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Books: 0	Journals: 2	Articles: 18

Abstract

G. Kreft, G.G. Kovacs, T. Voigtländer, C. Haberler, J.A. Hainfellner, H. Bernheimer and H. Budka

Abstract

Clinical Neuropathology, Vol. 29 – No. 5/2010 (271-288)

Current concepts of neuropathological diagnostics in practice: neurodegenerative diseases

G.G. Kovacs and H. Budka

Institute of Neurology, Medical University of Vienna, Vienna, Austria
Definitive diagnosis of neurodegenerative diseases (NDDs) relies on the neuropathological evaluation. NDDs are defined as disorders with progressive loss of neurons showing distinct anatomical distribution, and accordingly different clinical phenotypes. Recent research has identified a spectrum of immunohistochemically detectable proteins deposited in the central nervous system which serve as a basis for protein-based disease classification. Accordingly, diagnostic criteria and disease staging have been updated. Furthermore, it has become evident that there is considerable overlap between deposited proteins and pathologies. This review summarizes recent achievements in neuropathological diagnosis and classification of NDDs and recommends approaches to be used during the diagnostic procedure in practice, thus to serve as guideline for a common level of diagnostic quality.Correspondence to:
G.G. Kovacs, MD, PhD
Institute of Neurology, AKH 4J
Währinger Gürtel 18 – 20
1097 Vienna, Austria
Email: [email protected]

Abstract

Atemw.-Lungenkrkh., Jahrgang 36, Nr. 10/2010, S. 413–416

Aktuelle Fragestellungen und neue Möglichkeiten im Bereich der PAH

G. Kovacs und H. Olschewski

Klinische Abteilung für Pneumologie, Universitätsklinik für Innere Medizin, Medizinische Universität Graz, Österreich
Die pulmonal arterielle Hypertonie ist eine der aktivsten Forschungsgebiete der Medizin. In den vergangenen Jahren wurden effektive Behandlungsmöglichkeiten etabliert, die zu einem besseren Überleben und Lebensqualität geführt haben. Trotzdem bleibt die Prognose der Erkrankung schlecht. Von den bereits etablierten Medikamentengruppen wurden neue Phosphodiesterase-5 Inhibitoren (Tadalafil, Vardenafil), Endothelin-Rezeptor Antagonisten (Macitentan) und oral verfügbare Prostanoide entwickelt um die Prognose zu verbessern. Vielversprechende neue Medikamentgruppen sind die lösliche Guanylat Cyclase Aktivatoren (Riociguat) und die Tyrosine Kinase Inhibitoren. (Imatinib, Sorafenib). Darüber hinaus werden etablierte PAH Medikamente in neuen Indikationen - wie z.B. Lungenfibrose oder die diastolische Funktionsstörung des linken Ventrikels – eingesetzt, und diagnostische Studien werden iniziiert, um die Pathogenese der Erkrankung besser verstehen zu können. Correspondence to:
Dr. med. G. Kovacs
Klinische Abteilung für Pulmologie
Universitätsklinik für Innere Medizin
Medizinische Universität Graz
Auenbruggerplatz 20
A–8036 Graz
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 30 – No. 1/2011 (3-10)

Unclassifiable tauopathy associated with an A152T variation in MAPT exon 7

G.G. Kovacs¹, A. Wöhrer¹, T. Ströbel¹, G. Botond¹, J. Attems²,³ and H. Budka¹

¹Institute of Neurology, Medical University of Vienna, Vienna, Austria, ²Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK, ³Previous address: Department of Pathology, Otto Wagner Spital, Vienna, Austria
Mutations in the microtubule-associated tau (MAPT) gene are associated clinically with frontotemporal dementia with or without supranuclear palsy, corticobasal syndrome or parkinsonism. Here we present clinical, neuropathological, genetic and biochemical data on a patient with an A152T variation in exon 7 of MAPT. A 63-year-old man presented with memory disturbance and later speech disorder, followed by progressive dementia and terminally myoclonus together with periodic sharp waves in EEG. Duration of illness was 5 years. Similar neuropsychiatric symptoms were reported in the patient’s father. Neuropathological evaluation revealed neuronal loss mainly in the frontal and temporal cortices and substantia nigra. Abundant phospho-tau immunoreactive thread-like structures and diffuse staining of neuronal cytoplasm predominated in the frontal and temporal cortex, and hippocampus. There was a lack of astrocytic plaques and tufted astrocytes, and only a moderate number of oligodendroglial coiled bodies were seen. Tau pathology was characterized by the 4R tau isoform; immunoblot revealed bands at 64 and 68 kDa, and ultrastructure of filaments was compatible with twisted ribbons. Pathogenic mutations have not been reported in exon 7. Our observation of an apparently familial disorder with a novel neuropathological phenotype suggests a possible pathogenic role of thisMAPT gene variation, which might be different from mutations affecting the microtubule binding.Correspondence to:
G.G. Kovacs, MD, PhD
Institute of Neurology, AKH 4J
Währinger Gürtel 18 – 20
1097 Vienna, Austria
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 31 – No. 3/2012 (116-118)

