7,792 results match your criteria Frontotemporal Lobe Dementia


Emergence of artistic talent in progressive nonfluent aphasia: a case report.

Psychogeriatrics 2019 Feb 19. Epub 2019 Feb 19.

Department of Neuropsychiatry, Faculty of Life sciences, Kumamoto University, Kumamoto, Japan.

Some patients with frontotemporal lobar degeneration have developed artistic skills after the onset mainly in painting and music. Most of these cases have semantic dementia (SD), one of the frontotemporal lobar degeneration subtypes. In previously reported cases, the paintings made by patients with SD were usually hyper realistic, without a significant symbolic or abstract component. Read More

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http://dx.doi.org/10.1111/psyg.12437DOI Listing
February 2019

Artificial MicroRNAs Targeting C9orf72 Can Reduce Accumulation of Intra-nuclear Transcripts in ALS and FTD Patients.

Mol Ther Nucleic Acids 2019 Jan 30;14:593-608. Epub 2019 Jan 30.

Department of Research & Development, uniQure Biopharma B.V., Amsterdam, the Netherlands. Electronic address:

The most common pathogenic mutation in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is an intronic GGGGCC (GC) repeat in the chromosome 9 open reading frame 72 (C9orf72) gene. Cellular toxicity due to RNA foci and dipeptide repeat (DPR) proteins produced by the sense and antisense repeat-containing transcripts is thought to underlie the pathogenesis of both diseases. RNA sequencing (RNA-seq) data of C9orf72-ALS patients and controls were analyzed to better understand the sequence conservation of C9orf72 in patients. Read More

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http://dx.doi.org/10.1016/j.omtn.2019.01.010DOI Listing
January 2019

Molecular Mechanisms of Neurodegeneration Related to Hexanucleotide Repeat Expansion.

Behav Neurol 2019 15;2019:2909168. Epub 2019 Jan 15.

Department of Neuroscience, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Zagreb, Croatia.

Two clinically distinct diseases, amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), have recently been classified as two extremes of the FTD/ALS spectrum. The neuropathological correlate of FTD is frontotemporal lobar degeneration (FTLD), characterized by tau-, TDP-43-, and FUS-immunoreactive neuronal inclusions. An earlier discovery that a hexanucleotide repeat expansion mutation in chromosome 9 open reading frame 72 () gene causes ALS and FTD established a special subtype of ALS and FTLD with TDP-43 pathology (C9FTD/ALS). Read More

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http://dx.doi.org/10.1155/2019/2909168DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6350563PMC
January 2019

TARDBP mutation associated with semantic variant primary progressive aphasia, case report and review of the literature.

Neurocase 2019 Feb 16:1-5. Epub 2019 Feb 16.

a Department of Neurology , Hospital Universitario 12 de Octubre , Madrid , Spain.

Semantic variant primary progressive aphasia (svPPA) is a clinical syndrome included in the frontotemporal dementia (FTD) spectrum. Unlike other forms of FTD, it is sporadic in the majority of cases and not commonly associated with motor neuron disease (MND). We describe a case of svPPA associated with MND in the same family, due to a mutation of the transactive response DNA binding protein (TARDBP) gene, and review the literature. Read More

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http://dx.doi.org/10.1080/13554794.2019.1581225DOI Listing
February 2019

Clinical heterogeneity of frontotemporal dementia and Parkinsonism linked to chromosome 17 caused by MAPT N279K mutation in relation to tau positron emission tomography features.

Mov Disord 2019 Feb 17. Epub 2019 Feb 17.

Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.

Background: While mechanistic links between tau abnormalities and neurodegeneration have been proven in frontotemporal dementia and parkinsonism linked to chromosome 17 caused by MAPT mutations, variability of the tau pathogenesis and its relation to clinical progressions in the same MAPT mutation carriers are yet to be clarified.

Objectives: The present study aimed to analyze clinical profiles, tau accumulations, and their correlations in 3 kindreds with frontotemporal dementia and parkinsonism linked to chromosome 17 attributed to the MAPT N279K mutation.

Methods: Four patients with N279K mutant frontotemporal dementia and parkinsonism linked to chromosome 17/MAPT underwent [ C]PBB3-PET to estimate regional tau loads. Read More

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http://dx.doi.org/10.1002/mds.27623DOI Listing
February 2019

The underacknowledged PPA-ALS: A unique clinicopathologic subtype with strong heritability.

Neurology 2019 Feb 15. Epub 2019 Feb 15.

From the Brain and Mind Centre and Central Clinical School (R.H.T., B.G., C.D.-S., J.B.J.K., M.C.K., J.R.H., G.M.H.) and School of Medical Sciences (J.J.K.), Faculty of Medicine and Health, and Brain and Mind Centre and School of Psychology (O.P.), The University of Sydney; School of Medical Sciences (R.H.T., C.D.-S., G.M.H.), University of New South Wales & Neuroscience Research Australia; Department of Neurology (M.C.K.), Royal Prince Alfred Hospital; ARC Centre of Excellence in Cognition and its Disorders (J.R.H., O.P.); and Division of Neuroscience (B.G.), Garvan Institute of Medical Research and St Vincent's Clinical School, UNSW Sydney, New South Wales, Australia.

Objective: To assess the incidence, heritability, and neuropathology of primary progressive aphasia (PPA) with amyotrophic lateral sclerosis (ALS) in a large Australian cohort.

Methods: A total of 130 patients with a primary nonfluent variant of PPA (nfvPPA) or semantic variant of PPA (svPPA) were assessed for concomitant ALS and a strong family history of neurodegenerative diseases (Goldman score ≤3). Neuropathologic examination was carried out in 28% (n = 36) of these PPA and PPA-ALS cases that had come to autopsy. Read More

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http://dx.doi.org/10.1212/WNL.0000000000007146DOI Listing
February 2019
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Aberrant deposition of stress granule-resident proteins linked to C9orf72-associated TDP-43 proteinopathy.

