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Brain Pathology

D Bodez, S Georgin-Lavialle, G Grateau, D Buob
We would like to comment on the "Case of the Month" by Magaki et al, entitled "A 44-year old female with familial Mediterranean fever, cardiomyopathy, and end stage renal disease" (3). In this case report, the authors describe the autopsy findings in a patient with systemic AA amyloidosis secondary to familial Mediterranean fever. The patient also had cardiomyopathy with severely reduced left ventricular ejection and death due to cardiac arrest; however, no details about cardiovascular risk factors, cardiac pre-mortem explorations, and heart gross examination were provided...
February 1, 2019: Brain Pathology
Jan Traub, Sarah Traffehn, Jasmin Ochs, Silke Häusser-Kinzel, Schirin Stephan, Robert Scannevin, Wolfgang Brück, Imke Metz, Martin S Weber
In multiple sclerosis (MS), the effect of dimethyl fumarate (DMF) treatment is primarily attributed to its capacity to dampen pathogenic T cells. Here, we tested whether DMF also modulates B cells, which are newly recognized key players in MS, and to which extent DMF restricts ongoing loss of oligodendrocytes and axons in the central nervous system (CNS). Therefore, blood samples and brain tissue from DMF-treated MS patients were analyzed by flow cytometry or histopathological examination, respectively. Complementary mechanistic studies were conducted in inflammatory as well as non-inflammatory CNS demyelinating mouse models...
January 31, 2019: Brain Pathology
Jens Schittenhelm, Nadin Krischker, Irina Gepfner-Tuma, Felix Behling, Susan Noell, Franziska Eckert, Saskia Biskup, Ghazaleh Tabatabai
Kirsten rat sarcoma viral oncogene homolog (KRAS) belongs to the RAS oncogene family that encode intracellular signal transduction proteins (guanosine triphosphate hydrolases (GTPases) which regulate cell proliferation, motility, and apoptosis [9]. KRAS mutations account for up to 85% of RAS mutations in all human tumors. Cancer KRAS hotspot mutations at codons 12/13 and 61 usually prevent Ras protein from hydrolysing GTP and thus the protein remains in the active state [9]. While KRAS mutations are currently not druggable per se, the detection of KRAS mutations serves as a biomarker for targeted anti-cancer therapies and predicts therapeutic response, e...
January 24, 2019: Brain Pathology
Ana R Malheiro, Barbara Correia, Tiago Ferreira da Silva, Diogo Bessa-Neto, Paul P Van Veldhoven, Pedro Brites
Plasmalogens are the most abundant form of ether-phospholipids in myelin and their deficiency causes Rhizomelic Chondrodysplasia Punctata (RCDP), a severe developmental disorder. Using the Gnpat knockout (KO) mouse as a model of RCDP, we determined the consequences of a plasmalogen deficiency during myelination and myelin homeostasis in the central nervous system (CNS). We unraveled that the lack of plasmalogens causes a generalized hypomyelination in several CNS regions including optic nerve, corpus callosum and spinal cord...
January 22, 2019: Brain Pathology
Allison McIntosh, Virginia Mela, Conor Harty, Aedin M Minogue, Derek A Costello, Christian Kerskens, Marina A Lynch
Among the changes that typify Alzheimer's disease (AD) are neuroinflammation and microglial activation, amyloid deposition perhaps resulting from compromised microglial function, and iron accumulation. Data from Genome Wide Association Studies (GWAS) identified a number of gene variants that endow a significant risk of developing AD and several of these encode proteins expressed in microglia, and proteins that are implicated in the immune response. This suggests that neuroinflammation and the accompanying microglial activation are likely to contribute to the pathogenesis of the disease...
January 20, 2019: Brain Pathology
Oscar H Del Brutto
I read with interest the paper of Mejia Maza and coworkers on the presence of axonal swelling and spheroids development in humans, pigs and rats with neurocysticercosis [8]. Taking the advantage of a novel rat model of Taenia solium cysticercosis, the authors found not only local inflammatory changes in the brain parenchyma surrounding cysticerci, but axonal swelling with spheroid formation at a considerable distance from the parasites. From what can be understood from their work, these axons originated in neurons located near the parasites that were damaged as the result of inflammatory changes surrounding parenchymal brain cysticerci...
January 13, 2019: Brain Pathology
Robert H Gilman, Rogger P Carmen-Orozco, Emma Carter, Manuela R Verastegui
We appreciate Dr. Del Brutto's comments concerning our article entitled "Axonal swellings and spheroids: a new insight into the pathology of neurocysticercosis (NCC)'' (5). Axonal swellings have only recently been described in neurocysticercosis. While we agree with Dr. Del Brutto's view that axonal swellings can be the result of neuronal damage due to inflammatory change surrounding parenchymal brain cysts,,any injury to the axon as occurs with trauma, toxins, shearing or hypoxia will also produce this response...
