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Publisher: Biomed Central Ltd.   (Total: 302 journals)

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Showing 1 - 200 of 302 Journals sorted alphabetically
Acta Neuropathologica Communications     Open Access   (Followers: 1, SJR: 2.683, CiteScore: 5)
Acta Veterinaria Scandinavica     Open Access   (Followers: 2, SJR: 0.655, CiteScore: 1)
Addiction Science & Clinical Practice     Open Access   (Followers: 8, SJR: 1.224, CiteScore: 3)
Advances in Rheumatology     Open Access  
Advances in Simulation     Open Access   (Followers: 4)
Agriculture & Food Security     Open Access   (Followers: 15, SJR: 0.575, CiteScore: 2)
AIDS Research and Therapy     Open Access   (Followers: 14, SJR: 1.08, CiteScore: 2)
Algorithms for Molecular Biology     Open Access   (Followers: 4, SJR: 1.333, CiteScore: 2)
Allergy, Asthma and Clinical Immunology     Open Access   (Followers: 26, SJR: 0.732, CiteScore: 2)
Alzheimer's Research & Therapy     Open Access   (Followers: 3, SJR: 2.449, CiteScore: 6)
Animal Biotelemetry     Open Access   (Followers: 1, SJR: 1.067, CiteScore: 2)
Annals of Clinical Microbiology and Antimicrobials     Open Access   (Followers: 11, SJR: 1.104, CiteScore: 3)
Annals of General Psychiatry     Open Access   (Followers: 24, SJR: 0.784, CiteScore: 2)
Annals of Occupational and Environmental Medicine     Open Access   (Followers: 10, SJR: 0.452, CiteScore: 1)
Annals of Surgical Innovation and Research     Open Access   (Followers: 3, SJR: 0.328, CiteScore: 1)
Antimicrobial Resistance and Infection Control     Open Access   (Followers: 8, SJR: 1.573, CiteScore: 3)
Applied Cancer Research     Open Access  
Archives of Physiotherapy     Open Access   (Followers: 11)
Archives of Public Health     Open Access   (Followers: 12, SJR: 1.244, CiteScore: 3)
Arthritis Research & Therapy     Open Access   (Followers: 14, SJR: 2.154, CiteScore: 4)
Asia Pacific Family Medicine     Open Access   (Followers: 1, SJR: 0.538, CiteScore: 1)
Asthma Research and Practice     Open Access   (Followers: 1)
Basic and Clinical Andrology     Open Access   (SJR: 0.564, CiteScore: 2)
Behavioral and Brain Functions     Open Access   (Followers: 3, SJR: 0.986, CiteScore: 3)
Big Data Analytics     Open Access   (Followers: 27)
BioData Mining     Open Access   (Followers: 5, SJR: 0.982, CiteScore: 2)
Bioelectronic Medicine     Open Access  
Biological Procedures Online     Open Access   (SJR: 1.352, CiteScore: 4)
Biological Research     Open Access   (SJR: 0.654, CiteScore: 2)
Biology Direct     Open Access   (Followers: 7, SJR: 1.694, CiteScore: 3)
Biology of Mood & Anxiety Disorders     Open Access   (Followers: 5)
Biology of Sex Differences     Open Access   (Followers: 2, SJR: 1.902, CiteScore: 4)
Biomarker Research     Open Access   (Followers: 2)
Biomaterials Research     Open Access   (Followers: 4, SJR: 0.735, CiteScore: 3)
Biomedical Dermatology     Open Access  
BioMedical Engineering OnLine     Open Access   (Followers: 7, SJR: 0.542, CiteScore: 2)
BioPsychoSocial Medicine     Open Access   (Followers: 7, SJR: 0.416, CiteScore: 1)
Biotechnology for Biofuels     Open Access   (Followers: 10, SJR: 1.899, CiteScore: 6)
BMC Anesthesiology     Open Access   (Followers: 17, SJR: 0.807, CiteScore: 2)
BMC Biochemistry     Open Access   (Followers: 15, SJR: 0.708, CiteScore: 2)
BMC Bioinformatics     Open Access   (Followers: 141, SJR: 1.479, CiteScore: 2)
BMC Biology     Open Access   (Followers: 64, SJR: 3.842, CiteScore: 5)
BMC Biophysics     Open Access   (Followers: 3, SJR: 0.682, CiteScore: 2)
BMC Biotechnology     Open Access   (Followers: 17, SJR: 1.012, CiteScore: 3)
BMC Cancer     Open Access   (Followers: 29, SJR: 1.464, CiteScore: 3)
BMC Cardiovascular Disorders     Open Access   (Followers: 21, SJR: 0.909, CiteScore: 2)
BMC Cell Biology     Open Access   (Followers: 48, SJR: 1.277, CiteScore: 3)
BMC Clinical Pathology     Open Access   (Followers: 7, SJR: 1.141, CiteScore: 3)
BMC Complementary and Alternative Medicine     Open Access   (Followers: 15, SJR: 0.858, CiteScore: 3)
BMC Dermatology     Open Access   (Followers: 13, SJR: 0.796, CiteScore: 2)
BMC Developmental Biology     Open Access   (Followers: 13, SJR: 1.43, CiteScore: 2)
BMC Ear, Nose and Throat Disorders     Open Access   (Followers: 1, SJR: 0.653, CiteScore: 2)
BMC Ecology     Open Access   (Followers: 20, SJR: 1.076, CiteScore: 2)
BMC Emergency Medicine     Open Access   (Followers: 17, SJR: 0.572, CiteScore: 1)
BMC Endocrine Disorders     Open Access   (Followers: 7, SJR: 0.965, CiteScore: 2)
BMC Evolutionary Biology     Open Access   (Followers: 72, SJR: 1.656, CiteScore: 3)
BMC Family Practice     Open Access   (Followers: 13, SJR: 1.137, CiteScore: 2)
BMC Gastroenterology     Open Access   (Followers: 15, SJR: 1.231, CiteScore: 3)
BMC Genetics     Open Access   (Followers: 27, SJR: 1.16, CiteScore: 3)
BMC Genomics     Open Access   (Followers: 89, SJR: 2.11, CiteScore: 4)
BMC Geriatrics     Open Access   (Followers: 14, SJR: 1.257, CiteScore: 3)
BMC Health Services Research     Open Access   (Followers: 16, SJR: 1.151, CiteScore: 2)
BMC Hematology     Open Access   (Followers: 4, SJR: 0.545, CiteScore: 1)
BMC Immunology     Open Access   (Followers: 10, SJR: 0.993, CiteScore: 3)
