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Brain Pathology

Theresa Scholl, Angelika Mühlebner, Gerda Ricken, Victoria Gruber, Anna Fabing, Sharon Samueli, Gudrun Gröppel, Christian Dorfer, Thomas Czech, Johannes A Hainfellner, Avanita S Prabowo, Roy J Reinten, Lisette Hoogendijk, Jasper J Anink, Eleonora Aronica, Martha Feucht
Conventional antiepileptic drugs suppress the excessive firing of neurons during seizures. In drug-resistant patients, treatment failure indicates an alternative important epileptogenic trigger. Two epilepsy-associated pathologies show myelin deficiencies in seizure-related brain regions: Focal Cortical Dysplasia IIB (FCD) and cortical tubers in Tuberous Sclerosis Complex (TSC). Studies uncovering white matter-pathology mechanisms are therefore urgently needed to gain more insight into epileptogenesis, the propensity to maintain seizures, and their associated comorbidities such as cognitive defects...
October 17, 2016: Brain Pathology
Monika Albert, Alonso Barrantes-Freer, Melanie Lohrberg, Jack P Antel, John W Prineas, Miklós Palkovits, Joachim R Wolff, Wolfgang Brück, Christine Stadelmann
In multiple sclerosis, cerebellar symptoms are associated with clinical impairment and an increased likelihood of progressive course. Cortical atrophy and synaptic dysfunction play a prominent role in cerebellar pathology and although the dentate nucleus is a predilection site for lesion development, structural synaptic changes in this region remain largely unexplored. Moreover, the mechanisms leading to synaptic dysfunction have not yet been investigated at an ultrastructural level in multiple sclerosis. Here we report on synaptic changes of dentate nuclei in post-mortem cerebella of 16 multiple sclerosis patients and eight controls at the histological level as well as an electron microscopy evaluation of afferent synapses of the cerebellar dentate and pontine nuclei of one multiple sclerosis patient and one control...
October 5, 2016: Brain Pathology
Pawel Tacik, Michael A DeTure, Yari Carlomagno, Wen-Lang Lin, Melissa E Murray, Matthew C Baker, Keith A Josephs, Bradley F Boeve, Zbigniew K Wszolek, Neill R Graff-Radford, Joseph E Parisi, Leonard Petrucelli, Rosa Rademakers, Richard S Isaacson, Kenneth M Heilman, Ronald C Petersen, Dennis W Dickson, Naomi Kouri
Mutations in microtubule-associated protein tau gene (MAPT) cause frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17). Here, we describe a patient with FTDP-17 and a novel missense mutation in exon 13 of MAPT, p.E372G. We compare clinicopathologic features of this patient to two previously unreported patients with another exon 13 mutation, p.G389R. The patient with the p.E372G mutation was a 40-year-old man with behavioral variant frontotemporal dementia (bvFTD), who subsequently developed agrammatic speech and parkinsonism...
October 5, 2016: Brain Pathology
Arnault Cazorla, Alain Czorny, Aalain Cangemi, Gabriel Viennet
No abstract text is available yet for this article.
September 20, 2016: Brain Pathology
Patrick J Cimino, Richard J Perrin
No abstract text is available yet for this article.
September 20, 2016: Brain Pathology
Danijela Oštrić, Marija Todosijević, Anja Jeričević, Saša Šega Jazbec, Mara Popović
No abstract text is available yet for this article.
September 20, 2016: Brain Pathology
Jiancong Liang, Jenny Libien, Yuetsu Tanaka, Constantine A Axiotis, Charles Shao, Jinli Liu
No abstract text is available yet for this article.
September 20, 2016: Brain Pathology
Pankaj Pathak, Anupam Kumar, Prerana Jha, Suvendu Purkait, Mohammed Faruq, Ashish Suri, Vaishali Suri, Mehar C Sharma, Chitra Sarkar
Pilocytic astrocytomas occur rarely in adults and show aggressive tumor behavior. However, their underlying molecular-genetic events are largely uncharacterized. Hence, we studied 59 adult pilocytic astrocytoma (APA) cases of classical histology (MIB-1 LI:1-5%). Analysis of BRAF alterations using qRT-PCR, confirmed KIAA1549-BRAF fusion in 11(19%) and BRAF-gain in 2(3.4%) cases. BRAF-V600E mutation was noted in 1(1.7%) case by sequencing. FGFR1-mutation and FGFR-TKD duplication were seen in 7/59(11.9%) and 3/59(5%) cases respectively...