January 13, 2019: Brain Pathology
Xavier Gallart-Palau, Aida Serra, Yoshiki Hase, Chee Fan Tan, Christopher P Chen, Raj N Kalaria, Siu Kwan Sze
Vascular factors that reduce blood flow to the brain are involved in apparition and progression of dementia. We hypothesized that cerebral hypoperfusion (CH) might alter the molecular compositions of brain intercellular communication mechanisms while affecting the neurovascular unit in preclinical and clinical human dementias. To test that hypothesis, mice were subjected to bilateral common carotid stenosis (BCAS) and the molecular compositions of brain-derived and circulating extracellular vesicles (EVs) were assessed...
January 10, 2019: Brain Pathology
Nhat T T Le, Bei Wu, David A Harris
Although the mechanisms underlying prion propagation and infectivity are now well established, the processes accounting for prion toxicity and pathogenesis have remained mysterious. These processes are of enormous clinical relevance, since they hold the key to identification of new molecular targets for therapeutic intervention. In this review, we will discuss two broad areas of investigation relevant to understanding prion neurotoxicity. The first is the use of in vitro experimental systems that model key events in prion pathogenesis...
December 26, 2018: Brain Pathology
Simone Baiardi, Marcello Rossi, Sabina Capellari, Piero Parchi
Prion diseases are progressive neurodegenerative disorders affecting humans and other mammalian species. The term prion, originally put forward to propose the concept that a protein could be infectious, refers to PrPS c , a misfolded isoform of the cellular prion protein (PrPC ) that represents the pathogenetic hallmark of these disorders. The discovery that other proteins characterized by misfolding and seeded aggregation can spread from cell to cell, similarly to PrPS c , has increased interest in prion diseases...
December 26, 2018: Brain Pathology
Fiona Houston, Olivier Andréoletti
Transmissible spongiform encephalopathies (TSEs) or prion diseases of animals notably include scrapie in small ruminants, chronic wasting disease (CWD) in cervids, and classical bovine spongiform encephalopathy (C-BSE). Due to the transmission barrier phenomenon that naturally limits the propagation of prions from one species to another, and the lack of epidemiological evidence for an association with human prion diseases, the zoonotic potential of these diseases was for a long time considered negligible. However, in 1996 C-BSE was recognized as the cause of a new human prion disease, variant Creutzfeldt-Jakob disease (vCJD), which triggered an unprecedented public health crisis in Europe...
December 26, 2018: Brain Pathology
Markus Glatzel, Christina J Sigurdson
Prion diseases continue to fascinate scientists from different disciplines since the discovery that a misfolded prion protein can act as an infectious agent. Infectious prions have caused epidemics, including kuru in humans, cervid chronic wasting disease, bovine spongiform encephalopathy (BSE) or "mad cow disease", and most recently, camel prion disease, which was identified in 2018 (1). In Kuru, spread of the disease occurred from the ingestion of prion-infected, dead relatives as part of mourning practices, whereas in chronic wasting disease, prions may be transmitted not only through ingesting prion-contaminated food, but also by exposure to a prion-contaminated environment(8, 9)...
December 26, 2018: Brain Pathology
Lina Patterson, Steven P Rushton, Johannes Attems, Alan J Thomas, Christopher M Morris
AIMS: Depression is commonly observed even in prodromal stages of Lewy body disorders (LBD), and is associated with cognitive impairment and a faster rate of cognitive decline. Given the role of dopamine in the development of movement disorders, but also in motivation and reward, we investigated neurodegenerative pathology in dopaminergic circuitry in Parkinson's disease (PD), PD with dementia (PDD) and dementia with Lewy bodies (DLB) patients in relation to depressive symptoms. METHODS: α-synuclein, hyperphosphorylated tau and amyloid beta pathology was assessed in 17 DLB, 14 PDD and 8 PD cases within striatal and midbrain subregions, with neuronal cell density assessed in substantia nigra and ventral tegmental area...
December 24, 2018: Brain Pathology
Xiaona Zhang, Yuandi Xi, Huiyan Yu, Yu An, Ying Wang, Lingwei Tao, Yushan Wang, Wen Liu, Tao Wang, Rong Xiao
The oxysterol 27-hydroxycholesterol (27-OHC) has been considered to play a key role in the pathogenesis of Alzheimer's disease (AD). Because β-amyloid peptide (Aβ) is the pathological hallmark of AD, the aim of this study is to verify whether 27-OHC could lead to cognitive impairment through modulating Aβ accumulation and deposition. Regulation of Aβ metabolism was explored as the pathogenic mechanism of 27-OHC. Furthermore, microRNAs (miRNAs) and their relations with 27-OHC were also detected. In present study, matched case-control study and APP/PS1 transgenic mice research were conducted...
