1,971 results match your criteria Brain Pathology[Journal]


Phosphorylated NUB1 distinguishes α-synuclein in Lewy bodies from that in glial cytoplasmic inclusions in multiple system atrophy.

Brain Pathol 2019 Apr 21. Epub 2019 Apr 21.

Department of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki, 036-8562, Japan.

Posttranslational modifications by phosphorylation, ubiquitination, neddylation, and other pathways have emerged as major regulators of cellular functions. NEDD8 ultimate buster 1, NUB1, is an adaptor protein, which negatively regulates the levels of the ubiquitin-like protein NEDD8 as well as neddylated proteins through proteasomal degradation. We previously reported that NUB1 is highly involved in the pathogenesis of synucleinopathy including Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Read More

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http://dx.doi.org/10.1111/bpa.12728DOI Listing

Osteopontin and phospho-SMAD2/3 are associated with calcification of vessels in D-CAA, an hereditary cerebral amyloid angiopathy.

Brain Pathol 2019 Mar 13. Epub 2019 Mar 13.

Department of Human Genetics, Leiden University Medical Center, Leiden, the Netherlands.

In severe forms of cerebral amyloid angiopathy (CAA) pathology, vascular calcification has been observed in the cerebral cortex, both in vivo on MRI and CT, and post-mortem using histopathology. However, the pathomechanisms leading to calcification of CAA-laden arteries are unknown. Therefore, we investigated the correlation between calcification of cortical arterioles and several potential modulators of vascular calcification using immunohistochemistry in a unique collection of brain material of patients with a hereditary form of CAA, namely hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D or D-CAA). Read More

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http://dx.doi.org/10.1111/bpa.12721DOI Listing
March 2019
4 Reads

It is time to move on: Commentary to: Genotype-phenotype correlations in focal malformations of cortical development: a pathway to integrated pathological diagnosis in epilepsy surgery (DOI: 10.1111/bpa.12686).

Authors:
Ingmar Blumcke

Brain Pathol 2019 Mar 13. Epub 2019 Mar 13.

Institute of Neuropathology, University Hospitals Erlangen, Erlangen, Germany.

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http://dx.doi.org/10.1111/bpa.12714DOI Listing
March 2019
1 Read

Neuropathological lesions in the very old: results from a large Brazilian autopsy study.

Brain Pathol 2019 Mar 12. Epub 2019 Mar 12.

Department of Pathology, University of Sao Paulo Medical School, Sao Paulo, Brazil.

Objective: To compare neuropathological correlates of cognitive impairment between very old and younger individuals from a Brazilian clinicopathological study.

Methods: We assessed the frequency of neuropathological lesions and their association with cognitive impairment (Clinical Dementia Rating scale ≥0.5) in the 80 or over age group compared to younger participants, using logistic regression models adjusted for sex, race and education. Read More

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http://doi.wiley.com/10.1111/bpa.12719
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http://dx.doi.org/10.1111/bpa.12719DOI Listing
March 2019
9 Reads

Whole-exome sequencing revealed mutational profiles of giant cell glioblastomas.

Brain Pathol 2019 Mar 12. Epub 2019 Mar 12.

Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, 30-32 Ngan Shing Street, Shatin, Hong Kong, China.

Giant cell glioblastoma (gcGBM) is a rare histological variant of GBM, accounting for about 1% of all GBM. The prognosis is poor generally though gcGBM does slightly better than the other IDH-wild-type GBM. Because of the rarity of the cases, there has been no comprehensive molecular analysis of gcGBM. Read More

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http://doi.wiley.com/10.1111/bpa.12720
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http://dx.doi.org/10.1111/bpa.12720DOI Listing
March 2019
7 Reads

The center of olfactory bulb-seeded α-synucleinopathy is the limbic system and the ensuing pathology is higher in male than in female mice.

Brain Pathol 2019 Mar 10. Epub 2019 Mar 10.

Graduate School of Pharmaceutical Sciences, Duquesne University, Pittsburgh, PA.

At early disease stages, Lewy body disorders are characterized by limbic vs. brainstem α-synucleinopathy, but most preclinical studies have focused solely on the nigrostriatal pathway. Furthermore, male gender and advanced age are two major risk factors for this family of conditions, but their influence on the topographical extents of α-synucleinopathy and the degree of cell loss are uncertain. Read More

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http://dx.doi.org/10.1111/bpa.12718DOI Listing
March 2019
2 Reads

A 32-Year-Old Women with an Intra- and Paraspinal, Extradural Mass at T10-T12.

Brain Pathol 2019 03;29(2):309-310

University of Zurich, Zurich, Switzerland.