BMC Infectious Diseases     Open Access   (Followers: 18, SJR: 1.576, CiteScore: 3)
BMC Intl. Health and Human Rights     Open Access   (Followers: 6, SJR: 1.006, CiteScore: 2)
BMC Medical Education     Open Access   (Followers: 44, SJR: 0.765, CiteScore: 2)
BMC Medical Ethics     Open Access   (Followers: 21, SJR: 1.016, CiteScore: 2)
BMC Medical Genetics     Open Access   (Followers: 8, SJR: 1.109, CiteScore: 2)
BMC Medical Genomics     Open Access   (Followers: 4, SJR: 1.688, CiteScore: 3)
BMC Medical Imaging     Open Access   (Followers: 9, SJR: 0.536, CiteScore: 2)
BMC Medical Informatics and Decision Making     Open Access   (Followers: 23, SJR: 0.812, CiteScore: 2)
BMC Medical Physics     Open Access   (Followers: 6)
BMC Medical Research Methodology     Open Access   (Followers: 9, SJR: 2.221, CiteScore: 3)
BMC Medicine     Open Access   (Followers: 13, SJR: 4.219, CiteScore: 7)
BMC Microbiology     Open Access   (Followers: 14, SJR: 1.242, CiteScore: 3)
BMC Molecular Biology     Open Access   (Followers: 146, SJR: 1.216, CiteScore: 2)
BMC Musculoskeletal Disorders     Open Access   (Followers: 22, SJR: 0.951, CiteScore: 2)
BMC Nephrology     Open Access   (Followers: 8, SJR: 1.098, CiteScore: 3)
BMC Neurology     Open Access   (Followers: 21, SJR: 1.006, CiteScore: 2)
BMC Neuroscience     Open Access   (Followers: 15, SJR: 1.12, CiteScore: 2)
BMC Nursing     Open Access   (Followers: 26, SJR: 0.766, CiteScore: 2)
BMC Nutrition     Open Access   (Followers: 8)
BMC Obesity     Open Access   (Followers: 6)
BMC Ophthalmology     Open Access   (Followers: 16, SJR: 0.921, CiteScore: 2)
BMC Oral Health     Open Access   (Followers: 6, SJR: 0.867, CiteScore: 2)
BMC Palliative Care     Open Access   (Followers: 29, SJR: 1.105, CiteScore: 2)
BMC Pediatrics     Open Access   (Followers: 17, SJR: 1.278, CiteScore: 2)
BMC Pharmacology     Open Access   (Followers: 2)
BMC Pharmacology & Toxicology     Open Access   (Followers: 6, SJR: 0.785, CiteScore: 2)
BMC Physiology     Open Access   (Followers: 4, SJR: 0.936, CiteScore: 2)
BMC Plant Biology     Open Access   (Followers: 15, SJR: 1.887, CiteScore: 4)
BMC Pregnancy and Childbirth     Open Access   (Followers: 22, SJR: 1.427, CiteScore: 3)
BMC Proceedings     Full-text available via subscription   (Followers: 1, SJR: 0.302, CiteScore: 1)
BMC Psychiatry     Open Access   (Followers: 32, SJR: 1.346, CiteScore: 3)
BMC Psychology     Open Access   (Followers: 18, SJR: 0.817, CiteScore: 2)
BMC Public Health     Open Access   (Followers: 167, SJR: 1.337, CiteScore: 3)
BMC Pulmonary Medicine     Open Access   (Followers: 4, SJR: 1.373, CiteScore: 3)
BMC Research Notes     Open Access   (Followers: 4, SJR: 0.691, CiteScore: 2)
BMC Rheumatology     Open Access   (Followers: 1)
BMC Sports Science, Medicine and Rehabilitation     Open Access   (Followers: 27, SJR: 0.926, CiteScore: 2)
BMC Structural Biology     Open Access   (Followers: 8, SJR: 1.024, CiteScore: 2)
BMC Surgery     Open Access   (Followers: 10, SJR: 0.693, CiteScore: 2)
BMC Systems Biology     Open Access   (Followers: 12, SJR: 1.109, CiteScore: 2)
BMC Urology     Open Access   (Followers: 14, SJR: 0.853, CiteScore: 2)
BMC Veterinary Research     Open Access   (Followers: 17, SJR: 0.934, CiteScore: 2)
BMC Women's Health     Open Access   (Followers: 11, SJR: 0.931, CiteScore: 2)
BMC Zoology     Open Access   (Followers: 1)
Borderline Personality Disorder and Emotion Dysregulation     Open Access   (Followers: 10)
Breast Cancer Research     Open Access   (Followers: 15, SJR: 3.026, CiteScore: 6)
Burns & Trauma     Open Access   (Followers: 12)
Cancer & Metabolism     Open Access   (Followers: 6)
Cancer Cell Intl.     Open Access   (Followers: 6, SJR: 1.13, CiteScore: 3)
Cancer Communications     Open Access  
Cancer Convergence     Open Access  
Cancer Imaging     Open Access   (Followers: 3, SJR: 1.012, CiteScore: 3)
Cancer Nanotechnology     Open Access   (Followers: 2, SJR: 1.168, CiteScore: 4)
Cancers of the Head & Neck     Open Access   (Followers: 2)
Canine Genetics and Epidemiology     Open Access   (Followers: 1)
Carbon Balance and Management     Open Access   (Followers: 5, SJR: 0.977, CiteScore: 2)
Cardio-Oncology     Open Access  
Cardiovascular Diabetology     Open Access   (Followers: 10, SJR: 2.157, CiteScore: 5)
Cardiovascular Ultrasound     Open Access   (Followers: 4, SJR: 0.812, CiteScore: 2)
Cell Communication and Signaling     Open Access   (Followers: 2, SJR: 2.211, CiteScore: 4)
Cell Division     Open Access   (Followers: 1, SJR: 2.445, CiteScore: 4)
Cellular & Molecular Biology Letters     Hybrid Journal   (Followers: 3)
Cerebellum & Ataxias     Open Access   (Followers: 1)
Child and Adolescent Psychiatry and Mental Health     Open Access   (Followers: 24, SJR: 0.901, CiteScore: 2)
Chinese Medicine     Open Access   (Followers: 2, SJR: 0.57, CiteScore: 2)
Chinese Neurosurgical J.     Open Access  
Chiropractic & Manual Therapies     Open Access   (Followers: 5, SJR: 0.599, CiteScore: 2)
Cilia     Open Access   (SJR: 0.732, CiteScore: 1)
Clinical and Molecular Allergy     Open Access   (Followers: 5, SJR: 0.933, CiteScore: 3)
Clinical and Translational Allergy     Open Access   (Followers: 2, SJR: 1.425, CiteScore: 4)
