinal nerves and dorsal root ganglia of patients with LBD indicates that α‐synuclein pathology in the peripheral nerves is axonal‐predominant in LBD, whereas it is restricted to glial cells in MSA.
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Synphilin-1-binding protein NUB1 is colocalized with nonfibrillar, proteinase K-resistant α-synuclein in presynapses in Lewy body disease.

TL;DR: In the brain of patients with PD and DLB, NUB1 accumulates in the presynapses in the hippocampus, cerebral neocortex, and substantia nigra in which PK-resistant &agr;-synuclein is deposited.
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Autophagy mediators (FOXO1, SESN3 and TSC2) in Lewy body disease and aging.

TL;DR: The presence of FOXO1, SESN3 and TSC2 in brainstem-type LBs is demonstrated for the first time and suggests that autophagy modulators are incorporated into LBs and that the expression of these proteins can be increased by various factors including aging.
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Retinoic acid-inducible gene-I is induced by interferon-γ and regulates CXCL11 expression in HeLa cells

TL;DR: It is demonstrated that IFN-gamma stimulates endometrial epithelial cells to produce CXCL11, which is implicated in implantation and pregnancy and RNA interference against RIG-I resulted in the suppression of the IFN -gamma-induced CXCl11 expression.