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http://dx.doi.org/10.1111/bpa.12708DOI Listing
March 2019
1 Read

A Frontal Dural-Based Lesion in a 63-Year Old Male.

Brain Pathol 2019 03;29(2):301-302

Department of Neuro-Oncology, Moffitt Cancer Center, Tampa, FL.

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http://dx.doi.org/10.1111/bpa.12682DOI Listing

A 45-Year-Old Woman with Rash and Severe Weakness.

Brain Pathol 2019 03;29(2):303-304

Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.

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http://dx.doi.org/10.1111/bpa.12705DOI Listing
March 2019
3 Reads

42-Year-Old Man with Worsening Headache.

Brain Pathol 2019 03;29(2):305-306

Departments of Pathology, Neurology and Neurosurgery, Medical College of Georgia at Augusta University and Charlie Norwood Veterans Medical Center, Augusta, GA.

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http://dx.doi.org/10.1111/bpa.12706DOI Listing

A 44-year-old female with familial Mediterranean fever, cardiomyopathy and end stage renal disease.

Brain Pathol 2019 03;29(2):312

Section of Neuropathology, Brain Research Institute, Ronald Reagan University of California, Los Angeles, CA.

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http://dx.doi.org/10.1111/bpa.12713DOI Listing
March 2019
1 Read

Dear Reader: Data citation in changing times.

Brain Pathol 2019 03;29(2):153-154

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http://dx.doi.org/10.1111/bpa.12702DOI Listing

A 82-Year-Old Man with an Extra-Axial Frontal Mass.

Brain Pathol 2019 03;29(2):307-308

Department of Neurosurgery, Hospital Cuf Descobertas, Lisbon, Portugal.

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http://dx.doi.org/10.1111/bpa.12707DOI Listing
March 2019
1 Read

The relationship between the morphological subtypes of microglia and Alzheimer's disease neuropathology.

Brain Pathol 2019 Feb 25. Epub 2019 Feb 25.

Discipline of Pathology, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.

Microglial associations with both the major Alzheimer's disease (AD) pathognomonic entities, β-amyloid-positive plaques and tau-positive neurofibrillary tangles, have been noted in previous investigations of both human tissue and mouse models. However, the precise nature of their role in the pathogenesis of AD is debated; the major working hypothesis is that pro-inflammatory activities of activated microglia contribute to disease progression. In contrast, others have proposed that microglial dystrophy with a loss of physiological and neuroprotective activities promotes neurodegeneration. Read More

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http://dx.doi.org/10.1111/bpa.12717DOI Listing
February 2019

CDKL5 deficiency predisposes neurons to cell death through the deregulation of SMAD3 signaling.

Brain Pathol 2019 Feb 22. Epub 2019 Feb 22.

Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.

CDKL5 deficiency disorder (CDD) is a rare encephalopathy characterized by early onset epilepsy and severe intellectual disability. CDD is caused by mutations in the X-linked cyclin-dependent kinase-like 5 (CDKL5) gene, a member of a highly conserved family of serine-threonine kinases. Only a few physiological substrates of CDKL5 are currently known, which hampers the discovery of therapeutic strategies for CDD. Read More

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http://dx.doi.org/10.1111/bpa.12716DOI Listing
February 2019
2 Reads

Commentary to "A 44-year-old female with familial Mediterranean fever, cardiomyopathy and end stage renal disease" by Magaki et al.

Brain Pathol 2019 03;29(2):311

Department of Pathology, Sorbonne Université, AP-HP, Tenon Hospital, Paris, France.

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http://dx.doi.org/10.1111/bpa.12712DOI Listing
March 2019
3 Reads

Dimethyl fumarate impairs differentiated B cells and fosters central nervous system integrity in treatment of multiple sclerosis.

Brain Pathol 2019 Jan 31. Epub 2019 Jan 31.

Institute of Neuropathology, University Medical Center, Göttingen, Germany.

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. Read More

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http://dx.doi.org/10.1111/bpa.12711DOI Listing
January 2019
1 Read

Oncogenic KRAS hotspot mutations are rare in IDH-mutant gliomas.

Brain Pathol 2019 Jan 24. Epub 2019 Jan 24.

Center for CNS Tumors, Comprehensive Cancer Center Tuebingen-Stuttgart, University Hospital of Tuebingen, Eberhard Karls University of Tuebingen, Tuebingen, Germany.

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http://doi.wiley.com/10.1111/bpa.12709
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http://dx.doi.org/10.1111/bpa.12709DOI Listing
January 2019
4 Reads

Leukodystrophy caused by plasmalogen deficiency rescued by glyceryl 1-myristyl ether treatment.

