Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS

doi:10.1016/J.NEURON.2011.09.011

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Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS

Journal Article•DOI•

Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS

Mariely DeJesus-Hernandez¹, Ian R. A. Mackenzie², Bradley F. Boeve¹, Adam L. Boxer³, Matt Baker¹, Nicola J. Rutherford¹, Alexandra M. Nicholson¹, Ni Cole A. Finch¹, Heather C. Flynn¹, Jennifer Adamson¹, Naomi Kouri¹, Aleksandra Wojtas¹, Pheth Sengdy², Ging-Yuek Robin Hsiung², Anna Karydas³, William W. Seeley³, Keith A. Josephs¹, Giovanni Coppola⁴, Daniel H. Geschwind⁴, Zbigniew K. Wszolek¹, Howard Feldman², Howard Feldman⁵, David S. Knopman¹, Ronald C. Petersen¹, Bruce L. Miller³, Dennis W. Dickson¹, Kevin B. Boylan¹, Neill R. Graff-Radford¹, Rosa Rademakers¹ - Show less +25 more•Institutions (5)

Mayo Clinic¹, University of British Columbia², University of California, San Francisco³, Semel Institute for Neuroscience and Human Behavior⁴, Bristol-Myers Squibb⁵

20 Oct 2011-Neuron (NIH Public Access)-Vol. 72, Iss: 2, pp 245-256

TL;DR: It is found that repeat expansion in C9ORF72 is a major cause of both FTD and ALS, suggesting multiple disease mechanisms.

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About: This article is published in Neuron.The article was published on 2011-10-20 and is currently open access. It has received 4153 citations till now. The article focuses on the topics: Trinucleotide repeat expansion & C9orf72 Protein.

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Journal Article•DOI•

A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD

[...]

Alan E. Renton¹, Elisa Majounie¹, Adrian James Waite², Javier Simón-Sánchez³, Javier Simón-Sánchez⁴, Sara Rollinson⁵, J. Raphael Gibbs¹, J. Raphael Gibbs⁶, Jennifer C. Schymick¹, Hannu Laaksovirta⁷, John C. van Swieten³, John C. van Swieten⁴, Liisa Myllykangas⁷, Hannu Kalimo⁷, Anders Paetau⁷, Yevgeniya Abramzon¹, Anne M. Remes⁸, Alice Kaganovich¹, Sonja W. Scholz¹, Sonja W. Scholz⁹, Sonja W. Scholz¹⁰, Jamie Duckworth¹, Jinhui Ding¹, Daniel W. Harmer¹¹, Dena G. Hernandez⁶, Dena G. Hernandez¹, Janel O. Johnson¹, Janel O. Johnson⁶, Kin Y. Mok⁶, Mina Ryten⁶, Danyah Trabzuni⁶, Rita Guerreiro⁶, Richard W. Orrell⁶, James Neal², Alexandra Murray¹², J. P. Pearson², Iris E. Jansen³, David Sondervan³, Harro Seelaar⁴, Derek J. Blake², Kate Young⁵, Nicola Halliwell⁵, Janis Bennion Callister⁵, Greg Toulson⁵, Anna Richardson⁵, Alexander Gerhard⁵, Julie S. Snowden⁵, David M. A. Mann⁵, David Neary⁵, Mike A. Nalls¹, Terhi Peuralinna⁷, Lilja Jansson⁷, Veli-Matti Isoviita⁷, Anna-Lotta Kaivorinne⁸, Maarit Hölttä-Vuori⁷, Elina Ikonen⁷, Raimo Sulkava¹³, Michael Benatar¹⁴, Joanne Wuu¹⁴, Adriano Chiò¹⁵, Gabriella Restagno, Giuseppe Borghero¹⁶, Mario Sabatelli¹⁷, David Heckerman¹⁸, Ekaterina Rogaeva¹⁹, Lorne Zinman¹⁹, Jeffrey D. Rothstein⁹, Michael Sendtner²⁰, Carsten Drepper²⁰, Evan E. Eichler²¹, Can Alkan²¹, Ziedulla Abdullaev¹, Svetlana Pack¹, Amalia Dutra¹, Evgenia Pak¹, John Hardy⁶, Andrew B. Singleton¹, Nigel Williams², Peter Heutink³, Stuart Pickering-Brown⁵, Huw R. Morris², Huw R. Morris¹², Huw R. Morris²², Pentti J. Tienari⁷, Bryan J. Traynor⁹, Bryan J. Traynor¹ - Show less +82 more•Institutions (22)

National Institutes of Health¹, Cardiff University², VU University Amsterdam³, Erasmus University Rotterdam⁴, University of Manchester⁵, University College London⁶, University of Helsinki⁷, University of Oulu⁸, Johns Hopkins University⁹, Georgetown University¹⁰, Illumina¹¹, University Hospital of Wales¹², University of Eastern Finland¹³, University of Miami¹⁴, University of Turin¹⁵, University of Cagliari¹⁶, The Catholic University of America¹⁷, Microsoft¹⁸, University of Toronto¹⁹, University of Würzburg²⁰, University of Washington²¹, Aneurin Bevan University Health Board²²

20 Oct 2011-Neuron

TL;DR: The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases, and a large hexanucleotide repeat expansion in the first intron of C9ORF72 is shown.