Mol Neurodegener 2019 Feb 15;14(1). Epub 2019 Feb 15.

Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Rd, Jacksonville, FL, 32224, USA.

Background: A GC hexanucleotide repeat expansion in the noncoding region of C9orf72 is the major genetic cause of frontotemporal dementia and amyotrophic lateral sclerosis (c9FTD/ALS). Putative disease mechanisms underlying c9FTD/ALS include toxicity from sense GC and antisense GC repeat-containing RNA, and from dipeptide repeat (DPR) proteins unconventionally translated from these RNA products.

Methods: Intracerebroventricular injections with adeno-associated virus (AAV) encoding 2 or 149 GC repeats were performed on postnatal day 0, followed by assessment of behavioral and neuropathological phenotypes. Read More

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http://dx.doi.org/10.1186/s13024-019-0310-zDOI Listing
February 2019

Citalopram-Associated Alopecia: A Case Report and Brief Literature Review.

Curr Drug Saf 2019 Feb 14. Epub 2019 Feb 14.

Department of Psychiatry, Western Michigan University, Homer Stryker M.D. School of Medicine, Kalamazoo, MI . United States.

Background: Selective Serotonin Reuptake Inhibitors (SSRIs) are the first-line treatments for various psychiatric disorders. SSRIs offer improved side effect profile compared to older treatments, which improve patient adherence and quality of life.

Case Report: Here we discuss a case of an uncommon, but distressing side effect of citalopram. Read More

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http://dx.doi.org/10.2174/1574886314666190215115857DOI Listing
February 2019

C9orf72-dependent lysosomal functions regulate epigenetic control of autophagy and lipid metabolism.

Authors:
Yang Liu Jiou Wang

Autophagy 2019 Feb 15. Epub 2019 Feb 15.

a Department of Biochemistry and Molecular Biology, Department of Neuroscience , Johns Hopkins University , Baltimore , MD , 21205 , USA .

Cellular adaption to nutrient stress is exquisitely regulated, and its dysregulation could underlie human diseases including neurodegeneration. C9orf72 is linked to the most common forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) as well as rare cases of other neurological disorders. Recent studies have implicated C9orf72 functions in the autophagy-lysosome pathway, but the exact roles of C9orf72 remain unclear. Read More

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http://dx.doi.org/10.1080/15548627.2019.1580106DOI Listing
February 2019

Heterochromatin anomalies and double-stranded RNA accumulation underlie poly(PR) toxicity.

Science 2019 02;363(6428)

Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

How hexanucleotide GGGGCC (GC) repeat expansions in cause frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is not understood. We developed a mouse model engineered to express poly(PR), a proline-arginine (PR) dipeptide repeat protein synthesized from expanded GC repeats. The expression of green fluorescent protein-conjugated (PR) (a 50-repeat PR protein) throughout the mouse brain yielded progressive brain atrophy, neuron loss, loss of poly(PR)-positive cells, and gliosis, culminating in motor and memory impairments. Read More

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http://dx.doi.org/10.1126/science.aav2606DOI Listing
February 2019

Clinical and cortical decline in the aphasic variant of Alzheimer's disease.

Alzheimers Dement 2019 Feb 11. Epub 2019 Feb 11.

NU Feinberg School of Medicine, Department of Preventive Medicine, Chicago, IL, USA.

Introduction: Primary progressive aphasia (PPA) displays variable progression trajectories that require further elucidation.

Methods: Longitudinal quantitation of atrophy and language over 12 months was completed for PPA patients with and without positive amyloid PET (PPA and PPA), an imaging biomarker of underlying Alzheimer's disease.

Results: Over 12 months, both PPA groups showed significantly greater cortical atrophy rates in the left versus right hemisphere, with a more widespread pattern in PPA. Read More

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http://dx.doi.org/10.1016/j.jalz.2018.12.003DOI Listing
February 2019

Implications of Microglia in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.

J Mol Biol 2019 Feb 11. Epub 2019 Feb 11.

Group of Stem Cells and Modeling of Neurodegeneration, Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark, Grønnegårdsvej 7, 1870C. Electronic address:

Amyotrophic lateral sclerosis (ALS) and Frontotemporal dementia (FTD) are neurodegenerative disorders with clear similarities regarding their clinical, genetic and pathological features. Both are progressive, lethal disorders, with no current curative treatment available. Several genes correlated with ALS and FTD are implicated in the same molecular pathways. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222836193006
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http://dx.doi.org/10.1016/j.jmb.2019.02.004DOI Listing
February 2019
3 Reads

Dementia spectrum disorders: lessons learnt from decades with PET research.

J Neural Transm (Vienna) 2019 Feb 14. Epub 2019 Feb 14.

Neurodegeneration Imaging Group, Maurice Wohl Clinical Neuroscience Institute, 125 Coldharbour Lane, Camberwell, London, SE5 9NU, UK.

The dementia spectrum encompasses a range of disorders with complex diagnosis, pathophysiology and limited treatment options. Positron emission tomography (PET) imaging provides insights into specific neurodegenerative processes underlying dementia disorders in vivo. Here we focus on some of the most common dementias: Alzheimer's disease, Parkinsonism dementias including Parkinson's disease with dementia, dementia with Lewy bodies, progressive supranuclear palsy and corticobasal syndrome, and frontotemporal lobe degeneration. Read More

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http://dx.doi.org/10.1007/s00702-019-01975-4DOI Listing
February 2019
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Measuring network disruption in neurodegenerative diseases: New approaches using signal analysis.

J Neurol Neurosurg Psychiatry 2019 Feb 13. Epub 2019 Feb 13.