Brain Pathol 2019 Jan 22. Epub 2019 Jan 22.

Neurolipid Biology, Instituto de Investigação e Inovação em Saúde - i3S, Instituto de Biologia Molecular e Celular - IBMC e Universidade do Porto, Porto, Portugal.

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 the optic nerve, corpus callosum and spinal cord. Read More

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http://dx.doi.org/10.1111/bpa.12710DOI Listing
January 2019
1 Read

Iron accumulation in microglia triggers a cascade of events that leads to altered metabolism and compromised function in APP/PS1 mice.

Brain Pathol 2019 Jan 20. Epub 2019 Jan 20.

Trinity College Institute for Neuroscience, Trinity College, Dublin 2, Ireland.

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. Read More

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http://doi.wiley.com/10.1111/bpa.12704
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http://dx.doi.org/10.1111/bpa.12704DOI Listing
January 2019
29 Reads

Axonal swelling and spheroids in Taenia solium neurocysticercosis.

Brain Pathol 2019 Jan 13. Epub 2019 Jan 13.

School of Medicine, Universidad Espíritu Santo - Ecuador, Samborondón, Ecuador.

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http://dx.doi.org/10.1111/bpa.12701DOI Listing
January 2019
3 Reads

Letter in response to Del Brutto, axonal swelling and spheroids in Taenia solium neurocysticercosis.

Brain Pathol 2019 Jan 13. Epub 2019 Jan 13.

Infectious Diseases Laboratory Research-LID, Faculty of Science and Philosophy, Alberto Cazorla Talleri, Universidad Peruana Cayetano Heredia, Lima, Perú.

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http://dx.doi.org/10.1111/bpa.12700DOI Listing
January 2019
4 Reads

Brain-derived and circulating vesicle profiles indicate neurovascular unit dysfunction in early Alzheimer's disease.

Brain Pathol 2019 Jan 10. Epub 2019 Jan 10.

School of Biological Sciences, Nanyang Technological University, Singapore, Singapore.

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. Read More

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http://dx.doi.org/10.1111/bpa.12699DOI Listing
January 2019
15 Reads

An Infratentorial Tumor in a 44-Year-Old Female Patient.

Brain Pathol 2019 01;29(1):145-146

Department of Neuropathology, University Hospital of Zurich.

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http://dx.doi.org/10.1111/bpa.12684DOI Listing
January 2019
1 Read

A 33-Year-Old Male with Five Years of Neck Pain.

Brain Pathol 2019 01;29(1):141-142

Department of Neurosurgery, University Hospital Essen, Germany.

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http://dx.doi.org/10.1111/bpa.12681DOI Listing
January 2019
2 Reads

Two Male Infants each with a Cerebellar Mass.

Brain Pathol 2019 01;29(1):143-144

Division of Pediatric Neurosurgery, Seoul National University Children's Hospital, Seoul, Korea.

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http://dx.doi.org/10.1111/bpa.12683DOI Listing
January 2019
2 Reads

Prion neurotoxicity.

Brain Pathol 2019 03 17;29(2):263-277. Epub 2019 Jan 17.

Department of Biochemistry, Boston University School of Medicine, Boston, MA.

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 as 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. Read More

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http://dx.doi.org/10.1111/bpa.12694DOI Listing
March 2019
2 Reads

Recent advances in the histo-molecular pathology of human prion disease.

Brain Pathol 2019 03 22;29(2):278-300. Epub 2019 Jan 22.

IRCCS, Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.

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 PrP , a misfolded isoform of the cellular prion protein (PrP ) 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 PrP , has increased interest in prion diseases. Read More

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http://doi.wiley.com/10.1111/bpa.12695
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http://dx.doi.org/10.1111/bpa.12695DOI Listing
March 2019
15 Reads

Animal prion diseases: the risks to human health.

Brain Pathol 2019 03 22;29(2):248-262. Epub 2019 Jan 22.

UMR INRA ENVT 1225-IHAP, École Nationale Vétérinaire de Toulouse, Toulouse, France.

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). As the transmission barrier phenomenon 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. Read More

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http://dx.doi.org/10.1111/bpa.12696DOI Listing
March 2019
4 Reads

Recent advances on the molecular pathogenesis of prion diseases.

Brain Pathol 2019 03;29(2):245-247

Departments of Pathology and Medicine, UC San Diego, La Jolla, CA.

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http://dx.doi.org/10.1111/bpa.12693DOI Listing
March 2019
1 Read

Degeneration of dopaminergic circuitry influences depressive symptoms in Lewy body disorders.

Brain Pathol 2018 Dec 24. Epub 2018 Dec 24.

