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Dive into the research topics where Murray Grossman is active.

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Featured researches published by Murray Grossman.


Neurology | 2011

Classification of primary progressive aphasia and its variants

Maria Luisa Gorno-Tempini; Argye E. Hillis; Sandra Weintraub; Andrew Kertesz; Mario F. Mendez; S. F. Cappa; Jennifer M. Ogar; Jonathan D. Rohrer; Sandra E. Black; B. F. Boeve; Facundo Manes; Nina F. Dronkers; Rik Vandenberghe; Katya Rascovsky; Karalyn Patterson; Bruce L. Miller; D. S. Knopman; John R. Hodges; M.-Marsel Mesulam; Murray Grossman

This article provides a classification of primary progressive aphasia (PPA) and its 3 main variants to improve the uniformity of case reporting and the reliability of research results. Criteria for the 3 variants of PPA—nonfluent/agrammatic, semantic, and logopenic—were developed by an international group of PPA investigators who convened on 3 occasions to operationalize earlier published clinical descriptions for PPA subtypes. Patients are first diagnosed with PPA and are then divided into clinical variants based on specific speech and language features characteristic of each subtype. Classification can then be further specified as “imaging-supported” if the expected pattern of atrophy is found and “with definite pathology” if pathologic or genetic data are available. The working recommendations are presented in lists of features, and suggested assessment tasks are also provided. These recommendations have been widely agreed upon by a large group of experts and should be used to ensure consistency of PPA classification in future studies. Future collaborations will collect prospective data to identify relationships between each of these syndromes and specific biomarkers for a more detailed understanding of clinicopathologic correlations.


Medical Image Analysis | 2008

Symmetric Diffeomorphic Image Registration with Cross-Correlation: Evaluating Automated Labeling of Elderly and Neurodegenerative Brain

Brian B. Avants; Charles L. Epstein; Murray Grossman; James C. Gee

One of the most challenging problems in modern neuroimaging is detailed characterization of neurodegeneration. Quantifying spatial and longitudinal atrophy patterns is an important component of this process. These spatiotemporal signals will aid in discriminating between related diseases, such as frontotemporal dementia (FTD) and Alzheimers disease (AD), which manifest themselves in the same at-risk population. Here, we develop a novel symmetric image normalization method (SyN) for maximizing the cross-correlation within the space of diffeomorphic maps and provide the Euler-Lagrange equations necessary for this optimization. We then turn to a careful evaluation of our method. Our evaluation uses gold standard, human cortical segmentation to contrast SyNs performance with a related elastic method and with the standard ITK implementation of Thirions Demons algorithm. The new method compares favorably with both approaches, in particular when the distance between the template brain and the target brain is large. We then report the correlation of volumes gained by algorithmic cortical labelings of FTD and control subjects with those gained by the manual rater. This comparison shows that, of the three methods tested, SyNs volume measurements are the most strongly correlated with volume measurements gained by expert labeling. This study indicates that SyN, with cross-correlation, is a reliable method for normalizing and making anatomical measurements in volumetric MRI of patients and at-risk elderly individuals.


Neurology | 2013

Criteria for the diagnosis of corticobasal degeneration.

Melissa J. Armstrong; Irene Litvan; Anthony E. Lang; Thomas H. Bak; Kailash P. Bhatia; Barbara Borroni; Adam L. Boxer; Dennis W. Dickson; Murray Grossman; Mark Hallett; Keith A. Josephs; Andrew Kertesz; Suzee E. Lee; Bruce L. Miller; Stephen G. Reich; David E. Riley; Eduardo Tolosa; Alexander I. Tröster; Marie Vidailhet; William J. Weiner

