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Erschienen in: Molecular Neurodegeneration 1/2014

Open Access 01.12.2014 | Editorial

Molecular neurodegeneration: basic biology and disease pathways

verfasst von: Robert Vassar, Hui Zheng

Erschienen in: Molecular Neurodegeneration | Ausgabe 1/2014

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Abstract

The field of neurodegeneration research has been advancing rapidly over the past few years, and has provided intriguing new insights into the normal physiological functions and pathogenic roles of a wide range of molecules associated with several devastating neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, frontotemporal dementia, Huntington’s disease, and Down syndrome. Recent developments have also facilitated initial efforts to translate preclinical discoveries toward novel therapeutic approaches and clinical trials in humans. These recent developments are reviewed in the current Review Series on "Molecular Neurodegeneration : Basic Biology and Disease Pathways" in a number of state-of-the-art manuscripts that cover themes presented at the Third International Conference on Molecular Neurodegeneration: "Basic biology and disease pathways" held in Cannes, France, September, 2013.
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Electronic supplementary material

The online version of this article (doi:10.​1186/​1750-1326-9-34) contains supplementary material, which is available to authorized users.
Abkürzungen
Beta-amyloid
AD
Alzheimer’s disease
ALS
Amyotrophic lateral sclerosis
APP
Amyloid precursor protein
C9ORF72
Chromosome 9 open reading frame 72
CD33
Cluster of differentiation 33
DS
Down syndrome
FTD
Frontotemporal dementia
HD
Huntington’s disease
PD
Parkinson’s disease
TREM2
Triggering receptor expressed on myeloid cells 2.

Text

In September 2013, the Third International Conference on Molecular Neurodegeneration: "Basic biology and disease pathways" was held in Cannes, France. The three-day conference brought together scientists from around the world to present and discuss the results of their most recent research on the normal physiological functions and pathological mechanisms of molecular pathways that are relevant to neurodegenerative diseases (Figure 1). The current thematic review series in the journal, entitled "Molecular Neurodegeneration : Basic Biology and Disease Pathways", is intended to represent not only the scientific findings presented during the conference, but to also reflect the state-of-the-art in a given field. The review series will consist of a "rolling submission" format in which manuscripts by presenters at the conference will appear at regular intervals in the journal.
The conference covered a wide array of topics concerning neurodegeneration at the genetic, molecular, cellular, physiological, behavioral, and systems levels, and with a translational perspective of moving discoveries from preclinical models into human clinical trials. Sessions discussed the following areas of neurodegeneration research:
  •  The genetics of AD and other neurodegenerative diseases
  •  The structure and normal physiological functions of molecules involved in neurodegeneration
  •  Novel molecular mechanisms of AD, PD, ALS, FTD, DS, and HD
  •  Mechanisms of neurotoxicity in PD, AD and other tauopathies
  •  Novel therapeutic approaches for neurodegenerative diseases
Molecular mechanisms of neurodegeneration were dominant themes of the conference. Some highlights included novel insights into AD pathogenesis provided by genetic analyses revealing new AD risk factor genes like CD33 and TREM2 involved in innate immunity [14]. Deeper knowledge of the structures and normal physiological functions of APP and the α-, β- and γ-secretase enzymes that process APP is assisting the development of disease-modifying AD therapies that target the neurotoxic Aβ peptide [59]. Intriguing studies have revealed new molecules involved in neurodegeneration, like C9ORF72 in ALS and FTD, and begin to shed light on their pathogenic roles [1012]. New insights into the prion-like spread of Aβ and tau pathologies in AD and α-synuclein in PD have also been made [1315]. Additionally, innovative studies of mechanisms of neurotoxicity have revealed roles for micro-RNAs, transcription factors, and trafficking molecules in AD [1620]. Novel therapies based on many of these discoveries are also in development, like anti-tau antibodies for AD and other tauopathies [14].
In summary, this review series aims to encapsulate the themes discussed at the Third International Conference on Molecular Neurodegeneration and provide state-of-the-art knowledge of a wide range of fields in neurodegeneration research. It is the hope of the editors that the knowledge conveyed in the review series will provide quality information to readers and stimulate further scientific advances in molecular neurodegeneration that may someday bring an end to these devastating neurodegenerative disorders.