NIHR Biomedical Research Centre Newcastle, Biomedical Research Building, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK.

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. Read More

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http://dx.doi.org/10.1111/bpa.12697DOI Listing
December 2018
2 Reads

27-hydroxycholesterol promotes Aβ accumulation via altering Aβ metabolism in mild cognitive impairment patients and APP/PS1 mice.

Brain Pathol 2018 Dec 23. Epub 2018 Dec 23.

School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.

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. Read More

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http://dx.doi.org/10.1111/bpa.12698DOI Listing
December 2018
3 Reads

A 39-year-old female with cerebellar tumor and visual disturbance.

Brain Pathol 2018 11;28(6):1027-1028

Department of Neurosurgery, Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.

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http://dx.doi.org/10.1111/bpa.12668DOI Listing
November 2018
2 Reads

Dear Reader: another changing of the guard.

Authors:

Brain Pathol 2018 11;28(6):789

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http://dx.doi.org/10.1111/bpa.12671DOI Listing
November 2018
1 Read

43 Year Old Woman with Left Arm Paralysis.

Brain Pathol 2018 11;28(6):1021-1022

Department of Neurology, Peking University People's Hospital, Beijing, China.

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http://dx.doi.org/10.1111/bpa.12665DOI Listing
November 2018
1 Read

A 72-year old female with multiple supra- and infratentorial dural masses.

Brain Pathol 2018 11;28(6):1023-1024

Institute of Neuropathology, University Hospital Zurich, Zurich, Switzerland.

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http://dx.doi.org/10.1111/bpa.12666DOI Listing
November 2018
3 Reads
3.840 Impact Factor

An 83 year-old man with fever and speech difficulties.

Brain Pathol 2018 11;28(6):1025-1026

Division of Infectious Diseases, University of Colorado Denver, USA.

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http://dx.doi.org/10.1111/bpa.12667DOI Listing
November 2018
1 Read

Distribution and prognostic impact of microglia/macrophage subpopulations in gliomas.

Brain Pathol 2018 Dec 3. Epub 2018 Dec 3.

Edinger Institute, Institute of Neurology, Goethe University Frankfurt, Frankfurt am Main, Germany.

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). Read More

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http://doi.wiley.com/10.1111/bpa.12690
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http://dx.doi.org/10.1111/bpa.12690DOI Listing
December 2018
20 Reads

Aberrant accrual of BIN1 near Alzheimer's disease amyloid deposits in transgenic models.

Brain Pathol 2018 Nov 30. Epub 2018 Nov 30.

Department of Neurobiology, The University of Chicago, Chicago, IL.

Bridging integrator 1 (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. Read More

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http://dx.doi.org/10.1111/bpa.12687DOI Listing
November 2018
6 Reads
3.840 Impact Factor

The sterol regulatory element-binding protein 2 is dysregulated by tau alterations in Alzheimer disease.

Brain Pathol 2018 Dec 4. Epub 2018 Dec 4.

Department of Pathology, Case Western Reserve University, Cleveland, OH.

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. Read More

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http://dx.doi.org/10.1111/bpa.12691DOI Listing
December 2018
2 Reads

Early growth response-1 regulates acetylcholinesterase and its relation with the course of Alzheimer's disease.

Brain Pathol 2018 Dec 3. Epub 2018 Dec 3.

Department of Neurobiology, and Department of Neurology of the Second Affiliated Hospital, NHC and CAMS Key Laboratory of Medical Neurobiology, Zhejiang University School of Medicine, Hangzhou, P.R. China.

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). Read More

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http://dx.doi.org/10.1111/bpa.12688DOI Listing
December 2018
4 Reads
3.840 Impact Factor

Extravascular fibrinogen in the white matter of Alzheimer's disease and normal aged brains: implications for fibrinogen as a biomarker for Alzheimer's disease.

Brain Pathol 2018 Nov 28. Epub 2018 Nov 28.

Institute of Neuroscience, Newcastle University, Newcastle Upon Tyne, UK.

The blood-brain barrier (BBB) regulates cerebrovascular permeability and leakage of blood-derived fibrinogen. Dysfunction of the BBB has been associated with cerebral arteriolosclerosis small vessel disease (SVD) and 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. Read More

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http://dx.doi.org/10.1111/bpa.12685DOI Listing
November 2018
5 Reads

Genotype-phenotype correlations in focal malformations of cortical development: a pathway to integrated pathological diagnosis in epilepsy surgery.

Brain Pathol 2018 Nov 28. Epub 2018 Nov 28.

Developmental Biology and Cancer Programme, UCL GOS Institute of Child Health, London, UK.