Current criteria for the clinical diagnosis of pathologically confirmed corticobasal degeneration (CBD) no longer reflect the expanding understanding of this disease and its clinicopathologic correlations. An international consortium of behavioral neurology, neuropsychology, and movement disorders specialists developed new criteria based on consensus and a systematic literature review. Clinical diagnoses (early or late) were identified for 267 nonoverlapping pathologically confirmed CBD cases from published reports and brain banks. Combined with consensus, 4 CBD phenotypes emerged: corticobasal syndrome (CBS), frontal behavioral-spatial syndrome (FBS), nonfluent/agrammatic variant of primary progressive aphasia (naPPA), and progressive supranuclear palsy syndrome (PSPS). Clinical features of CBD cases were extracted from descriptions of 209 brain bank and published patients, providing a comprehensive description of CBD and correcting common misconceptions. Clinical CBD phenotypes and features were combined to create 2 sets of criteria: more specific clinical research criteria for probable CBD and broader criteria for possible CBD that are more inclusive but have a higher chance to detect other tau-based pathologies. Probable CBD criteria require insidious onset and gradual progression for at least 1 year, age at onset ≥50 years, no similar family history or known tau mutations, and a clinical phenotype of probable CBS or either FBS or naPPA with at least 1 CBS feature. The possible CBD category uses similar criteria but has no restrictions on age or family history, allows tau mutations, permits less rigorous phenotype fulfillment, and includes a PSPS phenotype. Future validation and refinement of the proposed criteria are needed.


Neurology | 2007

DLB and PDD boundary issues: Diagnosis, treatment, molecular pathology, and biomarkers

Carol F. Lippa; John E. Duda; Murray Grossman; Howard I. Hurtig; Dag Aarsland; Bradley F. Boeve; David J. Brooks; Dennis W. Dickson; Bruno Dubois; Murat Emre; Stanley Fahn; Jennifer M. Farmer; Douglas Galasko; James E. Galvin; Christopher G. Goetz; J. H. Growdon; Katrina Gwinn-Hardy; John Hardy; Peter Heutink; Takeshi Iwatsubo; Kenji Kosaka; Virginia M.-Y. Lee; Jim Leverenz; E. Masliah; Ian G. McKeith; Robert L. Nussbaum; C. W. Olanow; Bernard Ravina; Andrew Singleton; C. M. Tanner

For more than a decade, researchers have refined criteria for the diagnosis of dementia with Lewy bodies (DLB) and at the same time have recognized that cognitive impairment and dementia occur commonly in patients with Parkinson disease (PD). This article addresses the relationship between DLB, PD, and PD with dementia (PDD). The authors agreed to endorse “Lewy body disorders” as the umbrella term for PD, PDD, and DLB, to promote the continued practical use of these three clinical terms, and to encourage efforts at drug discovery that target the mechanisms of neurodegeneration shared by these disorders of α-synuclein metabolism. We concluded that the differing temporal sequence of symptoms and clinical features of PDD and DLB justify distinguishing these disorders. However, a single Lewy body disorder model was deemed more useful for studying disease pathogenesis because abnormal neuronal α-synuclein inclusions are the defining pathologic process common to both PDD and DLB. There was consensus that improved understanding of the pathobiology of α-synuclein should be a major focus of efforts to develop new disease-modifying therapies for these disorders. The group agreed on four important priorities: 1) continued communication between experts who specialize in PDD or DLB; 2) initiation of prospective validation studies with autopsy confirmation of DLB and PDD; 3) development of practical biomarkers for α-synuclein pathologies; 4) accelerated efforts to find more effective treatments for these diseases.


Annals of Neurology | 2006

Frontotemporal dementia: clinicopathological correlations.

Jennifer M. Farmer; Julene K. Johnson; Christopher M. Clark; Steven E. Arnold; H. Branch Coslett; Anjan Chatterjee; Howard I. Hurtig; Jason Karlawish; Howard J. Rosen; Vivianna M. Van Deerlin; Virginia M.-Y. Lee; Bruce L. Miller; John Q. Trojanowski; Murray Grossman

Frontotemporal lobar degeneration (FTLD) is characterized by impairments in social, behavioral, and/or language function, but postmortem studies indicate that multiple neuropathological entities lead to FTLD. This study assessed whether specific clinical features predict the underlying pathology.