Acknowledgements

We thank the editors of Molecular Neurodegeneration for the invitation for this review series, and particularly the authors of the review manuscripts for their efforts. We further want to express our thanks to all the speakers and participants of the Third International Conference on Molecular Neurodegeneration, who are too numerous to mention by name.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://​creativecommons.​org/​licenses/​by/​4.​0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://​creativecommons.​org/​publicdomain/​zero/​1.​0/​) applies to the data made available in this article, unless otherwise stated.
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Literatur
1.
Zurück zum Zitat Tanzi RE: The genetics of Alzheimer disease. Cold Spring Harbor Perspect Med. 2012, 2 (10): Epub 2012/10/03. doi:10.1101/cshperspect.a006296. PubMed PMID: 23028126 Tanzi RE: The genetics of Alzheimer disease. Cold Spring Harbor Perspect Med. 2012, 2 (10): Epub 2012/10/03. doi:10.1101/cshperspect.a006296. PubMed PMID: 23028126
2.
Zurück zum Zitat Griciuc A, Serrano-Pozo A, Parrado AR, Lesinski AN, Asselin CN, Mullin K, Hooli B, Choi SH, Hyman BT, Tanzi RE: Alzheimer's disease risk gene CD33 inhibits microglial uptake of amyloid beta. Neuron. 2013, 78 (4): 631-43. 10.1016/j.neuron.2013.04.014. doi:10.1016/j.neuron.2013.04.014, PubMed PMID: 23623698, PubMed Central PMCID: PMC3706457PubMedCentralCrossRefPubMed Griciuc A, Serrano-Pozo A, Parrado AR, Lesinski AN, Asselin CN, Mullin K, Hooli B, Choi SH, Hyman BT, Tanzi RE: Alzheimer's disease risk gene CD33 inhibits microglial uptake of amyloid beta. Neuron. 2013, 78 (4): 631-43. 10.1016/j.neuron.2013.04.014. doi:10.1016/j.neuron.2013.04.014, PubMed PMID: 23623698, PubMed Central PMCID: PMC3706457PubMedCentralCrossRefPubMed
3.
Zurück zum Zitat Guerreiro R, Wojtas A, Bras J, Carrasquillo M, Rogaeva E, Majounie E, Cruchaga C, Sassi C, Kauwe JS, Younkin S, Hazrati L, Collinge J, Pocock J, Lashley T, Williams J, Lambert JC, Amouyel P, Goate A, Rademakers R, Morgan K, Powell J, St George-Hyslop P, Singleton A, Hardy J: Alzheimer Genetic Analysis G. TREM2 variants in Alzheimer's disease. N Engl J Med. 2013, 368 (2): 117-27. 10.1056/NEJMoa1211851.PubMedCentralCrossRefPubMed Guerreiro R, Wojtas A, Bras J, Carrasquillo M, Rogaeva E, Majounie E, Cruchaga C, Sassi C, Kauwe JS, Younkin S, Hazrati L, Collinge J, Pocock J, Lashley T, Williams J, Lambert JC, Amouyel P, Goate A, Rademakers R, Morgan K, Powell J, St George-Hyslop P, Singleton A, Hardy J: Alzheimer Genetic Analysis G. TREM2 variants in Alzheimer's disease. N Engl J Med. 2013, 368 (2): 117-27. 10.1056/NEJMoa1211851.PubMedCentralCrossRefPubMed
4.
Zurück zum Zitat Naj AC, Jun G, Beecham GW, Wang LS, Vardarajan BN, Buros J, Gallins PJ, Buxbaum JD, Jarvik GP, Crane PK, Larson EB, Bird TD, Boeve BF, Graff-Radford NR, De Jager PL, Evans D, Schneider JA, Carrasquillo MM, Ertekin-Taner N, Younkin SG, Cruchaga C, Kauwe JS, Nowotny P, Kramer P, Hardy J, Huentelman MJ, Myers AJ, Barmada MM, Demirci FY, Baldwin CT, et al: Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease. Nat Genet. 2011, 43 (5): 436-41. 10.1038/ng.801. Epub 2011/04/05. doi:10.1038/ng.801. PubMed PMID: 21460841.PubMedCentralCrossRefPubMed Naj AC, Jun G, Beecham GW, Wang LS, Vardarajan BN, Buros J, Gallins PJ, Buxbaum JD, Jarvik GP, Crane PK, Larson EB, Bird TD, Boeve BF, Graff-Radford NR, De Jager PL, Evans D, Schneider JA, Carrasquillo MM, Ertekin-Taner N, Younkin SG, Cruchaga C, Kauwe JS, Nowotny P, Kramer P, Hardy J, Huentelman MJ, Myers AJ, Barmada MM, Demirci FY, Baldwin CT, et al: Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease. Nat Genet. 2011, 43 (5): 436-41. 10.1038/ng.801. Epub 2011/04/05. doi:10.1038/ng.801. PubMed PMID: 21460841.PubMedCentralCrossRefPubMed