Clinical Diabetes and Endocrinology     Open Access   (Followers: 20)
Clinical Epigenetics     Open Access   (Followers: 11, SJR: 2.435, CiteScore: 5)
Clinical Sarcoma Research     Open Access  
Conflict and Health     Open Access   (Followers: 7, SJR: 1.851, CiteScore: 3)
Contraception and Reproductive Medicine     Open Access   (Followers: 1)
COPD Research and Practice     Open Access   (SJR: 0.755, CiteScore: 2)
Cost Effectiveness and Resource Allocation     Open Access   (Followers: 4, SJR: 0.888, CiteScore: 2)
Critical Care     Open Access   (Followers: 59, SJR: 2.48, CiteScore: 5)
Current Opinion in Molecular Therapeutics     Full-text available via subscription   (Followers: 14)
Diabetology & Metabolic Syndrome     Open Access   (Followers: 7, SJR: 0.943, CiteScore: 2)
Diagnostic and Prognostic Research     Open Access  
Diagnostic Pathology     Open Access   (Followers: 10, SJR: 0.818, CiteScore: 2)
Disaster and Military Medicine     Open Access   (Followers: 4)
Emerging Themes in Epidemiology     Open Access   (Followers: 13, SJR: 1.003, CiteScore: 2)
Energy, Sustainability and Society     Open Access   (Followers: 16, SJR: 0.607, CiteScore: 2)
Environmental Health     Open Access   (Followers: 11, SJR: 1.662, CiteScore: 4)
Environmental Health and Preventive Medicine     Open Access   (Followers: 3, SJR: 0.5, CiteScore: 1)
Epigenetics & Chromatin     Open Access   (Followers: 8, SJR: 3.767, CiteScore: 5)
European J. of Medical Research     Open Access   (Followers: 1, SJR: 0.55, CiteScore: 1)
European Review of Aging and Physical Activity     Open Access   (Followers: 9, SJR: 1.308, CiteScore: 4)
Experimental & Translational Stroke Medicine     Open Access   (Followers: 8, SJR: 0.98, CiteScore: 3)
Experimental Hematology & Oncology     Open Access   (Followers: 3, SJR: 0.842, CiteScore: 2)
Eye and Vision     Open Access   (Followers: 1)
Fertility Research and Practice     Open Access   (Followers: 2)
Fibrogenesis & Tissue Repair     Open Access   (SJR: 1.531, CiteScore: 4)
Fisheries and Aquatic Sciences     Open Access   (Followers: 2, SJR: 0.199, CiteScore: 0)
Flavour     Open Access   (Followers: 3)
Fluids and Barriers of the CNS     Open Access   (Followers: 2, SJR: 2.054, CiteScore: 5)
Frontiers in Zoology     Open Access   (Followers: 7, SJR: 1.597, CiteScore: 3)
Genes and Environment     Open Access   (Followers: 1, SJR: 0.516, CiteScore: 1)
Genetics Selection Evolution     Open Access   (Followers: 8, SJR: 1.745, CiteScore: 4)
Genome Biology     Open Access   (Followers: 31)
Genome Medicine     Open Access   (Followers: 5, SJR: 4.537, CiteScore: 7)
Global Health Research and Policy     Open Access   (Followers: 4)
Globalization and Health     Open Access   (Followers: 5, SJR: 1.262, CiteScore: 2)
Gut Pathogens     Full-text available via subscription   (Followers: 5, SJR: 1.066, CiteScore: 3)
Gynecologic Oncology Research and Practice     Open Access   (Followers: 1)
Harm Reduction J.     Open Access   (SJR: 1.445, CiteScore: 3)
Head & Face Medicine     Open Access   (Followers: 1, SJR: 0.62, CiteScore: 2)
Health and Quality of Life Outcomes     Open Access   (Followers: 14, SJR: 1.069, CiteScore: 3)
Health Research Policy and Systems     Open Access   (Followers: 14, SJR: 1.11, CiteScore: 2)
Hereditary Cancer in Clinical Practice     Open Access   (SJR: 0.848, CiteScore: 2)
Hereditas     Open Access   (Followers: 1, SJR: 0.278, CiteScore: 1)
Human Genomics     Open Access   (Followers: 3, SJR: 1.501, CiteScore: 3)
Human Resources for Health     Open Access   (Followers: 9, SJR: 1.301, CiteScore: 2)
Immunity & Ageing     Open Access   (Followers: 10, SJR: 1.218, CiteScore: 3)
Implementation Science     Open Access   (Followers: 18, SJR: 2.443, CiteScore: 4)
Infectious Agents and Cancer     Open Access   (SJR: 0.855, CiteScore: 2)
Infectious Diseases of Poverty     Open Access   (Followers: 1, SJR: 1.212, CiteScore: 3)
Inflammation and Regeneration     Open Access   (Followers: 1)
Intl. Breastfeeding J.     Open Access   (Followers: 23, SJR: 0.913, CiteScore: 3)
Intl. J. for Equity in Health     Open Access   (Followers: 6, SJR: 1.04, CiteScore: 2)
Intl. J. of Behavioral Nutrition and Physical Activity     Open Access   (Followers: 24, SJR: 2.626, CiteScore: 6)
Intl. J. of Health Geographics     Open Access   (Followers: 6, SJR: 1.385, CiteScore: 3)
Intl. J. of Mental Health Systems     Open Access   (Followers: 7, SJR: 0.721, CiteScore: 2)
Intl. J. of Pediatric Endocrinology     Open Access   (Followers: 10)
Intl. J. of Retina and Vitreous     Open Access   (Followers: 2)
Investigative Genetics     Open Access   (Followers: 1, SJR: 1.809, CiteScore: 3)
Irish Veterinary J.     Open Access   (Followers: 5, SJR: 0.657, CiteScore: 1)
Israel J. of Health Policy Research     Open Access   (SJR: 0.488, CiteScore: 1)
Italian J. of Pediatrics     Open Access   (Followers: 1, SJR: 0.685, CiteScore: 2)
J. for ImmunoTherapy of Cancer     Open Access   (Followers: 5, SJR: 2.798, CiteScore: 6)
J. of Angiogenesis Research     Open Access   (Followers: 2)
J. of Animal Science and Biotechnology     Open Access   (Followers: 4, SJR: 1.228, CiteScore: 3)
J. of Animal Science and Technology     Open Access   (Followers: 2)
J. of Biological Engineering     Open Access   (Followers: 3, SJR: 1.34, CiteScore: 4)

