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Acta Neuropathologica Communications

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https://www.readbyqxmd.com/read/28228164/erratum-to-mitochondrial-dna-point-mutations-and-relative-copy-number-in-1363-disease-and-control-human-brains
#1
Wei Wei, Michael J Keogh, Ian Wilson, Jonathan Coxhead, Sarah Ryan, Sara Rollinson, Helen Griffin, Marzena Kurzawa-Akanbi, Mauro Santibanez-Koref, Kevin Talbot, Martin R Turner, Chris-Anne McKenzie, Claire Troakes, Johannes Attems, Colin Smith, Safa Al Sarraj, Christopher M Morris, Olaf Ansorge, Stuart Pickering-Brown, James W Ironside, Patrick F Chinnery
No abstract text is available yet for this article.
February 22, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28212663/isolation-of-primary-microglia-from-the-human-post-mortem-brain-effects-of-ante-and-post-mortem-variables
#2
Mark R Mizee, Suzanne S M Miedema, Marlijn van der Poel, Adelia, Karianne G Schuurman, Miriam E van Strien, Jeroen Melief, Joost Smolders, Debbie A Hendrickx, Kirstin M Heutinck, Jörg Hamann, Inge Huitinga
Microglia are key players in the central nervous system in health and disease. Much pioneering research on microglia function has been carried out in vivo with the use of genetic animal models. However, to fully understand the role of microglia in neurological and psychiatric disorders, it is crucial to study primary human microglia from brain donors. We have developed a rapid procedure for the isolation of pure human microglia from autopsy tissue using density gradient centrifugation followed by CD11b-specific cell selection...
February 17, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28212662/marked-central-nervous-system-pathology-in-cd59-knockout-rats-following-passive-transfer-of-neuromyelitis-optica-immunoglobulin-g
#3
Xiaoming Yao, Alan S Verkman
Neuromyelitis optica spectrum disorders (herein called NMO) is an inflammatory demyelinating disease of the central nervous system in which pathogenesis involves complement-dependent cytotoxicity (CDC) produced by immunoglobulin G autoantibodies targeting aquaporin-4 (AQP4-IgG) on astrocytes. We reported evidence previously, using CD59(-/-) mice, that the membrane-associated complement inhibitor CD59 modulates CDC in NMO (Zhang and Verkman, J. Autoimmun. 53:67-77, 2014). Motivated by the observation that rats, unlike mice, have human-like complement activity, here we generated CD59(-/-) rats to investigate the role of CD59 in NMO and to create NMO pathology by passive transfer of AQP4-IgG under conditions in which minimal pathology is produced in normal rats...
February 17, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28173876/high-plasticity-of-axonal-pathology-in-alzheimer-s-disease-mouse-models
#4
Lidia Blazquez-Llorca, Susana Valero-Freitag, Eva Ferreira Rodrigues, Ángel Merchán-Pérez, J Rodrigo Rodríguez, Mario M Dorostkar, Javier DeFelipe, Jochen Herms
Axonal dystrophies (AxDs) are swollen and tortuous neuronal processes that are associated with extracellular depositions of amyloid β (Aβ) and have been observed to contribute to synaptic alterations occurring in Alzheimer's disease. Understanding the temporal course of this axonal pathology is of high relevance to comprehend the progression of the disease over time. We performed a long-term in vivo study (up to 210 days of two-photon imaging) with two transgenic mouse models (dE9xGFP-M and APP-PS1xGFP-M)...
February 7, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28153046/mitochondrial-dna-point-mutations-and-relative-copy-number-in-1363-disease-and-control-human-brains
#5
Wei Wei, Michael J Keogh, Ian Wilson, Jonathan Coxhead, Sarah Ryan, Sara Rollinson, Helen Griffin, Marzena Kurzawa-Akinibi, Mauro Santibanez-Koref, Kevin Talbot, Martin R Turner, Chris-Anne McKenzie, Claire Troakes, Johannes Attems, Colin Smith, Safa Al Sarraj, Christopher M Morris, Olaf Ansorge, Stuart Pickering-Brown, James W Ironside, Patrick F Chinnery
Mitochondria play a key role in common neurodegenerative diseases and contain their own genome: mtDNA. Common inherited polymorphic variants of mtDNA have been associated with several neurodegenerative diseases, and somatic deletions of mtDNA have been found in affected brain regions. However, there are conflicting reports describing the role of rare inherited variants and somatic point mutations in neurodegenerative disorders, and recent evidence also implicates mtDNA levels. To address these issues we studied 1363 post mortem human brains with a histopathological diagnosis of Parkinson's disease (PD), Alzheimer's disease (AD), Frontotemporal dementia - Amyotrophic Lateral Sclerosis (FTD-ALS), Creutzfeldt Jacob disease (CJD), and healthy controls...