5.
Zurück zum Zitat Muller UC, Zheng H: Physiological functions of APP family proteins. Cold Spring Harbor Perspect Med. 2012, 2 (2): a006288-doi:10.1101/cshperspect.a006288, PubMed PMID: 22355794, PubMed Central PMCID: PMC3281588CrossRef Muller UC, Zheng H: Physiological functions of APP family proteins. Cold Spring Harbor Perspect Med. 2012, 2 (2): a006288-doi:10.1101/cshperspect.a006288, PubMed PMID: 22355794, PubMed Central PMCID: PMC3281588CrossRef
6.
Zurück zum Zitat Renzi F, Zhang X, Rice WJ, Torres-Arancivia C, Gomez-Llorente Y, Diaz R, Ahn K, Yu C, Li YM, Sisodia SS, Ubarretxena-Belandia I: Structure of gamma-secretase and its trimeric pre-activation intermediate by single-particle electron microscopy. J Biol Chem. 2011, 286 (24): 21440-9. 10.1074/jbc.M110.193326. doi:10.1074/jbc.M110.193326, PubMed PMID: 21454611, PubMed Central PMCID: PMC3122203PubMedCentralCrossRefPubMed Renzi F, Zhang X, Rice WJ, Torres-Arancivia C, Gomez-Llorente Y, Diaz R, Ahn K, Yu C, Li YM, Sisodia SS, Ubarretxena-Belandia I: Structure of gamma-secretase and its trimeric pre-activation intermediate by single-particle electron microscopy. J Biol Chem. 2011, 286 (24): 21440-9. 10.1074/jbc.M110.193326. doi:10.1074/jbc.M110.193326, PubMed PMID: 21454611, PubMed Central PMCID: PMC3122203PubMedCentralCrossRefPubMed
7.
Zurück zum Zitat Vassar R, Kuhn PH, Haass C, Kennedy ME, Rajendran L, Wong PC, Lichtenthaler SF: Function, therapeutic potential and cell biology of BACE proteases: current status and future prospects. J Neurochem. 2014, doi:10.1111/jnc.12715. PubMed PMID: 24646365 Vassar R, Kuhn PH, Haass C, Kennedy ME, Rajendran L, Wong PC, Lichtenthaler SF: Function, therapeutic potential and cell biology of BACE proteases: current status and future prospects. J Neurochem. 2014, doi:10.1111/jnc.12715. PubMed PMID: 24646365
8.
Zurück zum Zitat Chami L, Checler F: BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and beta-amyloid production in Alzheimer's disease. Mol Neurodegener. 2012, 7: 52-10.1186/1750-1326-7-52. doi:10.1186/1750-1326-7-52, PubMed PMID: 23039869, PubMed Central PMCID: PMC3507664PubMedCentralCrossRefPubMed Chami L, Checler F: BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and beta-amyloid production in Alzheimer's disease. Mol Neurodegener. 2012, 7: 52-10.1186/1750-1326-7-52. doi:10.1186/1750-1326-7-52, PubMed PMID: 23039869, PubMed Central PMCID: PMC3507664PubMedCentralCrossRefPubMed
9.
Zurück zum Zitat Walter J, van Echten-Deckert G: Cross-talk of membrane lipids and Alzheimer-related proteins. Mol Neurodegener. 2013, 8: 34-10.1186/1750-1326-8-34. doi:10.1186/1750-1326-8-34, PubMed PMID: 24148205, PubMed Central PMCID: PMC4016522PubMedCentralCrossRefPubMed Walter J, van Echten-Deckert G: Cross-talk of membrane lipids and Alzheimer-related proteins. Mol Neurodegener. 2013, 8: 34-10.1186/1750-1326-8-34. doi:10.1186/1750-1326-8-34, PubMed PMID: 24148205, PubMed Central PMCID: PMC4016522PubMedCentralCrossRefPubMed
10.