Clinical Neuropathology Practice News 3-2012: the “ABC” in AD – revised and updated guideline for the neuropathologic assessment of Alzheimer’s disease

Gabor G. Kovacs¹ and Ellen Gelpi²

¹Institute of Neurology, Medical University of Vienna, Vienna, Austria, and ²Neurological Tissue Bank of the Biobank-Hospital Clinic-IDIBAPS, Barcelona, Spain
The two major approaches for the neuropathological assessment of Alzheimer’s disease (AD) related pathology have been based on the assessment of neuritic plaques (CERAD) and neurofibrillary pathology (Braak and Braak). In 1997 these two approaches were integrated in the criteria and recommendations of the National Institute on Aging and the Reagan Institute Working group. Recently a new guideline has been published by the National Institute on Aging-Alzheimer’s Association. This new guideline recognizes the existence of a pre-clinical stage of AD as part of continuous neuropathological changes in the background of the disease process, and it fosters the assessment of amyloid-beta phases in addition to neurofibrillary degeneration and neuritic plaques following an “ABC” score. Further, it suggests protocols for the neuropathological assessment of additional/concomitant neurodegenerative and vascular pathologies. Altogether, the new guideline responds to the need for an update of the existing “1997 criteria” for AD. Continued studies will have to assess the added value of the new approach and the influence of interlaboratory and/or methodological differences on the implementation of these new recommendations.Correspondence to:
Gabor G. Kovacs, MD, PhD
Institute of Neurology, AKH 4J Medical
University of Vienna
1090-Vienna, Austria
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 32 – No. 1/2013 – Letters to the editor

Incidental corticobasal degeneration in a 76-year-old woman

Ivan Milenkovic and Gabor G. Kovacs

Institute of Neurology, Medical University of Vienna, Vienna, Austria
Correspondence to:
Gabor G. Kovacs, MD, PhD
Institute of Neurology, AKH 4J
Währinger Gürtel 18-20, 1097 Vienna, Austria
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 31 – No. 6/2012 (409-417)

Prominent oligodendroglial response in surgical specimens of patients with temporal lobe epilepsy

Harald Stefanits¹,², Thomas Czech², Ekaterina Pataraia³, Christoph Baumgartner⁴, Nina Derhaschnig¹,², Anka Slana¹,² and Gabor G. Kovacs¹

¹Institute of Neurology, ²Department of Neurosurgery, ³Department of Clinical Neurology, Medical University of Vienna, and ⁴Department of Neurology, General Hospital Hietzing with Neurological Center Rosenhügel, Vienna, Austria
Temporal lobe epilepsy (TLE) is characterized by distinct neuropathological findings, such as hippocampal sclerosis and reactive astrogliosis. Recently, MRI studies have revealed the presence of white matter pathology in brains of epilepsy patients. The purpose of this study is to evaluate the involvement of oligodendroglia in the epileptogenic process. Using TPPP/p25 as a marker for mature oligodendroglia, we evaluated the hippocampus in 26 surgical specimens from patients with TLE and 9 autopsy controls without neuropathological alterations for changes in oligodendroglial cell densities (mm²) in hippocampal, entorhinal, and temporal white matter, and the amount of perineuronal oligodendrocytes in CA1 subregion. Oligodendrocyte cell densities were significantly elevated in epilepsy patients compared to controls in all four examined white matter subregions. In addition, in the CA1 sector, the percentage of neurons showing more than one perineuronal oligodendrocyte was significantly higher in epilepsy patients. In conclusion, our study expands the glial reactions beyond astrogliosis and shows that prominent oligodendroglial response is a consistent pathological feature characteristic for TLE.Correspondence to:
Gabor G. Kovacs MD PhD
Institute of Neurology,
Medical University of Vienna, AKH 4J,
Waehringer Guertel 18-20
1090 Vienna, Austria
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 33 – No. 5/2014 (328)

