Volume 26, No. 2/2007(March/April)
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 Clinical Neuropathology
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Review
A brief history of tau: the evolving view of the microtubule-associated protein tau in neurodegenerative diseases
G.L. Lace, S.B. Wharton and P.G. Ince
Abstract
G.L. Lace, S.B. Wharton and P.G. Ince
Neuropathology Group, Academic Unit of Pathology, University of Sheffield Medical School, Sheffield, UK
The major historical milestones in tau-research are reviewed, with their implications for changing perspectives about the significance of tau-pathology in neurodegeneration. Abnormalities of tau-protein characterize the pathology of numerous neurodegenerative disorders, both sporadic and inherited. Over the years, opinions regarding the significance of tau in disease pathogenesis, particularly in Alzheimer’s disease, have fluctuated. Early caution about the role of tau as a significant factor in neurodegenerative disease, especially Alzheimer’s disease, has been superseded by acceptance of its key involvement in pathways which led to cell dysfunction and death. The discovery of familial “tauopathies”, associated with tau-gene mutations, has confirmed that tau-dysmetabolism can independently lead to neurodegeneration. Debate about the centrality of its role remains, but current evidence makes it difficult to ignore the importance of tau in many neurodegenerative diseases. By examining the evolution of research on tau, related to advances in technology and the emergence of new diseases, the future developments needed to resolve remaining issues in the tau-story may be discerned.Correspondence to:
Prof. P. Ince; Academic Unit of Pathology, Division of Genomic Medicine, University of Sheffield Medical School, Sheffield, UK
Email: p.g.ince@sheffield.ac.uk
CNS inflammation
Necrotizing neurosarcoid: three cases with varying presentations
J.M. Markert, K. Powell, R.S. Tubbs, K.O. Riley, M.N. Hadley and C.A. Palmer
Abstract
J.M. Markert, K. Powell, R.S. Tubbs, K.O. Riley, M.N. Hadley and C.A. Palmer
1Department of Surgery, Division of Neurosurgery, 2Department of Neurology, 3Department of Pathology, Division of Neuropathology, University of Alabama at Birmingham, AL, USA
Background: Neurosarcoid affects approximately 5% of patients with sarcoidosis. A significantly more rare entity, necrotizing sarcoidosis affecting the central nervous system, has been confirmed previously in only three case reports. This paper documents three additional cases of necrotizing neurosarcoid, involving a wide spectrum of central nervous system (CNS) locations. Results: One patient presented to the emergency department after being found unresponsive. The second patient was referred due to hearing loss and the third patient sought care due to weakness and numbness of his left lower extremity. Locations of involvement were diverse and included diffuse leptomeningeal involvement, a cerebello- pontine angle mass and a thoracic spinal cord lesion. All patients eventually underwent surgical biopsy, and histologic review of tissue samples revealed necrotizing granulomatous inflammation. Serum ACE levels were available for two of the patients and were within normal limits. Once the diagnosis of necrotizing neurosarcoid was confirmed, all patients were treated with systemic corticosteroid therapy; one patient was also treated with an immunosuppressive agent. Conclusions: Necrotizing neurosarcoid may occur more commonly than previously described and should be considered in the differential diagnosis of patients without systemic manifestations of sarcoidosis.Correspondence to:
C.A. Palmer, MD; Division of Neuropathology, University of Alabama at Birmingham, 1960 6th Avenue South; PD4 175E, Birmingham, AL 35294, USA
Email: palmer@path.uab.edu
CNS inflammation
Progressive multifocal leukoencephalopathy in a lymphoma patient with complete remission after treatment with cytostatics and rituximab: case report and review of the literature
S.G. Freim Wahl, M.R. Folvik and S.H. Torp
Abstract
S.G. Freim Wahl, M.R. Folvik and S.H. Torp
1Department of Pathology and Medical Genetics, 2Department of Radiology, St. Olav Hospital and 3Department of Laboratory Medicine, Children’s and Women’s Health, Faculty of Medicine, Norwegian University of Science and Technology, University Hospital, Trondheim, Norway
A 44-year-old woman presented with dysarthria, visual disturbances, ataxia and cognitive impairment. There was a rapid progression of her neurological disease, and she died 8 months later. She was previously treated for a low-grade follicular B-cell lymphoma; complete remission was achieved by conventional radiotherapy and chemotherapy, including rituximab. Two years later, the neurological symptoms and signs started. MRI revealed a cerebral demyelinating process. Serology was negative. Autopsy disclosed areas in cerebral white matter with grey discoloration. Microscopy revealed demyelination, oligodendroglial viral inclusions and gliosis with bizarre astrocytes. Polymerase chain reaction (PCR) was positive for JC virus. These findings were consistent with progressive multifocal leukoencephalopathy (PML). This is one of recent reports on PML occurring in a patient treated with the anti-20 monoclonal antibody rituximab.Correspondence to:
Dr. S.H. Torp MD, PhD; Associate Professor of Pathology, Department of Pathology and Medical Genetics, St. Olav Hospital, N-7006 Trondheim, Norway
Email: sverre.torp@ntnu.no
Vascular lesions
Three-dimensional analysis of pathological characteristics of a microaneurysm
H. Kojima, H. Eguchi, T. Mizutani, K. Tanaka, Y. Kikuchi and N. Fukudome
Abstract
H. Kojima, H. Eguchi, T. Mizutani, K. Tanaka, Y. Kikuchi and N. Fukudome
1Department of Clinical Neuropathology, Tokyo Metropolitan Institute for Neuroscience, 2Department of Neurosurgery, Tokyo Metropolitan Fuchu Hospital, Tokyo, 3Department of Environmental Security System, Chiba Institute of Science, Chiba, Japan
The etiology of Charcot-Bouchard microaneurysms (MAs), especially before rupture, has been unclear. Case report: A surgical specimen of an MA was removed from an acute intracerebral hemorrhage in a 69-year-old man. The MA was fixed with formalin and embedded in paraffin, and serial sections were cut and stained by the Azan and Elastica van Gieson methods and immunohistochemically. Three-dimensional reconstructive analysis was performed. Results and discussion: The MA presented as local enlargement of an artery with a maximal diameter of 840 mm, but was not ruptured. The wall of the MA consisted of thickened, fine collagen fibrils, which were found to be similar to adventitia immunohistochemically, but with no internal elastic lamina or medial smooth muscle layer. The lumen was empty, with no mural thrombi, but the inner wall endothelial cells had expanded from the normal and/or residual arterial wall, which suggested that the MA had been present for a long period of time. Because the bare wall of the MA consisted of thickened collagen fibrils, the MA was not ruptured, but the possibility of rupture in the future was deemed high, with the risk of intracerebral hemorrhage.Correspondence to:
Dr. H. Kojima; Department of Clinical Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Musashi-dai, 2-6, Fuchu, Tokyo, 183-8526, Japan
Email: hkojima-path@umin.net
Vascular lesions
Effects of caffeic acid phenethyl ester on cerebral cortex: structural changes resulting from middle cerebral artery ischemia reperfusion
N. Cengiz, N. Colakoglu, A. Kavakli, E. Sahna, H. Parlakpinar and A. Acet
Abstract
N. Cengiz, N. Colakoglu, A. Kavakli, E. Sahna, H. Parlakpinar and A. Acet
1Department of Histology, Faculty of Medicine Yuzuncu Yil, University Van, 2Departments of Histology, 3Anatomy and 4Pharmacology, Faculty of Medicine, Firat University, Elazig, 5Department of Pharmacology, Faculty of Medicine, Inonu University, Malatya, Turkey
Overproduction of free radicals is important in the pathogenesis of the cerebral damage induced by ischemia reperfusion. Caffeic acid phenethyl ester, an active component of propolis extract, exhibits antioxidant properties. The study was carried out in 16 male Wistar albino rats, divided into two groups: ischemia reperfusion and ischemia reperfusion with caffeic acid phenethyl ester. The middle cerebral artery was occluded for 60 min with an intraluminal suture, followed by 24-h reperfusion. In this study, widespread infarcted areas, red neurons (eosinophilic degeneration), pyknotic cells, vacuolization and neuroglial cell infiltration were observed in the cerebral cortex in the ischemia reperfusion group. In the caffeic acid phenethyl ester group, slightly infarcted areas were observed and neuroglial cell infiltration was not determined. Congestion of choroid plexus and pia mater was found more severe in the ischemia reperfusion group than in the caffeic acid phenethyl ester group. In the caffeic acid group, neuroglial cell activation was rare. Vacuolization, an indication of brain edema, was prevented by caffeic acid phenethyl ester. In the present study, we showed that pre-treatment with a single i.p. injection of caffeic acid phenethyl ester at 50 µM/kg dose reduced the structural changes.Correspondence to:
Yrd. Doç. Dr. N. Cengiz; Yüzüncü Yil Üniversitesi, Tip Fakültesi, Histoloji ve Embriyoloji Anabilim Dali, Temel Bilimler Binasi, Van, Turkey
Email: nurettincengiz@hotmail.com
Abstracts
The Spanish Club for Neuropathology – 2005 Meeting Barcelona, Spain, November 25 and 26, 2005
Organizers: F. Alameda and T. Tuñon
Abstract
Organizers: F. Alameda and T. Tuñon
Euro-CNS News
Society News of the European Confederation of Neuropathological Societies
Euro-CNS