September 8, 2016: Brain Pathology
Kiyomitsu Oyanagi, Michiaki Kinoshita, Emi Suzuki-Kouyana, Teruhiko Inoue, Asa Nakahara, Mika Tokiwai, Nobutaka Arai, Jun-Ichi Satoh, Naoya Aoki, Kenji Jinnai, Ikuru Yazawa, Kimihito Arai, Kenji Ishihara, Mitsuru Kawamura, Keisuke Ishizawa, Kazuko Hasegawa, Saburo Yagisita, Naoji Amano, Kunihiro Yoshida, Seishi Terada, Mari Yoshida, Haruhiko Akiyama, Yoshio Mitsuyama, Shu-Ichi Ikeda
The brains of 10 Japanese patients with adult onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) encompassing hereditary diffuse leukoencephalopathy with axonal spheroids (HDLS) and pigmentary orthochromatic leukodystrophy (POLD) and eight Japanese patients with Nasu-Hakola disease (N-HD) and five age-matched Japanese controls were examined neuropathologically with special reference to lesion staging and dynamic changes of microglial subsets. In both diseases, the pathognomonic neuropathological features included spherically swollen axons (spheroids and globules), axon loss and changes of microglia in the white matter...
September 8, 2016: Brain Pathology
Thomas Arendt, Markus Morawski, Ulrich Gärtner, Nadine Fröhlich, Falko Schulze, Nils Wohmann, Carsten Jäger, Christian Eisenlöffel, Hermann-Josef Gertz, Wolf Mueller, Kurt Brauer
Alzheimeŕs disease (AD) is neuropathologically characterized by neuritic plaques and neurofibrillary tangles. Progression of both plaques and tangles throughout the brain follows a hierarchical distribution which is defined by intrinsic cytoarchitectonic features and extrinsic connectivity patterns. What has less well been studied is how cortical convolutions influence the distribution of AD pathology. Here, we systematically compared the distribution of both plaques and tangles within subsulcal gyral components (fundi) to components forming their top regions at the subarachnoidal brain surface (crowns) by stereological methods in seven different cortical areas...
August 26, 2016: Brain Pathology
Christiane Muth, Katharina Schröck, Charlotte Madore, Kristin Hartmann, Zain Fanek, Oleg Butovsky, Markus Glatzel, Susanne Krasemann
Prion diseases are fatal transmissible diseases, where conversion of the endogenous prion protein (PrP(C) ) into a misfolded isoform (PrP(Sc) ) leads to neurodegeneration. Microglia, the immune cells of the brain, are activated in neurodegenerative disorders including prion diseases, however their impact on prion disease pathophysiology is unclear with both beneficial PrP(Sc) -clearing and detrimental potentially neurotoxic effects. Moreover, monocytes entering the brain from the periphery during disease course might add to disease pathophysiology...
August 25, 2016: Brain Pathology
Franck Bielle, François Ducray, Karima Mokhtari, Caroline Dehais, Homa Adle-Biassette, Catherine Carpentier, Anaïs Chanut, Marc Polivka, Sylvie Poggioli, Shaï Rosenberg, Marine Giry, Yannick Marie, Charles Duyckaerts, Marc Sanson, Pola Network, Dominique Figarella-Branger, Ahmed Idbaih
The integrated diagnosis of anaplastic oligodendroglioma, IDH mutant and 1p/19q co-deleted, grade III (O3(id) ) is a histomolecular entity that WHO 2016 classification distinguished from other diffuse gliomas by specific molecular alterations. In contrast, its cell portrait is less well-known. The present study is focused on intertumor and intratumor, cell lineage-oriented, heterogeneity in O3(id) . Based on pathological, transcriptomic and immunophenotypic studies, a novel subgroup of newly diagnosed O3(id) overexpressing neuronal intermediate progenitor (NIP) genes was identified...
August 20, 2016: Brain Pathology
Carmen Infante-Garcia, Juan Jose Ramos-Rodriguez, Yolanda Marin-Zambrana, Maria Teresa Fernandez-Ponce, Lourdes Casas, Casimiro Mantell, Monica Garcia-Alloza
Epidemiological studies reveal that metabolic disorders, and specifically type 2 diabetes (T2D), are relevant risk factors to develop Alzheimer's disease (AD) and vascular dementia (VaD), the most common causes of dementia. Due to the limited success of available treatments, AD patients are in a tremendous need of new therapeutic options. Natural polyphenols, and concretely Mangifera indica Linn extract (MGF), have been reported to have antiinflammatory, antioxidant and antidiabetic activities. We have analyzed the role of MGF in central complications associated with T2D, after long-term treatment of db/db mice with MGF...
