2013 Fiscal Year Final Research Report
Study on the sleep and gait of idiopathic normal pressure hydrocephalus
| Project/Area Number |
23791619
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | The Tazuke Kofukai |
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Principal Investigator |
NISHIDA Namiko 公益財団法人田附興風会, 医学研究所 第7研究部, 研究員 (80450237)
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| Project Period (FY) |
2011 – 2013
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| Keywords | iNPH / L-PGDS / tau / CSF biomarker / DESH / white matter damage / frontal lobe dysfunction / sleep |
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| Research Abstract |
Lipocalin-type prostaglandin D synthase (L-PGDS) is a cerebrospinal fluid (CSF) protein, and its concentration is decreased in idiopathic normal pressure hydrocephalus (iNPH). L-PGDS behaves as a chaperone to prevent the neurotoxic aggregation of amyloid beta. The aim of this study was to clarify the relevance of the L-PGDS decease for a unique morphological entity of iNPH called disproportionately enlarged subarachnoid-space hydrocephalus (DESH). We evaluated L-PGDS, amyloid beta and tau in CSF, the clinical signs, the extent of DESH and the severity of parenchymal damage. L-PGDS and tau levels were decreased in DESH CSF. L-PGDS levels correlated positively with tau levels, age, callosal angle, and ARWMC scores, and negatively with frontal assessment battery. Our data support the diagnostic value of L-PGDS as a surrogate marker for DESH features, white matter damage, and frontal lobe dysfunction in iNPH, and suggest a possible interaction between L-PGDS and tau protein.
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Research Products
(8 results)
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[Journal Article] Association of lipocalin-type prostaglandin D synthase with disproportionately enlarged subarachnoid-space in idiopathic normal pressure hydrocephalus2014
Author(s)
Nishida N, Nagata N, Toda H, Jingami N, Uemura K, Ozaki A, Mase M, Urade Y, Matsumoto S, Iwasaki K, Ishikawa, M.
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Journal Title
Fluids Barriers CNS
Volume: 11(9): (in press)
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