December 23, 2018: Brain Pathology
Chunyu Wang, Fanpeng Zhao, Katie Shen, Wenzhang Wang, Sandra L Siedlak, Hyoung-Gon Lee, Clyde F Phelix, George Perry, Lu Shen, Beisha Tang, Riqiang Yan, Xiongwei Zhu
Disturbed neuronal cholesterol homeostasis has been observed in Alzheimer disease (AD) and contributes to the pathogenesis of AD. As the master switch of cholesterol biosynthesis, the sterol regulatory element-binding protein 2 (SREBP-2) translocates to the nucleus after cleavage/activation, but its expression and activation have not been studied in AD which is the focus of the current study. We found both a significant decrease in the nuclear translocation of N-terminal SREBP-2 accompanied by a significant accumulation of C-terminal SREBP-2 in NFT-containing pyramidal neurons in AD...
December 4, 2018: Brain Pathology
Yu-Ting Hu, Xin-Lu Chen, Shu-Han Huang, Qiong-Bin Zhu, Si-Yang Yu, Yi Shen, Arja Sluiter, Joost Verhaagen, Juan Zhao, Dick Swaab, Ai-Min Bao
Our previous studies showed that the transcription factor early growth response-1 (EGR1) may play a role in keeping the brain cholinergic function intact in the preclinical stages of Alzheimer's disease (AD). In order to elucidate the mechanisms involved, we first performed data mining on our previous microarray study on postmortem human prefrontal cortex (PFC) for the changes in the expression of EGR1 and acetylcholinesterase (AChE) and the relationship between them during the course of AD. The study contained 49 patients, ranging from non-demented controls (Braak stage 0) to late AD patients (Braak stage VI)...
December 3, 2018: Brain Pathology
Pia S Zeiner, Corinna Preusse, Anna Golebiewska, Jenny Zinke, Ane Iriondo, Arnaud Muller, Tony Kaoma, Katharina Filipski, Monika Müller-Eschner, Simon Bernatz, Anna-Eva Blank, Peter Baumgarten, Elena Ilina, Anne Grote, Martin L Hansmann, Marcel A Verhoff, Kea Franz, Friedrich Feuerhake, Joachim P Steinbach, Jörg Wischhusen, Werner Stenzel, Simone P Niclou, Patrick N Harter, Michel Mittelbronn
While the central nervous system is considered an immunoprivileged site and brain tumors display immunosuppressive features, both innate and adaptive immune responses affect glioblastoma (GBM) growth and treatment resistance. However, the impact of the major immune cell population in gliomas, represented by glioma-associated microglia/macrophages (GAMs), on patients' clinical course is still unclear. Thus, we aimed at assessing the immunohistochemical expression of selected microglia and macrophage markers in 344 gliomas (including gliomas from WHO grade I-IV)...
December 3, 2018: Brain Pathology
Pierre De Rossi, Robert J Andrew, Timothy F Musial, Virginie Buggia-Prevot, Guilian Xu, Moorthi Ponnusamy, Han Ly, Sofia V Krause, Richard C Rice, Valentine de l'Estoile, Tess Valin, Someya Salem, Florin Despa, David R Borchelt, Vytas P Bindokas, Daniel A Nicholson, Gopal Thinakaran
BIN1 is the most significant late-onset Alzheimer's Disease (AD) susceptibility locus identified via genome-wide association studies. BIN1 is an adaptor protein that regulates membrane dynamics in the context of endocytosis and membrane remodeling. An increase in BIN1 expression and changes in the relative levels of alternatively-spliced BIN1 isoforms have been reported in the brains of patients with AD. BIN1 can bind to Tau, and an increase of BIN1 expression correlates with Tau pathology. In contrast, the loss of BIN1 expression in cultured cells elevates Aβ production and Tau propagation by influencing endocytosis and recycling...
November 30, 2018: Brain Pathology
Kirsty E McAleese, Sophie Graham, Madhurima Dey, Lauren Walker, Daniel Erskine, Mary Johnson, Eleanor Johnston, Alan J Thomas, Ian G McKeith, Charles DeCarli, Johannes Attems
The blood-brain barrier (BBB) regulates cerebrovascular permeability and leakage of blood-derived fibrinogen has been associated with cerebral arteriolosclerosis small vessel disease (SVD) and subsequent white matter lesions (WML). Furthermore, BBB-dysfunction is associated with the pathogenesis of Alzheimer's disease (AD) with the presence of CSF plasma proteins suggested to be a potential biomarker of AD. We aimed to determine if extravascular fibrinogen in the white matter was associated with the development of AD hallmark pathologies, i...
November 28, 2018: Brain Pathology
Barbora Benova, Thomas S Jacques
Malformations of cortical development (MCD) comprise a broad spectrum of developmental brain abnormalities. Patients presenting with MCDs often suffer from drug resistant focal epilepsy, and some become candidates for epilepsy surgery. Their likelihood of achieving freedom from seizures, however, remains uncertain, and depends in a major part on the underlying pathology. Tissue samples obtained in epilepsy surgery form the basis of definite histopathological diagnosis; however, new molecular-genetic methods have not yet been implemented in diagnostic process for MCD cases...
November 28, 2018: Brain Pathology
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