Academic Unit of Neurology, Trinity College Dublin, the University of Dublin, Dublin, Ireland

Advanced neuroimaging has increased understanding of the pathogenesis and spread of disease, and offered new therapeutic targets. MRI and positron emission tomography have shown that neurodegenerative diseases including Alzheimer's disease (AD), Lewy body dementia (LBD), Parkinson's disease (PD), frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) are associated with changes in brain networks. However, the underlying neurophysiological pathways driving pathological processes are poorly defined. Read More

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http://jnnp.bmj.com/lookup/doi/10.1136/jnnp-2018-319581
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http://dx.doi.org/10.1136/jnnp-2018-319581DOI Listing
February 2019
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Relative preservation of facial expression recognition in posterior cortical atrophy.

Neurology 2019 Feb 13. Epub 2019 Feb 13.

From the Department of Neurology, Division of Behavioral Neurology and Neuropsychiatry (P.P., V.P.), University of Colorado, Denver; Memory and Aging Center (P.P., K.G., S.M.S., B.L.M., C.M., K.P.R.), University of California, San Francisco; and Stanford Neuroscience Health Center (C.F.), Stanford University School of Medicine, Palo Alto, CA.

Objective: To compare recognition of facial expression (FE) vs recognition of facial identity (FI) in posterior cortical atrophy (PCA), with the hypothesis that FE recognition would be relatively preserved in PCA.

Methods: In this observational study, FI and expression recognition tasks were performed by 194 participants in 4 groups, including 39 with Alzheimer disease (AD) (non-PCA), 49 with behavioral variant frontotemporal dementia (bvFTD), 15 with PCA, and 91 healthy controls. Between-group differences in test scores were compared. Read More

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http://dx.doi.org/10.1212/WNL.0000000000007075DOI Listing
February 2019

Heterogeneous nuclear ribonucleoproteins R and Q accumulate in pathological inclusions in FTLD-FUS.

Acta Neuropathol Commun 2019 Feb 12;7(1):18. Epub 2019 Feb 12.

Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.

Frontotemporal lobar degeneration (FTLD) is pathologically subdivided based on the presence of particular pathological proteins that are identified in inclusion bodies observed post-mortem. The FTLD-FUS subgroup is defined by the presence of the fused in sarcoma protein (FUS) in pathological inclusions. FUS is a heterogeneous nuclear ribonucleoprotein (hnRNP) protein and a member of the FET (FUS, EWS, TAF15) protein family. Read More

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http://dx.doi.org/10.1186/s40478-019-0673-yDOI Listing
February 2019

Music Therapy and Physical Activity to Ease Anxiety, Restlessness, Irritability, and Aggression in Individuals With Dementia With Signs of Frontotemporal Lobe Degeneration.

J Psychosoc Nurs Ment Health Serv 2019 Feb 8:1-9. Epub 2019 Feb 8.

The purpose of the current study was to evaluate whether a combined intervention of physical activity and music therapy could reduce anxiety, restlessness, irritability, and aggression among individuals with severe dementia. An exploratory design was used to evaluate a combined intervention of physical activity, music therapy, and daily walking. Interventions were systematically implemented for 8 weeks. Read More

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http://dx.doi.org/10.3928/02793695-20190124-02DOI Listing
February 2019
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Morphology and Distribution of TDP-43 Pre-inclusions in Primary Progressive Aphasia.

J Neuropathol Exp Neurol 2019 Feb 8. Epub 2019 Feb 8.

Feinberg School of Medicine, Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University, Chicago, Illinois.

Diffusely stained phosphorylated 43-kDa TAR DNA-binding protein (TDP-43)-positive "pre-inclusions" have been described. This experiment investigated morphological subtypes of pre-inclusions and their relationship with TDP-43 inclusions in primary progressive aphasia (PPA), a dementia characterized by gradual dissolution of language. Brain sections from 5 PPA participants with postmortem diagnoses of frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP) were immunohistochemically stained using an antibody to phosphorylated TDP-43 and quantitatively examined for regional and hemispheric distribution using unbiased stereology. Read More

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http://dx.doi.org/10.1093/jnen/nlz005DOI Listing
February 2019
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Nuclear RNA foci from expansion mutation form paraspeckle-like bodies.

J Cell Sci 2019 02 11. Epub 2019 Feb 11.

Department of Biotechnology, Jozef Stefan Institute, Ljubljana 1000, Slovenia

The GGGGCC (GC) repeat expansion mutation in gene is the most common genetic cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). Transcription of the repeat and formation of nuclear RNA foci, which sequester specific RNA-binding proteins is one of the possible pathological mechanisms. Here, we show that (GC) repeat RNA predominantly associates with essential paraspeckle proteins SFPQ, NONO, RBM14, FUS and hnRNPH and co-localizes with known paraspeckle-associated RNA As formation of paraspeckles in motor neurons has been associated with early phases of ALS, we investigated the extent of similarity between paraspeckles and (GC) RNA foci. Read More

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http://jcs.biologists.org/lookup/doi/10.1242/jcs.224303
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http://dx.doi.org/10.1242/jcs.224303DOI Listing
February 2019
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Neural correlates of distinct cognitive phenotypes in early Parkinson's disease.

J Neurol Sci 2019 Feb 7;399:22-29. Epub 2019 Feb 7.

University of California San Diego, Department of Neurosciences, La Jolla, CA, USA.

Objective: Cognitive decline is common in Parkinson's disease (PD), but changes can occur in a variety of cognitive domains. The lack of a single cognitive phenotype complicates diagnosis and tracking. In an earlier study we used a data-driven approach to identify distinct cognitive phenotypes of early PD. Read More

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http://dx.doi.org/10.1016/j.jns.2019.02.013DOI Listing
February 2019
2 Reads

Detecting frontotemporal dementia syndromes using MRI biomarkers.