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3,784 citations

Journal Article•DOI•

National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease

[...]

Bradley T. Hyman¹, Creighton H. Phelps², Thomas G. Beach, Eileen H. Bigio³, Nigel J. Cairns⁴, Maria C. Carrillo⁵, Dennis W. Dickson⁶, Charles Duyckaerts, Matthew P. Frosch¹, Eliezer Masliah⁷, Suzanne S. Mirra⁸, Peter T. Nelson⁹, Julie A. Schneider¹⁰, Dietmar Rudolf Thal¹¹, Bill Thies⁵, John Q. Trojanowski¹², Harry V. Vinters¹³, Thomas J. Montine¹⁴ - Show less +14 more•Institutions (14)

Harvard University¹, National Institutes of Health², Northwestern University³, Washington University in St. Louis⁴, Alzheimer's Association⁵, Mayo Clinic⁶, University of California, San Diego⁷, SUNY Downstate Medical Center⁸, University of Kentucky⁹, Rush University Medical Center¹⁰, University of Ulm¹¹, University of Pennsylvania¹², University of California, Los Angeles¹³, University of Washington¹⁴

01 Jan 2012-Alzheimers & Dementia

TL;DR: The new guidelines recognize the pre‐clinical stage of AD, enhance the assessment of AD to include amyloid accumulation as well as neurofibrillary change and neuritic plaques, and establish protocols for the neuropathologic assessment of Lewy body disease, vascular brain injury, hippocampal sclerosis, and TDP‐43 inclusions.

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Abstract: A consensus panel from the United States and Europe was convened recently to update and revise the 1997 consensus guidelines for the neuropathologic evaluation of Alzheimer's disease (AD) and other diseases of brain that are common in the elderly. The new guidelines recognize the pre-clinical stage of AD, enhance the assessment of AD to include amyloid accumulation as well as neurofibrillary change and neuritic plaques, establish protocols for the neuropathologic assessment of Lewy body disease, vascular brain injury, hippocampal sclerosis, and TDP-43 inclusions, and recommend standard approaches for the workup of cases and their clinico-pathologic correlation.

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2,240 citations

Journal Article•DOI•

National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach

[...]

Thomas J. Montine¹, Creighton H. Phelps², Thomas G. Beach, Eileen H. Bigio³, Nigel J. Cairns⁴, Dennis W. Dickson⁵, Charles Duyckaerts, Matthew P. Frosch⁶, Eliezer Masliah⁷, Suzanne S. Mirra⁸, Peter T. Nelson⁹, Julie A. Schneider¹⁰, Dietmar Rudolf Thal¹¹, John Q. Trojanowski¹², Harry V. Vinters¹³, Bradley T. Hyman⁶ - Show less +12 more•Institutions (13)

University of Washington¹, National Institutes of Health², Northwestern University³, Washington University in St. Louis⁴, Mayo Clinic⁵, Harvard University⁶, University of California, San Diego⁷, SUNY Downstate Medical Center⁸, University of Kentucky⁹, Rush University Medical Center¹⁰, University of Ulm¹¹, University of Pennsylvania¹², University of California, Los Angeles¹³

01 Jan 2012-Acta Neuropathologica

TL;DR: A practical guide for the implementation of recently revised National Institute on Aging–Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer’s disease is presented.

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Abstract: We present a practical guide for the implementation of recently revised National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease (AD). Major revisions from previous consensus criteria are: (1) recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment, (2) an “ABC” score for AD neuropathologic change that incorporates histopathologic assessments of amyloid β deposits (A), staging of neurofibrillary tangles (B), and scoring of neuritic plaques (C), and (3) more detailed approaches for assessing commonly co-morbid conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA binding protein (TDP)-43 immunoreactive inclusions. Recommendations also are made for the minimum sampling of brain, preferred staining methods with acceptable alternatives, reporting of results, and clinico-pathologic correlations.

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1,965 citations

Cites background from "Expanded GGGGCC hexanucleotide repe..."