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. Read More

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http://doi.wiley.com/10.1111/bpa.12686
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http://dx.doi.org/10.1111/bpa.12686DOI Listing
November 2018
9 Reads

Dysregulation of TDP-43 intracellular localization and early onset ALS are associated with a TARDBP S375G variant.

Brain Pathol 2018 Nov 21. Epub 2018 Nov 21.

International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy.

We investigated the Central Nervous System (CNS) and skeletal muscle tissue from A woman was clinically diagnosed with amyotrophic lateral sclerosis (ALS) at the age of 22. Neuropathologic evaluation showed upper and lower motor neuron loss, corticospinal tract degeneration and skeletal muscle denervation. Analysis of the patient's Deoxyribonucleic acid (DNA) revealed a AGT>GGT change resulting in an S375G substitution in the C-terminal region of TDP-43. Read More

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http://dx.doi.org/10.1111/bpa.12680DOI Listing
November 2018
17 Reads

Genome-wide identification of microRNAs regulating the human prion protein.

Brain Pathol 2019 03 21;29(2):232-244. Epub 2018 Dec 21.

Institute of Neuropathology, University of Zürich, Zürich, Switzerland.

The cellular prion protein (PrP ) is best known for its misfolded disease-causing conformer, PrP . Because the availability of PrP is often limiting for prion propagation, understanding its regulation may point to possible therapeutic targets. We sought to determine to what extent the human microRNAome is involved in modulating PrP levels through direct or indirect pathways. Read More

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http://doi.wiley.com/10.1111/bpa.12679
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http://dx.doi.org/10.1111/bpa.12679DOI Listing
March 2019
8 Reads

Clarity reveals a more protracted temporal course of axon swelling and disconnection than previously described following traumatic brain injury.

Brain Pathol 2018 Nov 16. Epub 2018 Nov 16.

Department of Neurosurgery, Penn Center for Brain Injury and Repair, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.

Diffuse axonal injury (DAI) is an important consequence of traumatic brain injury (TBI). At the moment of trauma, axons rarely disconnect, but undergo cytoskeletal disruption and transport interruption leading to protein accumulation within swellings. The amyloid precursor protein (APP) accumulates rapidly and the standard histological evaluation of axonal pathology relies upon its detection. Read More

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http://doi.wiley.com/10.1111/bpa.12677
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http://dx.doi.org/10.1111/bpa.12677DOI Listing
November 2018
26 Reads

Oligodendroglial α-synucleinopathy-driven neuroinflammation in multiple system atrophy.

Brain Pathol 2018 Nov 16. Epub 2018 Nov 16.

Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.

Neuroinflammation and oligodendroglial cytoplasmic α-synuclein (α-syn) inclusions (GCIs) are important neuropathological characteristics of multiple system atrophy (MSA). GCIs are known to interfere with oligodendroglial maturation and consequently result in myelin loss. The neuroinflammatory phenotype in the context of MSA, however, remains poorly understood. Read More

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http://doi.wiley.com/10.1111/bpa.12678
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http://dx.doi.org/10.1111/bpa.12678DOI Listing
November 2018
26 Reads

Clinicopathologic features of anaplastic myxopapillary ependymomas.

Brain Pathol 2019 01;29(1):75-84

Department of Pathology, University of California, San Francisco, CA.

Myxopapillary ependymomas (MPE) are considered benign (World Health Organization (WHO) grade I) neoplasms with favorable prognosis. However, malignant behavior occurs in a small subset. To our knowledge, only five anaplastic MPEs have been reported without consensus on diagnostic criteria. Read More

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http://doi.wiley.com/10.1111/bpa.12673
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http://dx.doi.org/10.1111/bpa.12673DOI Listing
January 2019
18 Reads
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Regulation of glioma cell invasion by 3q26 gene products PIK3CA, SOX2 and OPA1.

Brain Pathol 2018 Nov 7. Epub 2018 Nov 7.

Laboratory of Brain Tumor Biology, Department of Biomedicine, University Hospital and University of Basel, Basel, Switzerland.

Diffuse gliomas progress by invading neighboring brain tissue to promote postoperative relapse. Transcription factor SOX2 is highly expressed in invasive gliomas and maps to chromosome region 3q26 together with the genes for PI3K/AKT signaling activator PIK3CA and effector molecules of mitochondria fusion and cell invasion, MFN1 and OPA1. Gene copy number analysis at 3q26 from 129 glioma patient biopsies revealed mutually exclusive SOX2 amplifications (26%) and OPA1 losses (19%). Read More

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Source
http://doi.wiley.com/10.1111/bpa.12670
Publisher Site
http://dx.doi.org/10.1111/bpa.12670DOI Listing
November 2018
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