Neuroimage Clin 2019 Feb 4;22:101711. Epub 2019 Feb 4.

Danish Dementia Research Centre, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark.

Background: Diagnosing frontotemporal dementia may be challenging. New methods for analysis of regional brain atrophy patterns on magnetic resonance imaging (MRI) could add to the diagnostic assessment. Therefore, we aimed to develop automated imaging biomarkers for differentiating frontotemporal dementia subtypes from other diagnostic groups, and from one another. Read More

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http://dx.doi.org/10.1016/j.nicl.2019.101711DOI Listing
February 2019
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RNA as a key factor in driving or preventing self-assembly of the TAR DNA-binding protein 43.

J Mol Biol 2019 Feb 8. Epub 2019 Feb 8.

UK Dementia Research Institute at King's College London, London, SE5 9RT, United Kingdom; The Wohl Institute at King's College London, London, SE5 9RT, United Kingdom; Department of Medicina Molecolare, University of Pavia, Pavia, 27100, Italy. Electronic address:

Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTD) are incurable motor neuron diseases associated with muscle weakness, paralysis and respiratory failure. Accumulation of TAR DNA-binding protein 43 (TDP-43) as toxic cytoplasmic inclusions is one of the hallmarks of these pathologies. TDP-43 is an RNA-binding protein responsible for regulating RNA transcription, splicing, transport and translation. Read More

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http://dx.doi.org/10.1016/j.jmb.2019.01.028DOI Listing
February 2019
2 Reads

Tau and TDP-43 proteinopathies: kindred pathologic cascades and genetic pleiotropy.

Lab Invest 2019 Feb 11. Epub 2019 Feb 11.

University of Kentucky College of Medicine, Lexington, KY, USA.

We review the literature on Tau and TDP-43 proteinopathies in aged human brains and the relevant underlying pathogenetic cascades. Complex interacting pathways are implicated in Alzheimer's disease and related dementias (ADRD), wherein multiple proteins tend to misfold in a manner that is "reactive," but, subsequently, each proteinopathy may contribute strongly to the clinical symptoms. Tau proteinopathy exists in brains of individuals across a broad spectrum of primary underlying conditions-e. Read More

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http://dx.doi.org/10.1038/s41374-019-0196-yDOI Listing
February 2019
2 Reads

MAPT mutations, tauopathy, and mechanisms of neurodegeneration.

Lab Invest 2019 Feb 11. Epub 2019 Feb 11.

Department of Neuroscience, College of Medicine, University of Florida, Gainesville, FL, 32610, USA.

In multiple neurodegenerative diseases, including Alzheimer's disease (AD), a prominent pathological feature is the aberrant aggregation and inclusion formation of the microtubule-associated protein tau. Because of the pathological association, these disorders are often referred to as tauopathies. Mutations in the MAPT gene that encodes tau can cause frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), providing the clearest evidence that tauopathy plays a causal role in neurodegeneration. Read More

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http://dx.doi.org/10.1038/s41374-019-0197-xDOI Listing
February 2019

Excessive Daytime Sleepiness in Major Dementia Syndromes.

Am J Alzheimers Dis Other Demen 2019 Feb 10:1533317519828046. Epub 2019 Feb 10.

1 Mayo Clinic, Rochester, MN, USA.

There has been no comparison of excessive daytime sleepiness (EDS) in patients with Alzheimer's disease dementia (AD), dementia with Lewy bodies (DLB), and behavioral variant frontotemporal dementia (bvFTD). We identified patients with mild dementia who met criteria for these disorders who also had the Epworth Sleepiness Scale (ESS) completed. The sample included 17 bvFTD, 111 AD, and 31 DLB. Read More

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http://dx.doi.org/10.1177/1533317519828046DOI Listing
February 2019
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Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD.

Authors:
Cyril Pottier Yingxue Ren Ralph B Perkerson Matt Baker Gregory D Jenkins Marka van Blitterswijk Mariely DeJesus-Hernandez Jeroen G J van Rooij Melissa E Murray Elizabeth Christopher Shannon K McDonnell Zachary Fogarty Anthony Batzler Shulan Tian Cristina T Vicente Billie Matchett Anna M Karydas Ging-Yuek Robin Hsiung Harro Seelaar Merel O Mol Elizabeth C Finger Caroline Graff Linn Öijerstedt Manuela Neumann Peter Heutink Matthis Synofzik Carlo Wilke Johannes Prudlo Patrizia Rizzu Javier Simon-Sanchez Dieter Edbauer Sigrun Roeber Janine Diehl-Schmid Bret M Evers Andrew King M Marsel Mesulam Sandra Weintraub Changiz Geula Kevin F Bieniek Leonard Petrucelli Geoffrey L Ahern Eric M Reiman Bryan K Woodruff Richard J Caselli Edward D Huey Martin R Farlow Jordan Grafman Simon Mead Lea T Grinberg Salvatore Spina Murray Grossman David J Irwin Edward B Lee EunRan Suh Julie Snowden David Mann Nilufer Ertekin-Taner Ryan J Uitti Zbigniew K Wszolek Keith A Josephs Joseph E Parisi David S Knopman Ronald C Petersen John R Hodges Olivier Piguet Ethan G Geier Jennifer S Yokoyama Robert A Rissman Ekaterina Rogaeva Julia Keith Lorne Zinman Maria Carmela Tartaglia Nigel J Cairns Carlos Cruchaga Bernardino Ghetti Julia Kofler Oscar L Lopez Thomas G Beach Thomas Arzberger Jochen Herms Lawrence S Honig Jean Paul Vonsattel Glenda M Halliday John B Kwok Charles L White Marla Gearing Jonathan Glass Sara Rollinson Stuart Pickering-Brown Jonathan D Rohrer John Q Trojanowski Vivianna Van Deerlin Eileen H Bigio Claire Troakes Safa Al-Sarraj Yan Asmann Bruce L Miller Neill R Graff-Radford Bradley F Boeve William W Seeley Ian R A Mackenzie John C van Swieten Dennis W Dickson Joanna M Biernacka Rosa Rademakers

Acta Neuropathol 2019 Feb 9. Epub 2019 Feb 9.

Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL, 32224, USA.

Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) represents the most common pathological subtype of FTLD. We established the international FTLD-TDP whole-genome sequencing consortium to thoroughly characterize the known genetic causes of FTLD-TDP and identify novel genetic risk factors. Through the study of 1131 unrelated Caucasian patients, we estimated that C9orf72 repeat expansions and GRN loss-of-function mutations account for 25. Read More

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http://link.springer.com/10.1007/s00401-019-01962-9
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http://dx.doi.org/10.1007/s00401-019-01962-9DOI Listing
February 2019
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Validation of the revised classification of cognitive and behavioural impairment in ALS.

J Neurol Neurosurg Psychiatry 2019 Feb 7. Epub 2019 Feb 7.

ALS Center, 'Rita Levi Montalcini' Department of Neuroscience, University of Turin, Torino, Italy

Objective: In 2017, the diagnostic criteria for cognitive and behavioural impairment in amyotrophic lateral sclerosis (ALS) with frontotemporal dementia (ALSFTD-1) have been modified (ALSFTD-2) with the inclusion of a novel category (ALS with combined cognitive and behavioural impairment, ALScbi) and with changes of operational criteria of the other categories (ALS with cognitive impairment (ALSci), ALS with behavioural impairment (ALSbi) and ALS with frontotemporal dementia (ALS-FTD)). We compared the two sets of criteria to assess the effect of the revised criteria on the cognitive classification of patients with ALS.

Methods: Two cohorts of patients with ALS were included in this study: a population-based cohort including patients identified through the Piemonte/Valle d'Aosta register for ALS in the 2014-2017 period (n=321), and a referral cohort recruited at the Turin ALS centre and at the ALS centre of the Maugeri Institute in Milan in the same period (n=205). Read More

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http://dx.doi.org/10.1136/jnnp-2018-319696DOI Listing
February 2019
2 Reads

Comparison of clinical and neuropathological diagnoses of neurodegenerative diseases in two centres from the Brains for Dementia Research (BDR) cohort.

J Neural Transm (Vienna) 2019 Feb 7. Epub 2019 Feb 7.

Department of Basic and Clinical Neuroscience, IoPPN, King's College London, London, UK.

Early detection and accurate diagnosis of neurodegenerative disorders may provide better epidemiological data, closer monitoring of disease progression and enable more specialised intervention. We analysed the clinical records and pathology of brain donations from 180 patients from two Brains for Dementia Research cohorts to determine the agreement between in-life clinical diagnosis and post-mortem pathological results. Clinical diagnosis was extracted from medical records and cases assigned into broad clinical groups; control, Alzheimer's disease (AD), vascular dementia (CVD), dementia with Lewy bodies (DLB), frontotemporal dementia (FTD) and combined diseases. Read More

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http://dx.doi.org/10.1007/s00702-018-01967-wDOI Listing
February 2019
2 Reads

Risk of caregiver burden in patients with three types of dementia.

Authors:
Tomoyuki Kawada

Int Psychogeriatr 2019 Jan;31(1):153

Department of Hygiene and Public Health,Nippon Medical School,Bunkyo-Ku,Tokyo,Japan.

Liu et al. (2017) investigated caregiver burden of patients with frontotemporal lobar degeneration (FTD) and dementia with Lewy bodies (DLB), which was compared with caregivers of patients with Alzheimer's disease. The authors concluded that the frequency and severity of behavioral disturbances in caregiver of patients with FTD and DLB were higher than those with caregivers of patients with Alzheimer's disease. Read More

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http://dx.doi.org/10.1017/S1041610218000662DOI Listing
January 2019
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Dementia with Lewy bodies presenting as frontotemporal dementia phenotype.

Psychogeriatrics 2019 Feb 6. Epub 2019 Feb 6.

Kawasaki Memorial Hospital, Kawasaki-city, Japan.

We herein report two patients with dementia with Lewy bodies (DLB) presenting characteristic symptoms suggestive of the behavioural variant of frontotemporal dementia (bvFTD). Patient 1 presented behavioural and personality changes from the onset, such as restlessness, compulsive behaviours, and stereotypical speech. A neuroimaging study showed preferential frontal involvement, and this patient fulfilled the diagnostic criteria for bvFTD. Read More

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http://dx.doi.org/10.1111/psyg.12405DOI Listing
February 2019
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PARylation regulates stress granule dynamics, phase separation, and neurotoxicity of disease-related RNA-binding proteins.

Cell Res 2019 Feb 6. Epub 2019 Feb 6.

Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, 201210, China.

Mutations in RNA-binding proteins (RBPs) localized in ribonucleoprotein (RNP) granules, such as hnRNP A1 and TDP-43, promote aberrant protein aggregation, which is a pathological hallmark of various neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Protein posttranslational modifications (PTMs) are known to regulate RNP granules. In this study, we investigate the function of poly(ADP-ribosyl)ation (PARylation), an important PTM involved in DNA damage repair and cell death, in RNP granule-related neurodegeneration. Read More

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http://dx.doi.org/10.1038/s41422-019-0141-zDOI Listing
February 2019
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Atypical globular glial tauopathy with a combination of types I and II pathology.

Neuropathology 2019 Feb 5. Epub 2019 Feb 5.