February 2, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28148299/propagation-of-pathological-%C3%AE-synuclein-in-marmoset-brain
#6
Aki Shimozawa, Maiko Ono, Daisuke Takahara, Airi Tarutani, Sei Imura, Masami Masuda-Suzukake, Makoto Higuchi, Kazuhiko Yanai, Shin-Ichi Hisanaga, Masato Hasegawa
α-Synuclein is a defining, key component of Lewy bodies and Lewy neurites in Parkinson's disease (PD) and dementia with Lewy bodies (DLB), as well as glial cytoplasmic inclusions in multiple system atrophy (MSA). The distribution and spreading of these pathologies are closely correlated with disease progression. Recent studies have revealed that intracerebral injection of synthetic α-synuclein fibrils or pathological α-synuclein prepared from DLB or MSA brains into wild-type or transgenic animal brains induced prion-like propagation of phosphorylated α-synuclein pathology...
February 2, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28143577/aav1-2-induced-overexpression-of-a53t-%C3%AE-synuclein-in-the-substantia-nigra-results-in-degeneration-of-the-nigrostriatal-system-with-lewy-like-pathology-and-motor-impairment-a-new-mouse-model-for-parkinson-s-disease
#7
Chi Wang Ip, Laura-Christin Klaus, Akua A Karikari, Naomi P Visanji, Jonathan M Brotchie, Anthony E Lang, Jens Volkmann, James B Koprich
α-Synuclein is a protein implicated in the etiopathogenesis of Parkinson's disease (PD). AAV1/2-driven overexpression of human mutated A53T-α-synuclein in rat and monkey substantia nigra (SN) induces degeneration of nigral dopaminergic neurons and decreases striatal dopamine and tyrosine hydroxylase (TH). Given certain advantages of the mouse, especially it being amendable to genetic manipulation, translating the AAV1/2-A53T α-synuclein model to mice would be of significant value. AAV1/2-A53T α-synuclein or AAV1/2 empty vector (EV) at a concentration of 5...
February 1, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28137310/serum-microrna-mir-501-3p-as-a-potential-biomarker-related-to-the-progression-of-alzheimer-s-disease
#8
Norikazu Hara, Masataka Kikuchi, Akinori Miyashita, Hiroyuki Hatsuta, Yuko Saito, Kensaku Kasuga, Shigeo Murayama, Takeshi Ikeuchi, Ryozo Kuwano
MicroRNAs (miRNAs) are attractive molecules to utilize as one of the blood-based biomarkers for neurodegenerative disorders such as Alzheimer's disease (AD) because miRNAs are relatively stable in biofluid, including serum or plasma. To determine blood miRNA biomarkers for AD with next-generation sequencing genome-wide, we first surveyed 45 serum samples. These came from 27 AD patients and 18 controls (discovery set) that underwent autopsy within two weeks after their serum sampling and were neuropathologically diagnosed...
January 31, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28126008/elevated-tmem106b-levels-exaggerate-lipofuscin-accumulation-and-lysosomal-dysfunction-in-aged-mice-with-progranulin-deficiency
#9
Xiaolai Zhou, Lirong Sun, Owen Adam Brady, Kira A Murphy, Fenghua Hu
Mutations resulting in haploinsufficiency of progranulin (PGRN) cause frontotemporal lobar degeneration with TDP-43-positive inclusions (FTLD-TDP), a devastating neurodegenerative disease. Accumulating evidence suggest a crucial role of progranulin in maintaining proper lysosomal function during aging. TMEM106B has been identified as a risk factor for frontotemporal lobar degeneration with progranulin mutations and elevated mRNA and protein levels of TMEM106B are associated with increased risk for frontotemporal lobar degeneration...
January 26, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28109312/locus-coeruleus-cellular-and-molecular-pathology-during-the-progression-of-alzheimer-s-disease
#10
Sarah C Kelly, Bin He, Sylvia E Perez, Stephen D Ginsberg, Elliott J Mufson, Scott E Counts
A major feature of Alzheimer's disease (AD) is the loss of noradrenergic locus coeruleus (LC) projection neurons that mediate attention, memory, and arousal. However, the extent to which the LC projection system degenerates during the initial stages of AD is still under investigation. To address this question, we performed tyrosine hydroxylase (TH) immunohistochemistry and unbiased stereology of noradrenergic LC neurons in tissue harvested postmortem from subjects who died with a clinical diagnosis of no cognitive impairment (NCI), amnestic mild cognitive impairment (aMCI, a putative prodromal AD stage), or mild/moderate AD...