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Journal Cover
Acta Neuropathologica Communications
Journal Prestige (SJR): 2.683
Citation Impact (citeScore): 5
Number of Followers: 1  

  This is an Open Access Journal Open Access journal
ISSN (Online) 2051-5960
Published by Biomed Central Ltd. Homepage  [302 journals]
  • BRAF activating mutations involving the β3-αC loop in V600E-negative
           anaplastic pleomorphic xanthoastrocytoma

    • PubDate: 2018-03-15
  • Preventing mutant huntingtin proteolysis and intermittent fasting promote
           autophagy in models of Huntington disease

    • Abstract: Huntington disease (HD) is caused by the expression of mutant huntingtin (mHTT) bearing a polyglutamine expansion. In HD, mHTT accumulation is accompanied by a dysfunction in basal autophagy, which manifests as specific defects in cargo loading during selective autophagy. Here we show that the expression of mHTT resistant to proteolysis at the caspase cleavage site D586 (C6R mHTT) increases autophagy, which may be due to its increased binding to the autophagy adapter p62. This is accompanied by faster degradation of C6R mHTT in vitro and a lack of mHTT accumulation the C6R mouse model with age. These findings may explain the previously observed neuroprotective properties of C6R mHTT. As the C6R mutation cannot be easily translated into a therapeutic approach, we show that a scheduled feeding paradigm is sufficient to lower mHTT levels in YAC128 mice expressing cleavable mHTT. This is consistent with a previous model, where the presence of cleavable mHTT impairs basal autophagy, while fasting-induced autophagy remains functional. In HD, mHTT clearance and autophagy may become increasingly impaired as a function of age and disease stage, because of gradually increased activity of mHTT-processing enzymes. Our findings imply that mHTT clearance could be enhanced by a regulated dietary schedule that promotes autophagy.
      PubDate: 2018-03-06
  • Intravenous injection of beta-amyloid seeds promotes cerebral amyloid
           angiopathy (CAA)

    • Abstract: Seeding and spread of beta-amyloid (Aβ) pathologies have been considered to be based on prion-like mechanisms. However, limited transmissibility of Aβ seeding activity upon peripheral exposure would represent a key difference to prions, not only in terms of pathogenesis but also in terms of potential transmission of disease. We partially characterized the seeded Aβ amyloidosis after intracerebral injection of various brain homogenates in APP/PS1 mice. One particularly seed-laden homogenate was selected to investigate the development of Aβ pathologies after intravenous exposure. We report here that a single intravenous injection of an Alzheimer disease patient’s-brain extract into APP/PS1 recipient mice led to cerebral amyloid angiopathy within 180 days post injection. Thus, vascular proteinopathies such as CAA are transmissible in mice via the intravenous route of peripheral exposure.
      PubDate: 2018-03-05
  • Three-dimensional analysis of synapses in the transentorhinal cortex of
           Alzheimer’s disease patients

    • Abstract: Synaptic dysfunction or loss in early stages of Alzheimer’s disease (AD) is thought to be a major structural correlate of cognitive dysfunction. Early loss of episodic memory, which occurs at the early stage of AD, is closely associated with the progressive degeneration of medial temporal lobe (MTL) structures of which the transentorhinal cortex (TEC) is the first affected area. However, no ultrastructural studies have been performed in this region in human brain samples from AD patients. In the present study, we have performed a detailed three-dimensional (3D) ultrastructural analysis using focused ion beam/scanning electron microscopy (FIB/SEM) to investigate possible synaptic alterations in the TEC of patients with AD. Surprisingly, the analysis of the density, morphological features and spatial distribution of synapses in the neuropil showed no significant differences between AD and control samples. However, light microscopy studies showed that cortical thickness of the TEC was severely reduced in AD samples, but there were no changes in the volume occupied by neuronal and glial cell bodies, blood vessels, and neuropil. Thus, the present results indicate that there is a dramatic loss of absolute number of synapses, while the morphology of synaptic junctions and synaptic spatial distribution are maintained. How these changes affect cognitive impairment in AD remains to be elucidated.
      PubDate: 2018-03-02
  • Rapid detection of 2-hydroxyglutarate in frozen sections of IDH mutant
           tumors by MALDI-TOF mass spectrometry

    • Abstract: All isocitrate dehydrogenase (IDH) mutant solid neoplasms exhibit highly elevated levels of D-2-hydroxyglutarate (D-2HG). Detection of 2HG in tumor tissues currently is performed by gas or liquid chromatography-mass spectrometry (GC- or LC-MS) or biochemical detection. While these methods are highly accurate, a considerable amount of time for tissue preparation and a relatively high amount of tissue is required for testing. We here present a rapid approach to detect 2HG in brain tumor tissue based on matrix-assisted laser desorption ionization - time of flight mass spectrometry (MALDI-TOF). We analyzed 26 brain tumor samples with known IDH1 or IDH2 mutation and compared readouts to those from 28 brain tumor samples of wildtype IDH status. IDH mutant samples exhibited a clear positive signal for 2HG which was not observed in any of the IDH wildtype tumors. Our analytical pipeline allowed for 2HG detection in less than 5 min. Data were validated by determining 2HG levels in all tissues with a biochemical assay. In conclusion, we developed a protocol for rapid detection of 2HG levels and illustrate the possibility to use MALDI-TOF for the detection of metabolites on frozen tissue sections in a diagnostic setting.
      PubDate: 2018-03-02
  • White matter changes in Alzheimer’s disease: a focus on myelin and