Department of Neuropathology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Globular glial tauopathy (GGT) is a group of 4-repeat tauopathies characterized by widespread globular glial inclusions (GGIs). GGT is now classified into three subtypes based on the distribution and morphology of the GGIs. We report an autopsy case of GGT in an 85-year-old woman who presented with semantic dementia, a rare phenotype in GGT. Read More

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https://onlinelibrary.wiley.com/doi/abs/10.1111/neup.12536
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http://dx.doi.org/10.1111/neup.12536DOI Listing
February 2019
6 Reads

Heritability in frontotemporal tauopathies.

Alzheimers Dement (Amst) 2019 Dec 24;11:115-124. Epub 2019 Jan 24.

Faculty of Medicine and Health, Charles Perkins Centre and Discipline of Pathology, University of Sydney, Sydney, Australia.

Introduction: Exploring the degree of heritability in a large cohort of frontotemporal lobar degeneration with tau-immunopositive inclusions (FTLD-tau) and determining if different FTLD-tau subtypes are associated with stronger heritability will provide important insight into disease pathogenesis.

Methods: Using modified Goldman pedigree classifications, heritability was examined in pathologically proven FTLD-tau cases with dementia at any time (n = 124) from the Sydney-Cambridge collection.

Results: Thirteen percent of the FTLD-tau cohort have a suggested autosomal dominant pattern of inheritance, 25% have some family history, and 62% apparently sporadic. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S23528729183008
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http://dx.doi.org/10.1016/j.dadm.2018.12.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6351353PMC
December 2019
2 Reads

Hippocampal atrophy and intrinsic brain network dysfunction relate to alterations in mind wandering in neurodegeneration.

Proc Natl Acad Sci U S A 2019 Feb 4;116(8):3316-3321. Epub 2019 Feb 4.

Brain and Mind Centre, University of Sydney, Sydney 2050, Australia;

Mind wandering represents the human capacity for internally focused thought and relies upon the brain's default network and its interactions with attentional networks. Studies have characterized mind wandering in healthy people, yet there is limited understanding of how this capacity is affected in clinical populations. This paper used a validated thought-sampling task to probe mind wandering capacity in two neurodegenerative disorders: behavioral variant frontotemporal dementia [(bvFTD); = 35] and Alzheimer's disease [(AD); = 24], compared with older controls ( = 37). Read More

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http://dx.doi.org/10.1073/pnas.1818523116DOI Listing
February 2019
1 Read

Parkinsonisms and Glucocerebrosidase Deficiency: A Comprehensive Review for Molecular and Cellular Mechanism of Glucocerebrosidase Deficiency.

Brain Sci 2019 Feb 1;9(2). Epub 2019 Feb 1.

Department of Neurology, Parkinson's Disease and Movement Disorders Section, Institute of Neuroscience of Buenos Aires (INEBA). Guardia Vieja 4435, Buenos Aires C1192AAW, Argentina.

In the last years, lysosomal storage diseases appear as a bridge of knowledge between rare genetic inborn metabolic disorders and neurodegenerative diseases such as Parkinson's disease (PD) or frontotemporal dementia. Epidemiological studies helped promote research in the field that continues to improve our understanding of the link between mutations in the glucocerebrosidase (GBA) gene and PD. We conducted a review of this link, highlighting the association in GBA mutation carriers and in Gaucher disease type 1 patients (GD type 1). Read More

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http://dx.doi.org/10.3390/brainsci9020030DOI Listing
February 2019
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The inner fluctuations of the brain in presymptomatic Frontotemporal Dementia: The chronnectome fingerprint.

Neuroimage 2019 Feb 1;189:645-654. Epub 2019 Feb 1.

Centre for Neurodegenerative Disorders, Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy. Electronic address:

Frontotemporal Dementia (FTD) is preceded by a long period of subtle brain changes, occurring in the absence of overt cognitive symptoms, that need to be still fully characterized. Dynamic network analysis based on resting-state magnetic resonance imaging (rs-fMRI) is a potentially powerful tool for the study of preclinical FTD. In the present study, we employed a "chronnectome" approach (recurring, time-varying patterns of connectivity) to evaluate measures of dynamic connectivity in 472 at-risk FTD subjects from the Genetic Frontotemporal dementia research Initiative (GENFI) cohort. Read More

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http://dx.doi.org/10.1016/j.neuroimage.2019.01.080DOI Listing
February 2019
1 Read
6.357 Impact Factor

A Case with Early Onset Alzheimer's Disease, Frontotemporal Hypometabolism, ApoE Genotype ɛ4/ɛ4 and C9ORF72 Intermediate Expansion: A Treviso Dementia (TREDEM) Registry Case Report.

J Alzheimers Dis 2019 ;67(3):985-993

Cognitive Impairment Center, Local Health Autority n.2 Marca Trevigiana, Treviso, Italy.

We report the case of a woman firstly referred to our Memory Clinic at the age of 61, following the development of cognitive complaints and difficulties in sustained attention. The investigation that was performed showed: predominant executive dysfunctions at the neuropsychological evaluation, with mild, partial and stable involvement of the memory domain; cortical and subcortical atrophy with well-preserved hippocampal structures at MRI; marked fronto-temporal and moderate parietal hypometabolism from 18F-FDG PET study with a sparing of the posterior cingulate and precuneus; positivity of amyloid-β at 18F-Flutemetamol PET; an hexanucleotide intermediate repeats expansion of C9ORF72 gene (12//38 repeats) and ApoE genotype ɛ4/ɛ4. The patient was diagnosed with probable early onset frontal variant of Alzheimer's disease (AD), presenting with a major executive function impairment. Read More

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http://dx.doi.org/10.3233/JAD-180715DOI Listing
January 2019
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18F-Florbetaben PET/CT to Assess Alzheimer's Disease: A new Analysis Method for Regional Amyloid Quantification.

J Neuroimaging 2019 Feb 3. Epub 2019 Feb 3.

