UpToDate Contents
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
English Journal
- Nanoscale intracortical iron injection induces chronic epilepsy in rodent.
- Jo A, Heo C, Schwartz TH, Suh M.Author information Center for Neuroscience Imaging Research, Institute for Basic Science (IBS), Sungkyunkwan University, Suwon 440-746, Republic of Korea; Department of Biological Science, Sungkyunkwan University, Suwon 440-746, Republic of Korea.AbstractWe studied the electrophysiological, hemodynamic, and cytomorphological consequences of microhemorrhagic brain injury induced by a nanoscale iron injection. Of particular interest were the etiology, development, and treatment of epilepsy associated with this injury. We developed an animal model of chronic epilepsy using nanoscale injection into the adult mouse cortex. Although injection of nanoamounts of iron did not cause clear cell death or damage in the cortex, it elicited varying degrees of spontaneous epileptiform events that could be recorded under anesthesia 3 months postinjection. The influence of these chronic epileptiform events on neurovascular coupling was probed by directly stimulating the cortex ipsilateral to the epileptic focus and by measuring cerebral blood volume simultaneously in both hemispheres using intrinsic signal optical imaging. The ipsilateral hemodynamic response was dramatically lower in animals that exhibited longer, more frequent epileptiform events, but it was unchanged in animals displaying infrequent, short events. In contrast, the contralateral hemodynamic response was augmented in all iron-injected animals compared with the control group. These abnormal hemodynamic responses in chronically epileptic animals were correlated with the degree of reduction in the number of GABAergic interneurons. Therefore, nanoscale iron injection, which mimics some aspects of microhemorrhagic brain injury, generated chronic, yet varying, degrees of spontaneous epileptiform events. Moreover, the severity of the epileptiform events corresponded to the degree of reduction in GABAergic interneurons in the iron-injected hemisphere and the level of autoregulatory dysfunction of cerebral blood flow. © 2013 Wiley Periodicals, Inc.
- Journal of neuroscience research.J Neurosci Res.2014 Mar;92(3):389-97. doi: 10.1002/jnr.23328. Epub 2013 Dec 21.
- We studied the electrophysiological, hemodynamic, and cytomorphological consequences of microhemorrhagic brain injury induced by a nanoscale iron injection. Of particular interest were the etiology, development, and treatment of epilepsy associated with this injury. We developed an animal model of c
- PMID 24375750
- The Presence and Role of Iron in Mild Traumatic Brain Injury: An Imaging Perspective.
- Nisenbaum EJ, Novikov DS, Lui YW.Author information Department of Radiology, NYU Langone Medical Center , New York, New York.AbstractAbstract Mild traumatic brain injury (mTBI), although often presenting without the gross structural abnormalities seen in more severe forms of brain trauma, can nonetheless result in lingering cognitive and behavioral problems along with subtle alterations in brain structure and function. Repeated injuries are associated with brain atrophy and dementia in the form of chronic traumatic encephalopathy (CTE). The mechanisms underlying these dysfunctions are poorly understood. There is a growing body of evidence that brain iron is abnormal after TBI, and brain iron has also been implicated in a host of neurodegenerative disorders. The purpose of this article is to review evidence about the function of iron in the pathophysiology of mTBI and the role that advanced imaging modalities can play in further elucidating said function. MRI techniques sensitive to field inhomogeneities provide supporting evidence for both deep gray matter non-heme iron accumulation as well as focal microhemorrhage resulting from mTBI. In addition, there is evidence that iron may contribute to pathology after mTBI through a number of mechanisms, including generation of reactive oxygen species (ROS), exacerbation of oxidative stress from other sources, and encouragement of tau phosphorylation and the formation of neurofibrillary tangles. Finally, recent animal studies suggest that iron may serve as a therapeutic target in mitigating the effects of mTBI. However, research on the presence and role of iron in mTBI and CTE is still relatively sparse, and further work is necessary to elucidate issues such as the sources of increased iron and the chain of secondary injury.
- Journal of neurotrauma.J Neurotrauma.2014 Jan 9. [Epub ahead of print]
- Abstract Mild traumatic brain injury (mTBI), although often presenting without the gross structural abnormalities seen in more severe forms of brain trauma, can nonetheless result in lingering cognitive and behavioral problems along with subtle alterations in brain structure and function. Repeated i
- PMID 24295521
- Safety and pharmacokinetics of PF-04360365 following a single-dose intravenous infusion in Japanese subjects with mild-to-moderate Alzheimer's disease: a multicenter, randomized, double-blind, placebo-controlled, dose-escalation study.
- Miyoshi I, Fujimoto Y, Yamada M, Abe S, Zhao Q, Cronenberger C, Togo K, Ishibashi T, Bednar MM, Kupiec JW, Binneman B.AbstractOBJECTIVE: PF-04360365 is a humanized IgG(2)Δa anti-amyloid β (Aβ) antibody designed to improve outcome in Alzheimer's disease (AD). Single doses of 0.1 - 10 mg/kg were safe and well tolerated in Western (mostly Caucasian) subjects with mild-to-moderate AD. This Phase 1, multicenter, randomized, double-blind, dose-escalation study was the first to evaluate the safety, pharmacokinetics, pharmacodynamics, and immunogenicity of PF-04360365 in Japanese subjects.
- International journal of clinical pharmacology and therapeutics.Int J Clin Pharmacol Ther.2013 Dec;51(12):911-23. doi: 10.5414/CP201816.
- OBJECTIVE: PF-04360365 is a humanized IgG(2)Δa anti-amyloid β (Aβ) antibody designed to improve outcome in Alzheimer's disease (AD). Single doses of 0.1 - 10 mg/kg were safe and well tolerated in Western (mostly Caucasian) subjects with mild-to-moderate AD. This Phase 1, multicenter, randomized,
- PMID 24131736
Japanese Journal
- Susceptibility-Weighted Magnetic Resonance Imaging for the Detection of Cerebral Microhemorrhage in Patients With Traumatic Brain Injury
- AKIYAMA Yukinori,MIYATA Kei,HARADA Kuniaki,MINAMIDA Yoshihiro,NONAKA Tadashi,KOYANAGI Izumi,ASAI Yasufumi,HOUKIN Kiyohiro
- Neurologia medico-chirurgica 49(3), 97-99, 2009-03-15
- The sensitivity of susceptibility-weighted magnetic resonance (MR) imaging was compared with conventional MR sequences, including T_2^*-weighted imaging, and computed tomography for the detection of c …
- NAID 110007131675
- Transcutaneous β-amyloid immunization reduces cerebral β-amyloid deposits without T cell infiltration and microhemorrhage
- Viswanathan Anand,Chabriat Hugues
- Stroke 1(1), 12-18, 2006-00-00
- NAID 40015823786
Related Links
- 1. J Neurosurg. 2006 Oct;105(4):576-80. Microhemorrhage, a possible mechanism for cyst formation in vestibular schwannomas. Park CK, Kim DC, Park SH, Kim JE, Paek SH, Kim DG, Jung HW. Department of Neurosurgery, Seoul ...
- Differential Diagnosis In the differential diagnosis of cerebral microhemorrhage, other causes of signal loss on GE sequences should be considered. Vascular flow voids of small cerebral vessels in cross-section may ...
Related Pictures