    • Abstract: Alzheimer’s disease (AD) is conceptualized as a progressive consequence of two hallmark pathological changes in grey matter: extracellular amyloid plaques and neurofibrillary tangles. However, over the past several years, neuroimaging studies have implicated micro- and macrostructural abnormalities in white matter in the risk and progression of AD, suggesting that in addition to the neuronal pathology characteristic of the disease, white matter degeneration and demyelination may be also important pathophysiological features. Here we review the evidence for white matter abnormalities in AD with a focus on myelin and oligodendrocytes, the only source of myelination in the central nervous system, and discuss the relationship between white matter changes and the hallmarks of Alzheimer’s disease. We review several mechanisms such as ischemia, oxidative stress, excitotoxicity, iron overload, Aβ toxicity and tauopathy, which could affect oligodendrocytes. We conclude that white matter abnormalities, and in particular myelin and oligodendrocytes, could be mechanistically important in AD pathology and could be potential treatment targets.
      PubDate: 2018-03-02
  • CD74 regulates complexity of tumor cell HLA class II peptidome in brain
           metastasis and is a positive prognostic marker for patient survival

    • Abstract: Despite multidisciplinary local and systemic therapeutic approaches, the prognosis for most patients with brain metastases is still dismal. The role of adaptive and innate anti-tumor response including the Human Leukocyte Antigen (HLA) machinery of antigen presentation is still unclear. We present data on the HLA class II-chaperone molecule CD74 in brain metastases and its impact on the HLA peptidome complexity. We analyzed CD74 and HLA class II expression on tumor cells in a subset of 236 human brain metastases, primary tumors and peripheral metastases of different entities in association with clinical data including overall survival. Additionally, we assessed whole DNA methylome profiles including CD74 promoter methylation and differential methylation in 21 brain metastases. We analyzed the effects of a siRNA mediated CD74 knockdown on HLA-expression and HLA peptidome composition in a brain metastatic melanoma cell line. We observed that CD74 expression on tumor cells is a strong positive prognostic marker in brain metastasis patients and positively associated with tumor-infiltrating T-lymphocytes (TILs). Whole DNA methylome analysis suggested that CD74 tumor cell expression might be regulated epigenetically via CD74 promoter methylation. CD74high and TILhigh tumors displayed a differential DNA methylation pattern with highest enrichment scores for antigen processing and presentation. Furthermore, CD74 knockdown in vitro lead to a reduction of HLA class II peptidome complexity, while HLA class I peptidome remained unaffected. In summary, our results demonstrate that a functional HLA class II processing machinery in brain metastatic tumor cells, reflected by a high expression of CD74 and a complex tumor cell HLA peptidome, seems to be crucial for better patient prognosis.
      PubDate: 2018-03-01
  • Integrated proteomics and network analysis identifies protein hubs and
           network alterations in Alzheimer’s disease

    • Abstract: Although the genetic causes for several rare, familial forms of Alzheimer’s disease (AD) have been identified, the etiology of the sporadic form of AD remains unclear. Here, we report a systems-level study of disease-associated proteome changes in human frontal cortex of sporadic AD patients using an integrated approach that combines mass spectrometry-based quantitative proteomics, differential expression analysis, and co-expression network analysis. Our analyses of 16 human brain tissues from AD patients and age-matched controls showed organization of the cortical proteome into a network of 24 biologically meaningful modules of co-expressed proteins. Of these, 5 modules are positively correlated to AD phenotypes with hub proteins that are up-regulated in AD, and 6 modules are negatively correlated to AD phenotypes with hub proteins that are down-regulated in AD. Our study generated a molecular blueprint of altered protein networks in AD brain and uncovered the dysregulation of multiple pathways and processes in AD brain, including altered proteostasis, RNA homeostasis, immune response, neuroinflammation, synaptic transmission, vesicular transport, cell signaling, cellular metabolism, lipid homeostasis, mitochondrial dynamics and function, cytoskeleton organization, and myelin-axon interactions. Our findings provide new insights into AD pathogenesis and suggest novel candidates for future diagnostic and therapeutic development.
      PubDate: 2018-03-01
  • Transcription factors Tp73 , Cebpd , Pax6, and Spi1 rather than DNA
           methylation regulate chronic transcriptomics changes after experimental
           traumatic brain injury

    • Abstract: Traumatic brain injury (TBI) induces a wide variety of cellular and molecular changes that can continue for days to weeks to months, leading to functional impairments. Currently, there are no pharmacotherapies in clinical use that favorably modify the post-TBI outcome, due in part to limited understanding of the mechanisms of TBI-induced pathologies. Our system biology analysis tested the hypothesis that chronic transcriptomics changes induced by TBI are controlled by altered DNA-methylation in gene promoter areas or by transcription factors. We performed genome-wide methyl binding domain (MBD)-sequencing (seq) and RNA-seq in perilesional, thalamic, and hippocampal tissue sampled at 3 months after TBI induced by lateral fluid percussion in adult male Sprague-Dawley rats. We investigated the regulated molecular networks and mechanisms underlying the chronic regulation, particularly DNA methylation and transcription factors. Finally, we identified compounds that modulate the transcriptomics changes and could be repurposed to improve recovery. Unexpectedly, DNA methylation was not a major regulator of chronic post-TBI transcriptomics changes. On the other hand, the transcription factors Cebpd, Pax6, Spi1, and Tp73 were upregulated at 3 months after TBI (False discovery rate < 0.05), which was validated using digital droplet polymerase chain reaction. Transcription regulatory network analysis revealed that these transcription factors regulate apoptosis, inflammation, and microglia, which are well-known contributors to secondary damage after TBI. Library of Integrated Network-based Cellular Signatures (LINCS) analysis identified 118 pharmacotherapies that regulate the expression of Cebpd, Pax6, Spi1, and Tp73. Of these, the antidepressant and/or antipsychotic compounds trimipramine, rolipramine, fluspirilene, and chlorpromazine, as well as the anti-cancer therapies pimasertib, tamoxifen, and vorinostat were strong regulators of the identified transcription factors, suggesting their potential to modulate the regulated transcriptomics networks to improve post-TBI recovery.
      PubDate: 2018-02-27
  • Type 2 diabetes impairs odour detection, olfactory memory and olfactory
           neuroplasticity; effects partly reversed by the DPP-4 inhibitor