January 21, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28086964/anti-%C3%AE-synuclein-immunotherapy-reduces-%C3%AE-synuclein-propagation-in-the-axon-and-degeneration-in-a-combined-viral-vector-and-transgenic-model-of-synucleinopathy
#11
Brian Spencer, Elvira Valera, Edward Rockenstein, Cassia Overk, Michael Mante, Anthony Adame, Wagner Zago, Peter Seubert, Robin Barbour, Dale Schenk, Dora Games, Robert A Rissman, Eliezer Masliah
Neurodegenerative disorders such as Parkinson's Disease (PD), PD dementia (PDD) and Dementia with Lewy bodies (DLB) are characterized by progressive accumulation of α-synuclein (α-syn) in neurons. Recent studies have proposed that neuron-to-neuron propagation of α-syn plays a role in the pathogenesis of these disorders. We have previously shown that antibodies against the C-terminus of α-syn reduce the intra-neuronal accumulation of α-syn and related deficits in transgenic models of synucleinopathy, probably by abrogating the axonal transport and accumulation of α-syn in in vivo models...
January 13, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28077174/mutant-hspb1-causes-loss-of-translational-repression-by-binding-to-pcbp1-an-rna-binding-protein-with-a-possible-role-in-neurodegenerative-disease
#12
Thomas Geuens, Vicky De Winter, Nicholas Rajan, Tilmann Achsel, Ligia Mateiu, Leonardo Almeida-Souza, Bob Asselbergh, Delphine Bouhy, Michaela Auer-Grumbach, Claudia Bagni, Vincent Timmerman
The small heat shock protein HSPB1 (Hsp27) is an ubiquitously expressed molecular chaperone able to regulate various cellular functions like actin dynamics, oxidative stress regulation and anti-apoptosis. So far disease causing mutations in HSPB1 have been associated with neurodegenerative diseases such as distal hereditary motor neuropathy, Charcot-Marie-Tooth disease and amyotrophic lateral sclerosis. Most mutations in HSPB1 target its highly conserved α-crystallin domain, while other mutations affect the C- or N-terminal regions or its promotor...
January 11, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28077166/threonine-175-a-novel-pathological-phosphorylation-site-on-tau-protein-linked-to-multiple-tauopathies
#13
Alexander J Moszczynski, Wencheng Yang, Robert Hammond, Lee Cyn Ang, Michael J Strong
Microtubule associated protein tau (tau) deposition is associated with a spectrum of neurodegenerative diseases collectively termed tauopathies. We have previously shown that amyotrophic lateral sclerosis (ALS) with cognitive impairment (ALSci) is associated with tau phosphorylation at Thr(175) and that this leads to activation of GSK3β which then induces phosphorylation at tau Thr(231). This latter step leads to dissociation of tau from microtubules and pathological tau fibril formation. To determine the extent to which this pathway is unique to ALS, we have investigated the expression of pThr(175) tau and pThr(231) tau across a range of frontotemporal degenerations...
January 11, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28073370/expression-site-of-p2ry12-in-residential-microglial-cells-in-astrocytomas-correlates-with-m1-and-m2-marker-expression-and-tumor-grade
#14
Changbin Zhu, Johan M Kros, Marcel van der Weiden, PingPin Zheng, Caroline Cheng, Dana A M Mustafa
The role of resident microglial cells in the pathogenesis and progression of glial tumors is still obscure mainly due to a lack of specific markers. Recently P2RY12, a P2 purinergic receptor, was introduced as a specific marker for microglial cells under normal and pathologic conditions. Here we analyzed the expression of P2RY12 in astrocytomas of various malignancy grades in relation to markers for M1 and M2 macrophage activation profiles by using two web-based glioma datasets and confocal immunohistochemistry to 28 astrocytoma samples grades II-IV...
January 10, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28069058/endosulfine-alpha-inhibits-membrane-induced-%C3%AE-synuclein-aggregation-and-protects-against-%C3%AE-synuclein-neurotoxicity
#15
Daniel Ysselstein, Benjamin Dehay, Isabel M Costantino, George P McCabe, Matthew P Frosch, Julia M George, Erwan Bezard, Jean-Christophe Rochet
Neuropathological and genetic findings suggest that the presynaptic protein α-synuclein (aSyn) is involved in the pathogenesis of synucleinopathy disorders, including Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy. Evidence suggests that the self-assembly of aSyn conformers bound to phospholipid membranes in an aggregation-prone state plays a key role in aSyn neurotoxicity. Accordingly, we hypothesized that protein binding partners of lipid-associated aSyn could inhibit the formation of toxic aSyn oligomers at membrane surfaces...