...With the exception of individuals with mutations in TARDBP, GRN, VCP or c9ORF72 [10, 18], it is not clear whether TDP-43 proteinopathy in these other neurodegenerative diseases is...
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Journal Article•DOI•

Decoding ALS: from genes to mechanism

[...]

J. Paul Taylor¹, Robert H. Brown², Don W. Cleveland³, Don W. Cleveland⁴•Institutions (4)

St. Jude Children's Research Hospital¹, University of Massachusetts Medical School², Ludwig Institute for Cancer Research³, University of California, San Diego⁴

10 Nov 2016-Nature

TL;DR: Extraordinary progress in understanding the biology of ALS provides new reasons for optimism that meaningful therapies will be identified, and emerging themes include dysfunction in RNA metabolism and protein homeostasis, with specific defects in nucleocytoplasmic trafficking.

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Abstract: Amyotrophic lateral sclerosis (ALS) is a progressive and uniformly fatal neurodegenerative disease. A plethora of genetic factors have been identified that drive the degeneration of motor neurons in ALS, increase susceptibility to the disease or influence the rate of its progression. Emerging themes include dysfunction in RNA metabolism and protein homeostasis, with specific defects in nucleocytoplasmic trafficking, the induction of stress at the endoplasmic reticulum and impaired dynamics of ribonucleoprotein bodies such as RNA granules that assemble through liquid-liquid phase separation. Extraordinary progress in understanding the biology of ALS provides new reasons for optimism that meaningful therapies will be identified.

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1,382 citations

Journal Article•DOI•

Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis.

[...]

Shuo-Chien Ling¹, Magdalini Polymenidou¹, Don W. Cleveland¹•Institutions (1)

University of California, San Diego¹

07 Aug 2013-Neuron

TL;DR: It is presented the case here that these two processes are intimately linked, with disease-initiated perturbation of either leading to further deviation of both protein and RNA homeostasis through a feedforward loop including cell-to-cell prion-like spread that may represent the mechanism for relentless disease progression.

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1,347 citations

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References

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Journal Article•DOI•

Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis

[...]

Daniel R. Rosen¹•Institutions (1)

Harvard University¹

04 Mar 1993-Nature

TL;DR: Tight genetic linkage between FALS and a gene that encodes a cytosolic, Cu/Zn-binding superoxide dismutase (SOD1), a homodimeric metalloenzyme that catalyzes the dismutation of the toxic superoxide anion O–2 to O2 and H2O2 is reported.

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Abstract: Amyotrophic lateral sclerosis (ALS) is a degenerative disorder of motor neurons in the cortex, brainstem and spinal cord. Its cause is unknown and it is uniformly fatal, typically within five years. About 10% of cases are inherited as an autosomal dominant trait, with high penetrance after the sixth decade. In most instances, sporadic and autosomal dominant familial ALS (FALS) are clinically similar. We have previously shown that in some but not all FALS pedigrees the disease is linked to a genetic defect on chromosome 21q (refs 8, 9). Here we report tight genetic linkage between FALS and a gene that encodes a cytosolic, Cu/Zn-binding superoxide dismutase (SOD1), a homodimeric metalloenzyme that catalyzes the dismutation of the toxic superoxide anion O2.- to O2 and H2O2 (ref. 10). Given this linkage and the potential role of free radical toxicity in other neurodenegerative disorders, we investigated SOD1 as a candidate gene in FALS. We identified 11 different SOD1 missense mutations in 13 different FALS families.