    • Abstract: Recent data suggest that olfactory deficits could represent an early marker and a pathogenic mechanism at the basis of cognitive decline in type 2 diabetes (T2D). However, research is needed to further characterize olfactory deficits in diabetes, their relation to cognitive decline and underlying mechanisms. The aim of this study was to determine whether T2D impairs odour detection, olfactory memory as well as neuroplasticity in two major brain areas responsible for olfaction and odour coding: the main olfactory bulb (MOB) and the piriform cortex (PC), respectively. Dipeptidyl peptidase-4 inhibitors (DPP-4i) are clinically used T2D drugs exerting also beneficial effects in the brain. Therefore, we aimed to determine whether DPP-4i could reverse the potentially detrimental effects of T2D on the olfactory system. Non-diabetic Wistar and T2D Goto-Kakizaki rats, untreated or treated for 16 weeks with the DPP-4i linagliptin, were employed. Odour detection and olfactory memory were assessed by using the block, the habituation-dishabituation and the buried pellet tests. We assessed neuroplasticity in the MOB by quantifying adult neurogenesis and GABAergic inhibitory interneurons positive for calbindin, parvalbumin and carletinin. In the PC, neuroplasticity was assessed by quantifying the same populations of interneurons and a newly identified form of olfactory neuroplasticity mediated by post-mitotic doublecortin (DCX) + immature neurons. We show that T2D dramatically reduced odour detection and olfactory memory. Moreover, T2D decreased neurogenesis in the MOB, impaired the differentiation of DCX+ immature neurons in the PC and altered GABAergic interneurons protein expression in both olfactory areas. DPP-4i did not improve odour detection and olfactory memory. However, it normalized T2D-induced effects on neuroplasticity. The results provide new knowledge on the detrimental effects of T2D on the olfactory system. This knowledge could constitute essentials for understanding the interplay between T2D and cognitive decline and for designing effective preventive therapies.
      PubDate: 2018-02-23
  • Clinical significance of polyglutamylation in primary central nervous
           system lymphoma

    • Abstract: The therapeutic response to high-dose methotrexate (HD-MTX) therapy for primary central nervous system lymphoma (PCNSL) varies. Polyglutamylation is a reversible protein modification with a high occurrence rate in tumor cells. MTX incorporated into cells is polyglutamylated and strongly binds to dihydrofolate reductase without competitive inhibition by leucovorin (LV). Tumor cells with high polyglutamylation levels are selectively killed, whereas normal cells with lower polyglutamylation are rescued by LV. We hypothesized that the extent of polyglutamylation in tumor cells determines treatment resistance. Here, we investigated the therapeutic response of PCNSL to HD-MTX therapy with LV rescue based on polyglutamylation status. Among 113 consecutive PCNSL patients who underwent HD-MTX therapy in our department between 2001 and 2014, polyglutamylation was evaluated by immunostaining in 82 cases, with relationships between polyglutamylation and therapeutic response retrospectively examined. Human malignant lymphoma lines were used for in vitro experiments, and folpolyglutamate synthetase (FPGS), which induces polyglutamylation, was knocked down with short-hairpin RNA, and a stable cell line with a low rate of polyglutamylation was established. Cell viability after MTX treatment with LV rescue was evaluated using sodium butyrate (NaBu), a histone-deacetylase inhibitor that induces polyglutamylation by elevating FPGS expression. The complete response rate was significantly higher in the group with polyglutamylation than in the non-polyglutamylation group [58.1% (25/43) and 33.3% (13/39), respectively] (p < 0.05), and progression-free survival was also significantly increased in the group with polyglutamylation (p < 0.01). In vitro, the relief effect of LV after MTX administration was significantly enhanced after FPGS knockdown in al cell lines, whereas enhancement of FPGS expression by NaBu treatment significantly reduced this relief effect. These findings suggested that polyglutamylation could be a predictor of therapeutic response to HD-MTX therapy with LV rescue in PCNSL. Combination therapy with HD-MTX and polyglutamylation-inducing agents might represent a promising strategy for PCNSL treatment.
      PubDate: 2018-02-23
  • Diffuse microvascular C5b-9 deposition is a common feature in muscle and
           nerve biopsies from diabetic patients

    • Abstract: Terminal complement complex deposition in endomysial capillaries detected by a C5b-9 immunostain is considered a diagnostic feature for dermatomyositis. However, we found widespread microvascular C5b-9 reactivity in a substantial subset of muscle biopsies with denervation changes, and in nerve biopsies of peripheral neuropathies, particularly in patients with diabetes. It is unclear whether the presence of C5b-9 deposition signifies active immune-mediated vascular injury that requires immune suppression therapy. We retrospectively identified 63 nerve biopsies in patients with a documented history of diabetes, 26 of which had concomitant muscle biopsies, as well as 54 control nerve biopsies in patients without a documented diabetes history, 18 of which had concomitant muscle biopsies. C5b-9 immunostain was performed on all cases. 87% of the nerve biopsies and 92% of the muscle biopsies from diabetic patients showed microvascular C5b-9 reactivity, compared to 34% and 50% in non-diabetic patients. The differences were statistically significant (p < 0.0001 for nerve and p = 0.002 for muscle). The C5b-9 reactivity was generally proportional to the extent of microvascular sclerosis in diabetic patients, but unrelated to inflammation or vasculitis. C5b-9 deposition in micro-vasculature in both muscle and nerve is therefore a common feature in patients with diabetic neuropathies and may have diagnostic utility. Precaution needs to be taken before using muscle capillary C5b-9 reactivity as evidence of myositis.
      PubDate: 2018-02-20
  • Familial human prion diseases associated with prion protein mutations
           Y226X and G131V are transmissible to transgenic mice expressing human
           prion protein

    • Abstract: Human familial prion diseases are associated with mutations at 34 different prion protein (PrP) amino acid residues. However, it is unclear whether infectious prions are found in all cases. Mutant PrP itself may be neurotoxic, or alternatively, PrP mutation might predispose to spontaneous formation of infectious PrP isoforms. Previous reports demonstrated transmission to animal models by human brain tissue expressing 7 different PrP mutations, but 3 other mutations were not transmissible. In the present work, we tested transmission using brain homogenates from patients expressing 3 untested PrP mutants: G131V, Y226X, and Q227X. Human brain homogenates were injected intracerebrally into tg66 transgenic mice overexpressing human PrP. Mice were followed for nearly 800 days. From 593 to 762 dpi, 4 of 8 mice injected with Y226X brain had PrPSc detectable in brain by immunostaining, immunoblot, and PrP amyloid seeding activity assayed by RT-QuIC. From 531 to 784 dpi, 11 of 11 G131V-injected mice had PrPSc deposition in brain, but none were positive by immunoblot or RT-QuIC assay. In contrast, from 529 to 798 dpi, no tg66 mice injected with Q227X brain had PrPSc or PrP amyloid seeding activity detectable by these methods. Y226X is the only one of 4 known PrP truncations associated with familial disease which has been shown to be transmissible. This transmission of prion infectivity from a patient expressing truncated human PrP may have implications for the spread and possible transmission of other aggregated truncated proteins in prion-like diseases such as Alzheimer’s disease, Parkinson’s disease and tauopathies.
      PubDate: 2018-02-20
  • Cooperative p16 and p21 action protects female astrocytes from