January 10, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28057080/combination-of-alpha-synuclein-immunotherapy-with-anti-inflammatory-treatment-in-a-transgenic-mouse-model-of-multiple-system-atrophy
#16
Elvira Valera, Brian Spencer, Jerel A Fields, Ivy Trinh, Anthony Adame, Michael Mante, Edward Rockenstein, Paula Desplats, Eliezer Masliah
Multiple system atrophy (MSA) is a fatal neurodegenerative disorder characterized by the pathological accumulation of alpha-synuclein (α-syn) in oligodendrocytes. Therapeutic efforts to stop or delay the progression of MSA have yielded suboptimal results in clinical trials, and there are no efficient treatments currently available for MSA patients. We hypothesize that combining therapies targeting different aspects of the disease may lead to better clinical outcomes. To test this hypothesis, we combined the use of a single-chain antibody targeting α-syn modified for improved central nervous system penetration (CD5-D5) with an unconventional anti-inflammatory treatment (lenalidomide) in the myelin basic protein (MBP)-α-syn transgenic mouse model of MSA...
January 5, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28057070/distinct-pattern-of-enteric-phospho-alpha-synuclein-aggregates-and-gene-expression-profiles-in-patients-with-parkinson-s-disease
#17
Martina Barrenschee, Dimitri Zorenkov, Martina Böttner, Christina Lange, François Cossais, Amelie Bernadette Scharf, Günther Deuschl, Susanne A Schneider, Mark Ellrichmann, Annette Fritscher-Ravens, Thilo Wedel
Phosphorylated alpha-synuclein (p-α-syn) containing Lewy bodies (LBs) and Lewy neurites (LNs) are neuropathological hallmarks of Parkinson's disease (PD) in the central nervous system (CNS). Since they have been also demonstrated in the enteric nervous system (ENS) of PD patients, the aim of the study was to analyze enteric p-α-syn positive aggregates and intestinal gene expression. Submucosal rectal biopsies were obtained from patients with PD and controls and processed for dual-label-immunohistochemistry for p-α-syn and PGP 9...
January 5, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/27955702/%C3%AE-amyloid-triggers-aberrant-over-scaling-of-homeostatic-synaptic-plasticity
#18
James Gilbert, Shu Shu, Xin Yang, Youming Lu, Ling-Qiang Zhu, Heng-Ye Man
The over-production of β-amyloid (Aβ) has been strongly correlated to neuronal dysfunction and altered synaptic plasticity in Alzheimer's disease (AD). Accordingly, it has been proposed that disrupted synaptic transmission and neuronal network instability underlie memory failure that is evident in the early phases of AD. Homeostatic synaptic plasticity (HSP) serves to restrain neuronal activity within a physiological range. Therefore a disruption of this mechanism may lead to destabilization in synaptic and neural circuit function...
December 13, 2016: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/27955679/post-mortem-histopathology-underlying-%C3%AE-amyloid-pet-imaging-following-flutemetamol-f-18-injection
#19
Milos D Ikonomovic, Chris J Buckley, Kerstin Heurling, Paul Sherwin, Paul A Jones, Michelle Zanette, Chester A Mathis, William E Klunk, Aruna Chakrabarty, James Ironside, Azzam Ismail, Colin Smith, Dietmar R Thal, Thomas G Beach, Gill Farrar, Adrian P L Smith
In vivo imaging of fibrillar β-amyloid deposits may assist clinical diagnosis of Alzheimer's disease (AD), aid treatment selection for patients, assist clinical trials of therapeutic drugs through subject selection, and be used as an outcome measure. A recent phase III trial of [(18)F]flutemetamol positron emission tomography (PET) imaging in 106 end-of-life subjects demonstrated the ability to identify fibrillar β-amyloid by comparing in vivo PET to post-mortem histopathology. Post-mortem analyses demonstrated a broad and continuous spectrum of β-amyloid pathology in AD and other dementing and non-dementing disease groups...
December 12, 2016: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/27938414/the-effects-of-the-novel-a53e-alpha-synuclein-mutation-on-its-oligomerization-and-aggregation
#20
Diana F Lázaro, Mariana Castro Dias, Anita Carija, Susanna Navarro, Carolina Silva Madaleno, Sandra Tenreiro, Salvador Ventura, Tiago F Outeiro
α-synuclein (aSyn) is associated with both sporadic and familial forms of Parkinson's disease (PD), the second most common neurodegenerative disorder after Alzheimer's disease. In particular, multiplications and point mutations in the gene encoding for aSyn cause familial forms of PD. Moreover, the accumulation of aSyn in Lewy Bodies and Lewy neurites in disorders such as PD, dementia with Lewy bodies, or multiple system atrophy, suggests aSyn misfolding and aggregation plays an important role in these disorders, collectively known as synucleinopathies...
December 9, 2016: Acta Neuropathologica Communications
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