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6,733 citations

"Expanded GGGGCC hexanucleotide repe..." refers background in this paper

...In familial ALS, 15%–20% of patients are found to have mutations in the Cu/Zn superoxide dismutase gene (SOD1) (Rosen et al., 1993)....
[...]
...MC Clinical FTD Familial 171 20 (11.7) 13 (7.6) 12 (6.3) n/a n/a n/a Sporadic 203 6 (3.0) 6 (3.0) 3 (1.5) n/a n/a n/a MCF Clinical ALS Familial 34 8 (23.5) n/a n/a 4 (11.8) 1 (2.9) 1 (2.9) Sporadic 195 8 (4.1) n/a n/a 0 (0.0) 2 (1.0) 3 (1.5) ALS = amyotrophic lateral sclerosis; c9FTD/ALS = (GGGGCC)n repeat expansion at chromosome 9p identified in this study; FTD = frontotemporal dementia; FTLD-TDP = frontotemporal lobar degeneration with TDP-43 pathology; FUS = fused in sarcoma gene; GRN = progranulin gene; MAPT =microtubule-associated protein tau gene; MC =Mayo Clinic; MCF =Mayo Clinic Florida; n/a = not assessed; SOD1 = superoxide dismutase 1 gene; TARDBP = TAR DNA-binding protein 43 gene; UBC = University of British Columbia. a Includes 22 individuals for which no information on family history was available. unrelated expanded repeat carriers had at least one copy of the ‘‘risk’’ haplotype (100...
[...]
...Importantly, a direct comparison of the frequency of repeat expansions in C9ORF72 with mutations in SOD1, TARDBP, and FUS revealed GGGGCC expansions to be the most common genetic cause of sporadic and familial ALS in our clinical series (Table 1)....
[...]
...Treatments shown to be effective in SOD1 mouse models, however, have generally not been effective in ALS clinical trials, and the absence of TDP-43 pathology in cases with SOD1 mutations suggests that motor neuron degeneration in these cases may result from a different mechanism (Mackenzie et al., 2007)....
[...]
...This familial association is not well explained by the currently recognized genetic defects; GRNmutations are not associated with significant motor neuron deficits, while patients carrying mutations in SOD1, TARDBP, or FUS are rarely affected by FTD. Linkage analysis in several autosomal-dominant families in which affected members develop either ALS or FTD or both, and where the pathology is consistently TDP positive, have suggested a major locus for FTD/ALS on chromosome 9p21....
[...]

Journal Article•DOI•

Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

[...]

Manuela Neumann¹, Deepak M. Sampathu¹, Linda K. Kwong¹, Adam C. Truax¹, Matthew Micsenyi¹, Thomas T. Chou¹, Jennifer Bruce¹, Theresa Schuck¹, Murray Grossman¹, Christopher M. Clark¹, Leo McCluskey¹, Bruce L. Miller², Eliezer Masliah³, Ian R. A. Mackenzie⁴, Howard Feldman⁴, Wolfgang Feiden, Hans A. Kretzschmar⁵, John Q. Trojanowski¹, Virginia M.-Y. Lee¹ - Show less +15 more•Institutions (5)

University of Pennsylvania¹, University of California, San Francisco², University of California, San Diego³, University of British Columbia⁴, Ludwig Maximilian University of Munich⁵

06 Oct 2006-Science

TL;DR: It is shown that TDP-43 is the major disease protein in both frontotemporal lobar degeneration with ubiquitin-positive inclusions and amyotrophic lateral sclerosis.

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Abstract: Ubiquitin-positive, tau- and alpha-synuclein-negative inclusions are hallmarks of frontotemporal lobar degeneration with ubiquitin-positive inclusions and amyotrophic lateral sclerosis. Although the identity of the ubiquitinated protein specific to either disorder was unknown, we showed that TDP-43 is the major disease protein in both disorders. Pathologic TDP-43 was hyper-phosphorylated, ubiquitinated, and cleaved to generate C-terminal fragments and was recovered only from affected central nervous system regions, including hippocampus, neocortex, and spinal cord. TDP-43 represents the common pathologic substrate linking these neurodegenerative disorders.

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5,440 citations

Journal Article•DOI•

Frontotemporal lobar degeneration A consensus on clinical diagnostic criteria

[...]

David Neary¹, Julie S. Snowden, L. Gustafson, U. Passant, Donald T. Stuss, Sandra E. Black, Morris Freedman, Andrew Kertesz², Philippe Robert, Marilyn S. Albert³, Kyle B. Boone, Bruce L. Miller, Jeffrey L. Cummings, D. F. Benson - Show less +10 more•Institutions (3)

Manchester Royal Infirmary¹, University of Western Ontario², Harvard University³

01 Dec 1998-Neurology

TL;DR: Consensus criteria for the three prototypic syndromes-frontotemporal dementia, progressive nonfluent aphasia, and semantic dementia-were developed by members of an international workshop on frontotem temporal lobar degeneration and ought to provide the foundation for research work into the neuropsychology, neuropathology, genetics, molecular biology, and epidemiology of these important clinical disorders.

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Abstract: Objective: To improve clinical recognition and provide research diagnostic criteria for three clinical syndromes associated with frontotemporal lobar degeneration. Methods: Consensus criteria for the three prototypic syndromes-frontotemporal dementia, progressive nonfluent aphasia, and semantic dementia-were developed by members of an international workshop on frontotemporal lobar degeneration. These criteria build on earlier published clinical diagnostic guidelines for frontotemporal dementia produced by some of the workshop members. Results: The consensus criteria specify core and supportive features for each of the three prototypic clinical syndromes and provide broad inclusion and exclusion criteria for the generic entity of frontotemporal lobar degeneration. The criteria are presented in lists, and operational definitions for features are provided in the text. Conclusions: The criteria ought to provide the foundation for research work into the neuropsychology, neuropathology, genetics, molecular biology, and epidemiology of these important clinical disorders that account for a substantial proportion of cases of primary degenerative dementia occurring before the age of 65 years.