U.O.C. Neurologia, Fondazione IstitutoG. Giglio, Contrada Pietrapollastra-Pisciotto, 90015, Cefalù, Italy.

Background And Purpose: While AD can be definitively confirmed by postmortem histopathologic examination, in vivo imaging may improve the clinician's ability to identify AD at the earliest stage. The aim of the study was to test the performance of amyloid PET using new processing imaging algorithm for more precise diagnosis of AD.

Methods: Amyloid PET results using a new processing imaging algorithm (MRI-Less and AAL Atlas) were correlated with clinical, cognitive status, CSF analysis, and other imaging. Read More

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http://dx.doi.org/10.1111/jon.12601DOI Listing
February 2019
3 Reads

Diagnostic and Prognostic Performance of Neurofilaments in ALS.

Front Neurol 2018 18;9:1167. Epub 2019 Jan 18.

Laboratory of Neurobiology, Department of Neurosciences, KU Leuven and Center for Brain & Disease Research VIB Leuven, Leuven, Belgium.

There is a need for biomarkers for amyotrophic lateral sclerosis (ALS), to support the diagnosis of the disease, to predict disease progression and to track disease activity and treatment responses. Over the last decade multiple studies have investigated the potential of neurofilament levels, both in cerebrospinal fluid and blood, as biomarker for ALS. The most widely studied neurofilament subunits are neurofilament light chain (NfL) and phosphorylated neurofilament heavy chain (pNfH). Read More

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https://www.frontiersin.org/article/10.3389/fneur.2018.01167
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http://dx.doi.org/10.3389/fneur.2018.01167DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6345692PMC
January 2019
4 Reads

Depression and risk of Cognitive Dysfunctions in Amyotrophic Lateral Sclerosis.

Acta Neurol Scand 2019 Feb 3. Epub 2019 Feb 3.

Department of Neurology, University of Piemonte Orientale, Maggiore della Carità Hospital, Novara, Italy.

Objectives: ALS is not only a motor disorder: more than 50% of patients have cognitive dysfunctions over the course of the disease. At the same time, mood disorders may also occur in ALS patients following diagnosis due to the fatal prognosis; however little data is available on any depression beforehand. Starting from these considerations, the aim of our study was to investigate the occurrence of depression in Italian ALS patients prior to diagnosis, evaluating its prevalence in the subjects who have developed cognitive dysfunctions and in those who did not. Read More

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http://doi.wiley.com/10.1111/ane.13073
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http://dx.doi.org/10.1111/ane.13073DOI Listing
February 2019
3 Reads

Progression of logopenic aphasia to frontotemporal dementia in an amyloid β-negative and F-THK-5351-positive patient.

Psychogeriatrics 2019 Feb 3. Epub 2019 Feb 3.

Department of Neuropsychiatry, Faculty of Medicine, Kindai University, Osaka, Japan.

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http://dx.doi.org/10.1111/psyg.12396DOI Listing
February 2019
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Clinical and biomarker changes in presymptomatic genetic frontotemporal dementia.

Neurobiol Aging 2019 Jan 7;76:133-140. Epub 2019 Jan 7.

Department of Clinical and Experimental Sciences, Neurology Unit, University of Brescia, Brescia, Italy. Electronic address:

Presymptomatic carriers of GRN and C9orf72 mutations, the most frequent genetic causes of frontotemporal lobar degeneration, represent the optimal target population for the development of disease-modifying drugs. Preclinical biomarkers are needed to monitor the effect of therapeutic interventions in this population. We assessed clinical, functional, and neurophysiological measures in 113 GRN or C9orf72 carriers and in 73 noncarrier first-degree relatives. Read More

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http://dx.doi.org/10.1016/j.neurobiolaging.2018.12.018DOI Listing
January 2019
5.013 Impact Factor

Proinflammatory and anti-inflammatory cytokines in the CSF of patients with Alzheimer's disease and their correlation with cognitive decline.

Neurobiol Aging 2019 Jan 7;76:125-132. Epub 2019 Jan 7.

Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus de Gualtar, Braga, Portugal; ICVS/3B's - PT Government Associate Laboratory, Braga, Guimarães, Portugal; Centro Clínico Académico (2CA), Braga, Portugal.

Cumulative data suggest that neuroinflammation plays a prominent role in Alzheimer's disease (AD) pathogenesis. The purpose of this work was to assess if patients with AD present a specific cerebrospinal fluid (CSF) cytokine profile and if it correlates to disease progression. We determined the levels of 27 cytokines in CSF of patients with AD and compared them with patients with frontotemporal dementia and nondemented controls. Read More

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http://dx.doi.org/10.1016/j.neurobiolaging.2018.12.019DOI Listing
January 2019
2 Reads

Gray and white matter changes in presymptomatic genetic frontotemporal dementia: a longitudinal MRI study.

Neurobiol Aging 2019 Jan 7;76:115-124. Epub 2019 Jan 7.

Department of Neurology, Erasmus Medical Center, Rotterdam, the Netherlands. Electronic address:

In genetic frontotemporal dementia, cross-sectional studies have identified profiles of presymptomatic neuroanatomical loss for C9orf72 repeat expansion, MAPT, and GRN mutations. In this study, we characterize longitudinal gray matter (GM) and white matter (WM) brain changes in presymptomatic frontotemporal dementia. We included healthy carriers of C9orf72 repeat expansion (n = 12), MAPT (n = 15), GRN (n = 33) mutations, and related noncarriers (n = 53), that underwent magnetic resonance imaging at baseline and 2-year follow-up. Read More

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http://dx.doi.org/10.1016/j.neurobiolaging.2018.12.017DOI Listing
January 2019
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Clinical and neuroimaging investigations of language disturbance in frontotemporal dementia-motor neuron disease patients.