Clinical Neuropathology image 5-2014: α-synuclein pathology in the ependyma in Parkinson’s disease

Gabor G. Kovacs

Correspondence to:
Gabor G. Kovacs, MD, PhD
Institute of Neurology
Medical University of Vienna, AKH 4J
Währinger Gürtel 18-20
1097 Vienna, Austria
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 33 – No. 5/2014 (329-334)

Detection of disease-associated α-synuclein in the cerebrospinal fluid: a feasibility study

Ursula Unterberger¹, Ingolf Lachmann², Till Voigtländer¹, Walter Pirker³, Anna S. Berghoff¹,⁴, Katharina Flach², Uta Wagner², Aline Geneste⁵, Armand Perret-Liaudet⁵, and Gabor G. Kovacs¹

¹Institute of Neurology, Medical University of Vienna, Vienna, Austria, ²AJ Roboscreen GmbH, Leipzig, Germany, ³Department of Neurology, ⁴present address: Department of Medicine I, Clinical Division of Oncology, Medical University of Vienna, Vienna, Austria, and ⁵Neurobiologie, CMRR, Hospices Civils de Lyon, Université Lyon, Lyon, France
With the aim to evaluate the significance and reliability of detecting disease-specific α-synuclein in the cerebrospinal fluid (CSF) we developed an ELISA and bead-assay. We used a commercial antibody (5G4) that does not bind to the physiological monomeric form of α-synuclein, but is highly specific for the disease-associated forms, including high molecular weight fraction of β-sheet rich oligomers. We applied both tests in CSF from a series of neuropathologically confirmed αsynucleinopathy cases, including Parkinson’ disease dementia (PDD) and dementia with Lewy bodies (DLB) (n = 7), as well as Alzheimer’ disease (n = 6), and control patients without neurodegenerative pathologies (n = 9). Disease-specific α-synuclein was detectable in the CSF in a subset of patients with α-synuclein pathology in the brain. When combined with the analysis of total α-synuclein, the bead-assay for disease-specific α-synuclein was highly specific for PDD/DLB. Detection of disease-associated αsynuclein combined with the total levels of α-synuclein is a promising tool for the in-vivo diagnosis of αsynucleinopathies, including PDD and LBD.Correspondence to:
Gabor G. Kovacs, MD, PhD
Institute of Neurology,
Medical University of Vienna
Waehringer Guertel 18-20
1097 Vienna, Austria
and
Armand Perret-Liaudet, PhD
Neurobiology, CBPE, Groupement Hospitalier Est
Hospices Civils de Lyon
59 Boulevard Pinel
69677 Bron cedex, France
Email: [email protected] or [email protected]

Abstract

Clinical Neuropathology, Vol. 33 – No. 6/2014 (378-379)

Clinical Neuropathology image 6-2014: Corpora amylacea replacing cornu ammonis (CACA)

Gabor G. Kovacs¹ and Daniele Risser²

¹Institute of Neurology and ²Department of Forensic Pathology, Medical University of Vienna, Vienna, Austria
Correspondence to:
Gabor G. Kovacs, MD, PhD
Institute of Neurology, AKH 4J
Währinger Gürtel 18-20
1097 Vienna, Austria
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 34 – No. 1/2015 (4-5)

Clinical Neuropathology image 1-2015: Crystal-storing histiocytosis of the central nervous system

Adelheid Woehrer and Gabor G. Kovacs

Institute of Neurology, Medical University of Vienna, Vienna, Austria
Correspondence to:
Adelheid Woehrer, MD, PhD
Institute of Neurology, AKH 4J
Währinger Gürtel 18-20
1097 Vienna, Austria
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 34 – No. 4/2015 (178-180)

Clinical Neuropathology teaching case 4-2015: Heterogenous brain pathologies temporally and spatially coinciding in limbic regions