August 18, 2016: Brain Pathology
Mar Puigdellívol, Ana Saavedra, Esther Pérez-Navarro
One of the main focuses in Huntington's disease (HD) research, as well as in most of the neurodegenerative diseases, is the development of new therapeutic strategies, as currently there is no treatment to delay or prevent the progression of the disease. Neuronal dysfunction and neuronal death in HD are caused by a combination of interrelated pathogenic processes that lead to motor, cognitive and psychiatric symptoms. Understanding how mutant huntingtin impacts on a plethora of cellular functions could help to identify new molecular targets...
August 16, 2016: Brain Pathology
Isidro Ferrer
No abstract text is available yet for this article.
August 16, 2016: Brain Pathology
Marta Fernández-Nogales, María Santos-Galindo, Ivó H Hernández, Jorge R Cabrera, José J Lucas
Huntington's disease (HD) is caused by a CAG-repeat encoding a polyglutamine (polyQ) tract in the huntingtin protein. There is plenty of evidence of polyQ-driven toxicity. However, CAG repeat RNA-driven alteration of splicing has recently been proposed in analogy to CUG-repeat diseases. Here we review the reported alteration of the CAG-repeat associated splicing factor SRSF6 in brains of HD patients and mouse models and how this correlates with altered splicing of, at least, two microtubule-associated proteins in HD, namely MAPT (tau) and MAP2...
August 16, 2016: Brain Pathology
Malvindar K Singh-Bains, Henry J Waldvogel, Richard L M Faull
Huntington's disease (HD) is characterized by pronounced pathology of the basal ganglia, with numerous studies documenting the pattern of striatal neurodegeneration in the human brain. However, a principle target of striatal outflow, the globus pallidus (GP), has received limited attention in comparison, despite being a core component of the basal ganglia. The external segment (GPe) is a major output of the dorsal striatum, connecting widely to other basal ganglia nuclei via the indirect motor pathway. The internal segment (GPi) is a final output station of both the direct and indirect motor pathways of the basal ganglia...
August 16, 2016: Brain Pathology
Eulàlia Martí
Huntington's disease (HD) belongs to the group of inherited polyglutamine (PolyQ) diseases caused by an expanded CAG repeat in the coding region of the Huntingtin (HTT) gene that results in an elongated polyQ stretch. Abnormal function and aggregation of the mutant protein has been typically delineated as the main molecular cause underlying disease development. However, the most recent advances have revealed novel pathogenic pathways directly dependent on an RNA toxic gain-of-function. Expanded CAG repeats within exon 1 of the HTT mRNA induce toxicity through mechanisms involving, at least in part, gene expression perturbations...
August 16, 2016: Brain Pathology
U Rüb, K Seidel, H Heinsen, J P Vonsattel, W F den Dunnen, H W Korf
Huntington's disease (HD) is an autosomal dominantly inherited, and currently untreatable, neuropsychiatric disorder. This progressive and ultimately fatal disease is named after the American physician George Huntington and according to the underlying molecular biological mechanisms is assigned to the human polyglutamine or CAG-repeat diseases. In the present article we give an overview of the currently known neurodegenerative hallmarks of the brains of HD patients. Subsequent to recent pathoanatomical studies the prevailing reductionistic concept of HD as a human neurodegenerative disease, which is primarily and more or less exclusively confined to the striatum (i...
August 16, 2016: Brain Pathology
Michael Qize Jiang, Ying-Ying Zhao, Wenyuan Cao, Zheng Zachory Wei, Xiaohuan Gu, Ling Wei, Shan Ping Yu
Focal cerebral ischemia results in an ischemic core surrounded by the peri-infarct region (penumbra). Most research attention has been focused on penumbra while the pattern of cell fates inside the ischemic core is poorly defined. In the present investigation, we tested the hypothesis that, inside the ischemic core, some neuronal and vascular cells could survive the initial ischemic insult while regenerative niches might exist many days after stroke in the adult brain. Adult mice were subjected to focal cerebral ischemia induced by permanent occlusion of distal branches of the middle cerebral artery (MCA) plus transient ligations of bilateral common carotid artery (CCA)...
August 11, 2016: Brain Pathology
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