J Neurol 2019 Feb 1. Epub 2019 Feb 1.

Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia.

This study systematically investigated the neuropsychological profile of language disturbance in frontotemporal dementia-motor neuron disease (FTD-MND) using a data-driven approach. Neuroanatomical correlates of language profiles were also examined. Patients with FTD-MND (N = 26), pure motor neuron disease (N = 34), progressive non-fluent aphasia (N = 30), semantic dementia (N = 17), and controls (N = 31) underwent comprehensive language assessments. Read More

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http://dx.doi.org/10.1007/s00415-019-09216-0DOI Listing
February 2019
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Hippocampal Sclerosis, Argyrophilic Grain Disease, and Primary Age-Related Tauopathy.

Continuum (Minneap Minn) 2019 Feb;25(1):208-233

Purpose Of Review: Hippocampal sclerosis, argyrophilic grain disease, and primary age-related tauopathy are common Alzheimer disease mimics that currently lack clinical diagnostic criteria. Increased understanding of these pathologic entities is important for the neurologist who may encounter patients with an unusually slowly progressive degenerative dementia that may appear to meet criteria for Alzheimer disease but who progress to develop symptoms that are unusual for classic Alzheimer disease RECENT FINDINGS: Hippocampal sclerosis has traditionally been associated with hypoxic/ischemic injury and poorly controlled epilepsy, but it is now recognized that hippocampal sclerosis may also be associated with a unique degenerative disease of aging or may be an associated pathologic finding in many cases of frontotemporal lobar degeneration. Argyrophilic grain disease has been recognized as an enigma in the field of pathology for over 30 years, but recent discoveries suggest that it may overlap with other tau-related disorders within the spectrum of frontotemporal lobar degeneration. Read More

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http://Insights.ovid.com/crossref?an=00132979-201902000-0001
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http://dx.doi.org/10.1212/CON.0000000000000697DOI Listing
February 2019
5 Reads

Behavioral Variant Frontotemporal Dementia.

Authors:
William W Seeley

Continuum (Minneap Minn) 2019 Feb;25(1):76-100

Purpose Of Review: This article describes the clinical, anatomic, genetic, and pathologic features of behavioral variant frontotemporal dementia (bvFTD) and discusses strategies to improve diagnostic accuracy, emphasizing common pitfalls to avoid. Key aspects of management and the future of diagnosis and care for the disorder are highlighted.

Recent Findings: BvFTD is a clinical syndrome, not a disease. Read More

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http://dx.doi.org/10.1212/CON.0000000000000698DOI Listing
February 2019

F-flortaucipir (AV-1451) tau PET in frontotemporal dementia syndromes.

Alzheimers Res Ther 2019 Jan 31;11(1):13. Epub 2019 Jan 31.

Memory and Aging Center, University of California at San Francisco, 675 Nelson Rising Lane, Suite 190, San Francisco, CA, USA.

Background: The tau positron emission tomography (PET) ligand F-flortaucipir binds to paired helical filaments of tau in aging and Alzheimer's disease (AD), but its utility in detecting tau aggregates in frontotemporal dementia (FTD) is uncertain.

Methods: We performed F-flortaucipir imaging in patients with the FTD syndromes (n = 45): nonfluent variant primary progressive aphasia (nfvPPA) (n = 11), corticobasal syndrome (CBS) (n = 10), behavioral variant frontotemporal dementia (bvFTD) (n = 10), semantic variant primary progressive aphasia (svPPA) (n = 2) and FTD associated pathogenic genetic mutations microtubule-associated protein tau (MAPT) (n = 6), chromosome 9 open reading frame 72 (C9ORF72) (n = 5), and progranulin (GRN) (n = 1). All patients underwent MRI and β-amyloid biomarker testing via C-PiB or cerebrospinal fluid. Read More

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https://alzres.biomedcentral.com/articles/10.1186/s13195-019
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http://dx.doi.org/10.1186/s13195-019-0470-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6357510PMC
January 2019
11 Reads

[Antidementia Drug Therapy of Alzheimer's Dementia: Status 2018 and Outlook].

Dtsch Med Wochenschr 2019 Feb 31;144(3):156-160. Epub 2019 Jan 31.

Abteilung für Gerontopsychiatrie, ZI Mannheim, Medizinische Fakultät Mannheim, Universität Heidelberg.

Antidementia therapy: The clinical use of acetylcholinesterase inhibitors (AChE-I) for the symptomatic treatment of mild to moderate Alzheimer's dementia is recognized worldwide, despite its modest effectiveness. AChE-I may be continued to be used into severe stages of the dementia. In moderate to severe Alzheimer's dementia, the NMDA-receptor-antagonist Memantin is indicated. Read More

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http://dx.doi.org/10.1055/a-0658-6720DOI Listing
February 2019
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The longitudinal decline of white matter microstructural integrity in behavioral variant frontotemporal dementia and its association with executive function.

Neurobiol Aging 2018 Dec 25;76:62-70. Epub 2018 Dec 25.

The State Key Laboratory of Brain and Cognitive Sciences, Department of Psychology, The University of Hong Kong, Hong Kong; Laboratory of Neuropsychology, Department of Psychology, The University of Hong Kong, Hong Kong; Institute of Clinical Neuropsychology, Department of Psychology, The University of Hong Kong, Hong Kong. Electronic address:

The longitudinal decline in the integrity of several white matter (WM) tracts in behavioral variant frontotemporal dementia (bvFTD) has been documented. However, there is yet a clear relationship between this decline and that of executive function (EF), for the WM changes to meaningfully track progression in bvFTD. We sought to validate the use of diffusion tensor imaging (DTI) in tracking the progression of bvFTD with its associated decline in EF. Read More

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http://dx.doi.org/10.1016/j.neurobiolaging.2018.12.005DOI Listing
December 2018