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4,708 citations

Journal Article•DOI•

A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD

[...]

Alan E. Renton¹, Elisa Majounie¹, Adrian James Waite², Javier Simón-Sánchez³, Javier Simón-Sánchez⁴, Sara Rollinson⁵, J. Raphael Gibbs¹, J. Raphael Gibbs⁶, Jennifer C. Schymick¹, Hannu Laaksovirta⁷, John C. van Swieten⁴, John C. van Swieten³, Liisa Myllykangas⁷, Hannu Kalimo⁷, Anders Paetau⁷, Yevgeniya Abramzon¹, Anne M. Remes⁸, Alice Kaganovich¹, Sonja W. Scholz⁹, Sonja W. Scholz¹⁰, Sonja W. Scholz¹, Jamie Duckworth¹, Jinhui Ding¹, Daniel W. Harmer¹¹, Dena G. Hernandez¹, Dena G. Hernandez⁶, Janel O. Johnson¹, Janel O. Johnson⁶, Kin Y. Mok⁶, Mina Ryten⁶, Danyah Trabzuni⁶, Rita Guerreiro⁶, Richard W. Orrell⁶, James Neal², Alexandra Murray¹², J. P. Pearson², Iris E. Jansen³, David Sondervan³, Harro Seelaar⁴, Derek J. Blake², Kate Young⁵, Nicola Halliwell⁵, Janis Bennion Callister⁵, Greg Toulson⁵, Anna Richardson⁵, Alexander Gerhard⁵, Julie S. Snowden⁵, David M. A. Mann⁵, David Neary⁵, Mike A. Nalls¹, Terhi Peuralinna⁷, Lilja Jansson⁷, Veli-Matti Isoviita⁷, Anna-Lotta Kaivorinne⁸, Maarit Hölttä-Vuori⁷, Elina Ikonen⁷, Raimo Sulkava¹³, Michael Benatar¹⁴, Joanne Wuu¹⁴, Adriano Chiò¹⁵, Gabriella Restagno, Giuseppe Borghero¹⁶, Mario Sabatelli¹⁷, David Heckerman¹⁸, Ekaterina Rogaeva¹⁹, Lorne Zinman¹⁹, Jeffrey D. Rothstein⁹, Michael Sendtner²⁰, Carsten Drepper²⁰, Evan E. Eichler²¹, Can Alkan²¹, Ziedulla Abdullaev¹, Svetlana Pack¹, Amalia Dutra¹, Evgenia Pak¹, John Hardy⁶, Andrew B. Singleton¹, Nigel Williams², Peter Heutink³, Stuart Pickering-Brown⁵, Huw R. Morris², Huw R. Morris¹², Huw R. Morris²², Pentti J. Tienari⁷, Bryan J. Traynor⁹, Bryan J. Traynor¹ - Show less +82 more•Institutions (22)

20 Oct 2011-Neuron

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3,784 citations

"Expanded GGGGCC hexanucleotide repe..." refers background or result in this paper

...Foci were never observed in any of the samples using a probe targeting the unrelated CCTG repeat (probe (CAGG)6), implicated in myotonic dystrophy type 2 (DM2) (Liquori et al., 2001), further supporting the specificity of the RNA foci composed of GGGGCC in these patients (Figure 5D)....
[...]
...While our manuscript was in preparation we learned of another group who independently identified repeat expansions in C9ORF72 as the cause of FTD and ALS linked to chromosome 9p (Renton et al. 2011)....
[...]

Journal Article•

Hudson et al.

[...]

E. N. Anderson

01 Jul 1977-Journal of California Anthropology, The

TL;DR: The Eye of Flute: Chumash Traditional History and Ritual as Told by Fernando Librado Kitsepawit to John P. Harrington as discussed by the authors, was published by the Santa Barbara Museum of Natural History.

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Abstract: The Eye of the Flute: Chumash Traditional History and Ritual as Told by Fernando Librado Kitsepawit to John P. Harrington . Travis Hudson, Thomas Blackburn, Rosario Curletti, and Janice Timbrook, eds. lllustrated by Campbell Grant. Santa Barbara: Santa Barbara Museum of Natural History, Santa Barbara Bicentennial Historical Series iv. 1977. 130 pp., map, 19 illus., 4 appendices, indexed, clothbound. No price given.

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2,612 citations