    • Abstract: Mechanisms underlying sex differences in cancer incidence are not defined but likely involve dimorphism (s) in tumor suppressor function at the cellular and organismal levels. As an example, sexual dimorphism in retinoblastoma protein (Rb) activity was shown to block transformation of female, but not male, murine astrocytes in which neurofibromin and p53 function was abrogated (GBM astrocytes). Correlated sex differences in gene expression in the murine GBM astrocytes were found to be highly concordant with sex differences in gene expression in male and female GBM patients, including in the expression of components of the Rb and p53 pathways. To define the basis of this phenomenon, we examined the functions of the cyclin dependent kinase (CDK) inhibitors, p16, p21 and p27 in murine GBM astrocytes under conditions that promote Rb-dependent growth arrest. We found that upon serum deprivation or etoposide-induced DNA damage, female, but not male GBM astrocytes, respond with increased p16 and p21 activity, and cell cycle arrest. In contrast, male GBM astrocytes continue to proliferate, accumulate chromosomal aberrations, exhibit enhanced clonogenic cell activity and in vivo tumorigenesis; all manifestations of broad sex differences in cell cycle regulation and DNA repair. Differences in tumorigenesis disappeared when female GBM astrocytes are also rendered null for p16 and p21. These data elucidate mechanisms underlying sex differences in cancer incidence and demonstrate sex-specific effects of cytotoxic and targeted therapeutics. This has critical implications for lab and clinical research.
      PubDate: 2018-02-20
  • Exosomes taken up by neurons hijack the endosomal pathway to spread to
           interconnected neurons

    • Abstract: In Alzheimer disease and related disorders, the microtubule-associated protein tau aggregates and forms cytoplasmic lesions that impair neuronal physiology at many levels. In addition to affecting the host neuron, tau aggregates also spread to neighboring, recipient cells where the misfolded tau aggregates, in a manner similar to prions, actively corrupt the proper folding of soluble tau, and thereby impair cellular functions. One vehicle for the transmission of tau aggregates are secretory nanovesicles known as exosomes. Here, we established a simple model of a neuronal circuit using a microfluidics culture system in which hippocampal neurons A and B were seeded into chambers 1 and 2, respectively, extending axons via microgrooves in both directions and thereby interconnecting. This system served to establish two models to track exosome spreading. In the first model, we labeled the exosomal membrane by coupling tetraspanin CD9 with either a green or red fluorescent tag. This allowed us to reveal that interconnected neurons exchange exosomes only when their axons extend in close proximity. In the second model, we added exosomes isolated from the brains of tau transgenic rTg4510 mice (i.e. exogenous, neuron A-derived) to neurons in chamber 1 (neuron B) interconnected with neuron C in chamber 2. This allowed us to demonstrate that a substantial fraction of the exogenous exosomes were internalized by neuron B and passed then on to neuron C. This transportation from neuron B to C was achieved by a mechanism that is consistent with the hijacking of secretory endosomes by the exogenous exosomes, as revealed by confocal, super-resolution and electron microscopy. Together, these findings suggest that fusion events involving the endogenous endosomal secretory machinery increase the pathogenic potential and the radius of action of pathogenic cargoes carried by exogenous exosomes.
      PubDate: 2018-02-15
  • Brain region-specific enhancement of remyelination and prevention of
           demyelination by the CSF1R kinase inhibitor BLZ945

    • Abstract: Multiple sclerosis (MS) is a chronic inflammatory disease affecting the central nervous system (CNS). While multiple effective immunomodulatory therapies for MS exist today, they lack the scope of promoting CNS repair, in particular remyelination. Microglia play a pivotal role in regulating myelination processes, and the colony-stimulating factor 1 (CSF-1) pathway is a key regulator for microglia differentiation and survival. Here, we investigated the effects of the CSF-1 receptor kinase inhibitor, BLZ945, on central myelination processes in the 5-week murine cuprizone model by non-invasive and longitudinal magnetic resonance imaging (MRI) and histology. Therapeutic 2-week BLZ945 treatment caused a brain region-specific enhancement of remyelination in the striatum/cortex, which was absent in the corpus callosum/external capsule. This beneficial effect correlated positively with microglia reduction, increased oligodendrocytes and astrogliosis. Prophylactic BLZ945 treatment prevented excessive demyelination in the corpus callosum by reducing microglia and increasing oligondendrocytes. In the external capsule oligodendrocytes were depleted but not microglia and a buildup of myelin debris and axonal damage was observed. A similar microglial dysfunction in the external capsule with an increase of myelin debris was obvious in triggering receptor expressed on myeloid cells 2 (TREM2) knock-out mice treated with cuprizone. Finally, therapeutic BLZ945 treatment did not change the disease course in experimental autoimmune encephalomyelitis mice, a peripherally driven neuroinflammation model. Taken together, our data suggest that a short-term therapeutic inhibition of the CSF-1 receptor pathway by BLZ945 in the murine cuprizone model enhances central remyelination by modulating neuroinflammation. Thus, microglia-modulating therapies could be considered clinically for promoting myelination in combination with standard-of-care treatments in MS patients.
      PubDate: 2018-02-15
  • Rapid and ultra-sensitive quantitation of disease-associated α-synuclein
           seeds in brain and cerebrospinal fluid by αSyn RT-QuIC