Science | 2015

Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways

Elizabeth T. Cirulli; Brittany N. Lasseigne; Slavé Petrovski; Peter C. Sapp; Patrick A. Dion; Claire S. Leblond; Julien Couthouis; Yi Fan Lu; Quanli Wang; Brian Krueger; Zhong Ren; Jonathan Keebler; Yujun Han; Shawn Levy; Braden E. Boone; Jack R. Wimbish; Lindsay L. Waite; Angela L. Jones; John P. Carulli; Aaron G. Day-Williams; John F. Staropoli; Winnie Xin; Alessandra Chesi; Alya R. Raphael; Diane McKenna-Yasek; Janet Cady; J.M.B.Vianney de Jong; Kevin Kenna; Bradley Smith; Simon Topp

New players in Lou Gehrigs disease Amyotrophic lateral sclerosis (ALS), often referred to as “Lou Gehrigs disease,” is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. Cirulli et al. sequenced the expressed genes of nearly 3000 ALS patients and compared them with those of more than 6000 controls (see the Perspective by Singleton and Traynor). They identified several proteins that were linked to disease in patients. One such protein, TBK1, is implicated in innate immunity and autophagy and may represent a therapeutic target. Science, this issue p. 1436; see also p. 1422 Analysis of the expressed genes of nearly 2900 patients with amyotrophic lateral sclerosis and about 6400 controls reveals a disease predisposition–associated gene. [Also see Perspective by Singleton and Traynor] Amyotrophic lateral sclerosis (ALS) is a devastating neurological disease with no effective treatment. We report the results of a moderate-scale sequencing study aimed at increasing the number of genes known to contribute to predisposition for ALS. We performed whole-exome sequencing of 2869 ALS patients and 6405 controls. Several known ALS genes were found to be associated, and TBK1 (the gene encoding TANK-binding kinase 1) was identified as an ALS gene. TBK1 is known to bind to and phosphorylate a number of proteins involved in innate immunity and autophagy, including optineurin (OPTN) and p62 (SQSTM1/sequestosome), both of which have also been implicated in ALS. These observations reveal a key role of the autophagic pathway in ALS and suggest specific targets for therapeutic intervention.


Annals of Neurology | 2013

Stages of pTDP-43 pathology in amyotrophic lateral sclerosis

Johannes Brettschneider; Kelly Del Tredici; Jon B. Toledo; John L. Robinson; David J. Irwin; Murray Grossman; EunRan Suh; Vivianna M. Van Deerlin; Elisabeth McCarty Wood; Young Min Baek; Linda Kwong; Edward B. Lee; Lauren Elman; Leo McCluskey; Lubin Fang; Simone Feldengut; Albert C. Ludolph; Virginia M.-Y. Lee; Heiko Braak; John Q. Trojanowski

To see whether the distribution patterns of phosphorylated 43kDa TAR DNA‐binding protein (pTDP‐43) intraneuronal inclusions in amyotrophic lateral sclerosis (ALS) permit recognition of neuropathological stages.


Annals of Neurology | 2000

Assessment of cerebral blood flow in Alzheimer's disease by spin‐labeled magnetic resonance imaging

David C. Alsop; John A. Detre; Murray Grossman

To evaluate the utility of arterial spin‐labeled blood flow magnetic resonance imaging for the detection of cerebral blood flow abnormalities in Alzheimers disease, arterial spin‐labeled blood flow images in 16 contiguous 5‐mm axial sections were acquired in 18 patients diagnosed with probable Alzheimers disease and 11 age‐matched controls. Blood flow images from all subjects were transformed to a standard anatomical space for voxel‐by‐voxel statistical analysis. High quality blood flow images were obtained from all but 1 subject. Statistical analysis demonstrated significant flow decreases relative to control subjects in temporal, parietal, frontal, and posterior cingulate cortices. Increased severity of disease, as measured by Mini‐Mental State Examination, correlated with posterior parietal and posterior cingulate decreases but not temporal decreases. Arterial spin‐labeled magnetic resonance imaging was found to be an effective tool for characterizing flow decreases accompanying Alzheimers disease. The absence of ionizing radiation or injection and the ability to obtain high quality anatomical images within the same scanning session make arterial spin labeling an attractive technique for the study of Alzheimers disease, for the evaluation of pharmacological therapies, and, possibly, for early diagnosis. Ann Neural 2000; 47:93–100