Gabor G. Kovacs and Johannes A. Hainfellner

Institute of Neurology Medical University of Vienna, Vienna, Austria
Correspondence to:
Gabor G. Kovacs, MD, PhD
Institute of Neurology, AKH 4J
Währinger Gürtel 18-20
1097 Vienna, Austria
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 35 – No. 3/2016 (122-128)

Gaucher cells are not associated with α-synuclein neuropathology in infants

Evelyn Berger-Sieczkowski¹, Mirjam I. Lutz², Eduard Auff¹, and Gabor G. Kovacs²

¹Department of Neurology, Medical University of Vienna and ²Institute of Neurology, Medical University of Vienna, Vienna, Austria
A link between Gaucher disease (GD) and Parkinson disease (PD) has been suggested by many studies. Lewy-body-like α-synuclein inclusions have been shown in older GD patients who developed Parkinsonism. It has been proposed that decreased levels of glucocerebrosidase mediate impaired α-synuclein degradation and hence its accumulation. Nevertheless, this phenomenon is less investigated in the infantile form of GD. The aim of the study was to evaluate α-synuclein and τ-pathology in the brain and non-neural tissues (liver, spleen, pancreas, myocardial muscle, and lung) of 5 infants (age range from 1 month to 4 years) with GD. Our immunohistochemical study did not provide evidence that pathological α-synuclein or τ-accumulates early in tissues where Gaucher cells are already prominently present. Although recent finding of altered plasma α-synuclein levels in infantile GD patients suggest an early imbalance of α-synuclein homeostasis, our findings indicate that this does not inevitably coincide with α-synuclein pathology in the brain. Understanding this temporal variance of plasma levels and brain accumulation of α-synuclein might also be important when interpreting blood-based α-synuclein assays for the diagnosis of PD.Correspondence to:
Gabor G. Kovacs, MD PhD
Institute of Neurology, Medical University of Vienna, AKH 4J
Währinger Gürtel 18 – 20, 1097 Vienna, Austria
Email: [email protected]

Abstract

Atemwegs- und Lungenkrankheiten, Jahrgang 44, Nr. 1/2018, S. 39-50

Wirksamkeit, Sicherheit und Benutzerfreundlichkeit der Trockenpulver-Inhalation von Aclidiniumbromid bei COPD

H. Olschewski¹#⁴, R. Voves², E. Wallner³, S. Scheidl¹, G. Kovacs¹#⁴ und M. Trinker¹

¹Klinische Abteilung für Pulmonologie, Universitätsklinik für Innere Medizin, Medizinische Universität Graz, ²Ordination Dr. Robert Voves, Feldbach, ³A. Menarini Pharma GmbH, Wien, ⁴Ludwig Boltzmann Institut für Lungengefäßforschung, Graz, Österreich
Aclidiniumbromid ist ein langwirkendes, inhalierbares Anticholinergikum zur Behandlung der chronisch obstruktiven Lungenkrankheit (COPD). Die nicht interventionelle Studie ON AIR untersuchte die Wirksamkeit, Benutzerfreundlichkeit und Sicherheit von Aclidiniumbromid an 843 Patienten unter Alltagsbedingungen. Vor und während der Behandlung wurden die Krankheitsaktivität und die Erfahrungen der Patienten und Verordner strukturiert erfasst. Nach etwa 12 Wochen wurde bei 85% der Patienten eine klinisch relevante Verbesserung beobachtet, die nächtliche Beschwerden einschloss und in allen Schweregraden nachweisbar war. Insgesamt wurden sechs unerwünschte Ereignisse berichtet. Die Benutzerfreundlichkeit wurde von 65% der Patienten und 83% der Ärzte als sehr gut eingestuft. Kein Arzt und 1% der Patienten beurteilten die Benutzerfreundlichkeit als mäßig oder schlecht. Diese Daten stehen im Einklang mit randomisierten kontrollierten Studien zur Wirksamkeit und Sicherheit von Aclidiniumbromid.Correspondence to:
Univ.-Prof. Dr. med. Horst Olschewski
Klinische Abteilung für Pulmonologie
Universitätsklinik für Innere Medizin
Medizinische Universität Graz
Auenbruggerplatz 20
8036 Graz, Österreich
Email: [email protected]

Abstract

Clinical Neuropathology, Vol. 37 – No. 6/2018 (252-253)

Clinical Neuropathology image 6-2018: Metastasis of breast carcinoma to meningioma