    • Abstract: The diagnosis and treatment of synucleinopathies such as Parkinson disease and dementia with Lewy bodies would be aided by the availability of assays for the pathogenic disease-associated forms of α-synuclein (αSynD) that are sufficiently sensitive, specific, and practical for analysis of accessible diagnostic specimens. Two recent αSynD seed amplification tests have provided the first prototypes for ultrasensitive and specific detection of αSynD in patients’ cerebrospinal fluid. These prototypic assays require 5–13 days to perform. Here, we describe an improved α-synuclein real time quaking-induced conversion (αSyn RT-QuIC) assay that has similar sensitivity and specificity to the prior assays, but can be performed in 1–2 days with quantitation. Blinded analysis of cerebrospinal fluid from 29 synucleinopathy cases [12 Parkinson’s and 17 dementia with Lewy bodies] and 31 non-synucleinopathy controls, including 16 Alzheimer’s cases, yielded 93% diagnostic sensitivity and 100% specificity for this test so far. End-point dilution analyses allowed quantitation of relative amounts of αSynD seeding activity in cerebrospinal fluid samples, and detection in as little as 0.2 μL. These results confirm that αSynD seeding activity is present in cerebrospinal fluid. We also demonstrate that it can be rapidly detected, and quantitated, even in early symptomatic stages of synucleinopathy.
      PubDate: 2018-02-09
  • Lack of pathogenic potential of peripheral α-synuclein aggregates from
           Parkinson’s disease patients

    • Abstract: In Parkinson’s disease (PD) there is widespread accumulation in the brain of abnormal α-synuclein aggregates forming intraneuronal Lewy bodies (LB). It is now well established that LB-type α-synuclein aggregates also occur in the peripheral autonomic nervous system in PD, from where it has been speculated they may progressively spread to the central nervous system through synaptically-connected brain networks and reach the substantia nigra to trigger herein dopaminergic dysfunction/degeneration and subsequent parkinsonism. Supporting a pathogenic role for α-synuclein aggregates we have previously shown that LB purified from postmortem PD brains promote α-synuclein pathology and dopaminergic neurodegeneration when intracerebrally inoculated into wild-type mice. However, the pathogenic capacity of PD-derived peripheral α-synuclein aggregates remains unknown. Here we addressed this question using purified LB-type α-synuclein aggregates from postmortem PD stellate ganglia (SG), a paravertebral sympathetic ganglion that exhibits consistent and conspicuous Lewy pathology in all PD patients. In contrast to our previous findings using nigral LB extracts, intracerebral inoculation of SG-derived LB into mice did not trigger long-term nigrostriatal neurodegeneration nor α-synuclein pathology. The differential pathogenic capacities of central- and peripheral-derived α-synuclein aggregates appear independent of the absolute amount and basic biochemical properties of α-synuclein within these aggregates and may rely instead on differences in α-synuclein conformation and/or yet unrecognized brain region-specific intrinsic factors. Our results argue against a putative pathogenic capacity of peripheral α-synuclein aggregates to promote α-synuclein pathology in the brain, propagate between neuronal networks or induce neurodegeneration.
      PubDate: 2018-02-08
  • Exceptional in vivo catabolism of neurodegeneration-related aggregates

    • Abstract: Neurodegenerative diseases are linked to a systemic enzyme resistance of toxic aggregated molecules and their pathological consequences. This paper presents a unique phenomenon that Philodina acuticornis, a bdelloid rotifer, is able to catabolize different types of neurotoxic peptide and protein aggregates (such as beta-amyloids /Aβ/, alpha-synuclein, and prion) without suffering any damage. P. acuticornis is capable of using these aggregates as an exclusive energy source (i.e., as ‘food’, identified in the digestive system and body) in a hermetically isolated microdrop environment, increasing their survival. As regards Aβ1–42, five other bdelloid rotifer species were also found to be able to perform this phenomenon. Based on our experiments, the Aβ1–42-treated bdelloid rotifers demonstrate significantly increased survival (e.g. mean lifespan = 51 ± 2.71 days) compared to their untreated controls (e.g. mean lifespan = 14 ± 2.29 days), with similar improvements in a variety of phenotypic characteristics. To our knowledge, no other animal species have so far been reported to have a similar capability. For all other microscopic species tested, including monogonant rotifers and non-rotifers, the treatment with Aβ1–42 aggregates proved to be either toxic or simply ineffective. This paper describes and proves the existence of an unprecedented in vivo catabolic capability of neurotoxic aggregates by bdelloid rotifers, with special focus on P. acuticornis. Our results may provide the basis for a new preclinical perspective on therapeutic research in human neurodegenerative diseases.
      PubDate: 2018-01-29
  • Iatrogenic Creutzfeldt-Jakob disease with Amyloid-β pathology: an
           international study

    • Abstract: The presence of pathology related to the deposition of amyloid-β (Aβ) has been recently reported in iatrogenic Creutzfeldt-Jakob disease (iCJD) acquired from inoculation of growth hormone (GH) extracted from human cadaveric pituitary gland or use of cadaveric dura mater (DM) grafts. To investigate this phenomenon further, a cohort of 27 iCJD cases – 21 with adequate number of histopathological sections – originating from Australia, France, Italy, and the Unites States, were examined by immunohistochemistry, amyloid staining, and Western blot analysis of the scrapie prion protein (PrPSc), and compared with age-group matched cases of sporadic CJD (sCJD), Alzheimer disease (AD) or free of neurodegenerative diseases (non-ND). Cases of iCJD and sCJD shared similar profiles of proteinase K-resistant PrPSc with the exception of iCJD harboring the “MMi” phenotype. Cerebral amyloid angiopathy (CAA), either associated with, or free of, Thioflavin S-positive amyloid core plaques (CP), was observed in 52% of 21 cases of iCJD, which comprised 37.5% and 61.5% of the cases of GH- and DM-iCJD, respectively. If only cases younger than 54 years were considered, Aβ pathology affected 41%, 2% and 0% of iCJD, sCJD and non-ND, respectively. Despite the patients’ younger age CAA was more severe in iCJD than sCJD, while Aβ diffuse plaques, in absence of Aβ CP, populated one third of sCJD. Aβ pathology was by far most severe in AD. Tau pathology was scanty in iCJD and sCJD. In conclusion, (i) despite the divergences in the use of cadaveric GH and DM products, our cases combined with previous studies showed remarkably similar iCJD and Aβ phenotypes indicating that the occurrence of Aβ pathology in iCJD is a widespread phenomenon, (ii) CAA emerges as the hallmark of the Aβ phenotype in iCJD since it is observed in nearly 90% of all iCJD with Aβ pathology reported to date including ours, and it is shared by GH- and DM-iCJD, (iii) although the contributions to Aβ pathology of other factors, including GH deficiency, cannot be discounted, our findings increase the mounting evidence that this pathology is acquired by a mechanism resembling that of prion diseases.
      PubDate: 2018-01-08
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
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