Nature Genetics | 2010

Common variants at 7p21 are associated with frontotemporal lobar degeneration with TDP-43 inclusions

Vivianna M. Van Deerlin; Patrick Sleiman; Maria Martinez-Lage; Alice Chen-Plotkin; Li-San Wang; Neill R. Graff-Radford; Dennis W. Dickson; Rosa Rademakers; Bradley F. Boeve; Murray Grossman; Steven E. Arnold; David Mann; Stuart Pickering-Brown; Harro Seelaar; Peter Heutink; John C. van Swieten; Jill R. Murrell; Bernardino Ghetti; Salvatore Spina; Jordan Grafman; John R. Hodges; Maria Grazia Spillantini; Sid Gilman; Andrew P. Lieberman; Jeffrey Kaye; Randall L. Woltjer; Eileen H. Bigio; M.-Marsel Mesulam; Safa Al-Sarraj; Claire Troakes

Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. The predominant neuropathology is FTLD with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP). FTLD-TDP is frequently familial, resulting from mutations in GRN (which encodes progranulin). We assembled an international collaboration to identify susceptibility loci for FTLD-TDP through a genome-wide association study of 515 individuals with FTLD-TDP. We found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM106B. Three SNPs retained genome-wide significance following Bonferroni correction (top SNP rs1990622, P = 1.08 × 10−11; odds ratio, minor allele (C) 0.61, 95% CI 0.53–0.71). The association replicated in 89 FTLD-TDP cases (rs1990622; P = 2 × 10−4). TMEM106B variants may confer risk of FTLD-TDP by increasing TMEM106B expression. TMEM106B variants also contribute to genetic risk for FTLD-TDP in individuals with mutations in GRN. Our data implicate variants in TMEM106B as a strong risk factor for FTLD-TDP, suggesting an underlying pathogenic mechanism.


Journal of Neuropathology and Experimental Neurology | 2008

Concomitant TAR-DNA-Binding Protein 43 Pathology Is Present in Alzheimer Disease and Corticobasal Degeneration but Not in Other Tauopathies

Kunihiro Uryu; Hanae Nakashima-Yasuda; Linda K. Kwong; Christopher M. Clark; Murray Grossman; Bruce L. Miller; Hans A. Kretzschmar; Virginia M.-Y. Lee; John Q. Trojanowski; Manuela Neumann

Pathologic TAR-DNA-binding protein 43 (TDP-43) is a disease protein in frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis. We studied the presence, frequency, and distribution of TDP-43 pathology by immunohistochemistry and biochemistry in a series of clinically well-characterized tauopathy patient brains, including 182 Alzheimer disease (AD), 39 corticobasal degeneration, 77 progressive supranuclear palsy, and 12 Pick disease cases and investigated the clinical impact of concomitant TDP-43 pathology in these cases. TAR-DNA-binding protein 43 pathology was found in 25.8% of AD cases. It was restricted to the dentate gyrus and entorhinal cortex in approximately 75% of cases; approximately 25% showed more widespread TDP-43 pathology in frontal and temporal cortices, resembling the FTLD-U subtype associated with progranulin mutations. TAR-DNA-binding protein 43 pathology in AD was associated with significantly longer disease duration, but there was no association with the clinical presentation (148 cases diagnosed as AD and 34 cases diagnosed as frontotemporal lobar degeneration). Progressive supranuclear palsy and Pick disease cases showed no TDP-43 inclusions and no biochemical alterations of TDP-43. There was, however, a unique, predominantly glial TDP-43 pathology with staining of astrocytic plaque-like structures and coiled bodies in 15.4% of corticobasal degeneration cases; this was associated with biochemical TDP-43 changes similar to those in FTLD-U. These findings provide further insight into the burden and clinical significance of TDP-43 pathology in disorders other than FTLD-U and amyotrophic lateral sclerosis.

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Corey T. McMillan

University of Pennsylvania

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David J. Irwin

University of Pennsylvania

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Peachie Moore

University of Pennsylvania

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Katya Rascovsky

University of Pennsylvania

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James C. Gee

University of Pennsylvania

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Leo McCluskey

University of Pennsylvania

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Lauren Elman

University of Pennsylvania

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