Sigrid Klotz¹, Christian Matula², Matthias Pones³, Merima Herac¹#⁴, Anna Grisold⁵, Johannes A. Hainfellner¹, Gabor G. Kovacs¹, and Ellen Gelpi¹

¹Institute of Neurology, Medical University of Vienna, Vienna,  ²Department of Neurosurgery, Medical University of Vienna, Vienna,  ³Department of Radiology, Medical University of Vienna, Vienna,  ⁴Institute of Pathology, and ⁵Department of Neurology, Medical University  of Vienna, Vienna, Austria
Correspondence to:
Ellen Gelpi, MD, PhD, EFN
Institute of Neurology, Medical University of Vienna
AKH Leitstelle 4J
Währinger Gürtel 18 – 20, 1090 Vienna, Austria
and
Neurological Tissue Bank
Biobanc-Hospital Clinic-IDIBAPS
Barcelona, Spain
Email: [email protected] and [email protected]

Abstract

Clinical Neuropathology, Vol. 38 – No. 2/2019 (48-50)

Macrophagic scavenging of Aβ

Ellen Gelpi¹#², Sigrid Klotz¹, Alexandra Lang¹, Elisabeth Stögmann³, and Gabor G. Kovacs¹

¹Institute of Neurology, Medical University of Vienna, Vienna, Austria, ²Neurological Tissue Bank of the Biobanc-Hospital Clinic-IDIBAPS, Barcelona, Spain, and ³Department of Neurology, Medical University of Vienna, Vienna, Austria
Correspondence to:
Ellen Gelpi, MD, EFN
Institute of Neurology
Medical University of Vienna
Waehringer Guertel 18 – 20, 1090 Vienna, Austria
Email: ellen.gelpi@ meduniwien.ac.at

Abstract

Atemwegs- und Lungenkrankheiten, Jahrgang 48, Nr. 1/2022, S. 22-25

Pulmonale Hypertonie bei rheumatischen Erkrankungen

K. Zeder¹#², G. Kovacs¹#² und H. Olschewski¹#²

¹Ludwig Boltzmann Institut für Lungengefäßforschung, Graz, ²Klinische Abteilung für Pneumologie, Interne Medizin, Medizinische Universität Graz, Österreich
Das zentrale Symptom der pulmonalen Hypertonie ist die Belastungsdyspnoe. Bei vorliegender rheumatischer Grunderkrankung, insbesondere der systemischen Sklerose, sollte an die mögliche pulmonale Mitbeteiligung im Sinne einer pulmonalen Hypertonie gedacht werden. Das Screeningtool ist die Echokardiographie und ist bei der systemischen Sklerose einmal jährlich zu empfehlen. Die definitive Abklärung der PH sollte in einem spezialisierten Zentrum erfolgen und erfordert immer eine Rechtsherzkatheteruntersuchung.Correspondence to:
Assoz. Prof. Dr. Gabor Kovacs
Klinische Abteilung für Pneumologie
Interne Medizin, Medizinische Universität Graz
Auenbruggerplatz 15
8036 Graz, Österreich
Email: [email protected]

Abstract

Atemwegs- und Lungenkrankheiten, Jahrgang 49, Nr. 9/2023, S. 404-408

Definition und Klassifikation der pulmonalen Hypertonie

G. Kovacs

Medizinische Universität Graz, Universitätsklinik für Innere Medizin, Klinische Abteilung für Pulmonologie, Graz, Österreich
2022 wurden die aktuellen Leitlinien der European Society of Cardiology (ESC) und der European Respiratory Society (ERS) zur Diagnostik und Behandlung der pulmonalen Hypertonie (PH) veröffentlicht. In diesen Leitlinien wurden die hämodynamischen Definitionen der PH im Vergleich zu früheren europäischen Leitlinien geändert und auch die klinische Klassifikation der PH wurde modifiziert. Im Folgenden soll ein Überblick über diese Änderungen gegeben werden und es soll erklärt werden, welche Überlegungen dazu geführt haben und welche Bedeutung sie in der klinischen Praxis haben werden.Correspondence to:
Assoz. Prof. Dr. Gabor Kovacs
Medizinische Universität Graz
Universitätsklinik für Innere Medizin
Klinische Abteilung für Pulmonologie
Auenbruggerplatz 20
8036 Graz, Österreich
Email: [email protected]

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