Zurück zum Zitat Meyer K, Ferraiuolo L, Miranda CJ, Likhite S, McElroy S, Renusch S, Ditsworth D, Lagier-Tourenne C, Smith RA, Ravits J, Burghes AH, Shaw PJ, Cleveland DW, Kolb SJ, Kaspar BK: Direct conversion of patient fibroblasts demonstrates non-cell autonomous toxicity of astrocytes to motor neurons in familial and sporadic ALS. Proc Natl Acad Sci U S A. 2014, 111 (2): 829-32. 10.1073/pnas.1314085111. doi:10.1073/pnas.1314085111, PubMed PMID: 24379375; PubMed Central PMCID: PMC3896192PubMedCentralCrossRefPubMed Meyer K, Ferraiuolo L, Miranda CJ, Likhite S, McElroy S, Renusch S, Ditsworth D, Lagier-Tourenne C, Smith RA, Ravits J, Burghes AH, Shaw PJ, Cleveland DW, Kolb SJ, Kaspar BK: Direct conversion of patient fibroblasts demonstrates non-cell autonomous toxicity of astrocytes to motor neurons in familial and sporadic ALS. Proc Natl Acad Sci U S A. 2014, 111 (2): 829-32. 10.1073/pnas.1314085111. doi:10.1073/pnas.1314085111, PubMed PMID: 24379375; PubMed Central PMCID: PMC3896192PubMedCentralCrossRefPubMed
11.
Zurück zum Zitat Ling SC, Polymenidou M, Cleveland DW: Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis. Neuron. 2013, 79 (3): 416-38. 10.1016/j.neuron.2013.07.033. doi:10.1016/j.neuron.2013.07.033, PubMed PMID: 23931993PubMedCentralCrossRefPubMed Ling SC, Polymenidou M, Cleveland DW: Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis. Neuron. 2013, 79 (3): 416-38. 10.1016/j.neuron.2013.07.033. doi:10.1016/j.neuron.2013.07.033, PubMed PMID: 23931993PubMedCentralCrossRefPubMed
12.
Zurück zum Zitat Xu ZS: Does a loss of TDP-43 function cause neurodegeneration?. Mol Neurodegener. 2012, 7: 27-10.1186/1750-1326-7-27. doi:10.1186/1750-1326-7-27, PubMed PMID: 22697423, PubMed Central PMCID: PMC3419078PubMedCentralCrossRefPubMed Xu ZS: Does a loss of TDP-43 function cause neurodegeneration?. Mol Neurodegener. 2012, 7: 27-10.1186/1750-1326-7-27. doi:10.1186/1750-1326-7-27, PubMed PMID: 22697423, PubMed Central PMCID: PMC3419078PubMedCentralCrossRefPubMed
13.
Zurück zum Zitat Jucker M, Walker LC: Self-propagation of pathogenic protein aggregates in neurodegenerative diseases. Nature. 2013, 501 (7465): 45-51. 10.1038/nature12481. 10.1038/nature12481, PubMed PMID: 24005412, PubMed Central PMCID: PMC3963807PubMedCentralCrossRefPubMed Jucker M, Walker LC: Self-propagation of pathogenic protein aggregates in neurodegenerative diseases. Nature. 2013, 501 (7465): 45-51. 10.1038/nature12481. 10.1038/nature12481, PubMed PMID: 24005412, PubMed Central PMCID: PMC3963807PubMedCentralCrossRefPubMed
14.
Zurück zum Zitat Yanamandra K, Kfoury N, Jiang H, Mahan TE, Ma S, Maloney SE, Wozniak DF, Diamond MI, Holtzman DM: Anti-tau antibodies that block tau aggregate seeding in vitro markedly decrease pathology and improve cognition in vivo. Neuron. 2013, 80 (2): 402-14. 10.1016/j.neuron.2013.07.046. 10.1016/j.neuron.2013.07.046, PubMed PMID: 24075978; PubMed Central PMCID: PMC3924573PubMedCentralCrossRefPubMed Yanamandra K, Kfoury N, Jiang H, Mahan TE, Ma S, Maloney SE, Wozniak DF, Diamond MI, Holtzman DM: Anti-tau antibodies that block tau aggregate seeding in vitro markedly decrease pathology and improve cognition in vivo. Neuron. 2013, 80 (2): 402-14. 10.1016/j.neuron.2013.07.046. 10.1016/j.neuron.2013.07.046, PubMed PMID: 24075978; PubMed Central PMCID: PMC3924573PubMedCentralCrossRefPubMed
15.
Zurück zum Zitat Guo JL, Covell DJ, Daniels JP, Iba M, Stieber A, Zhang B, Riddle DM, Kwong LK, Xu Y, Trojanowski JQ, Lee VM: Distinct alpha-synuclein strains differentially promote tau inclusions in neurons. Cell. 2013, 154 (1): 103-17. 10.1016/j.cell.2013.05.057. doi:10.1016/j.cell.2013.05.057, PubMed PMID: 23827677; PubMed Central PMCID: PMC3820001CrossRefPubMed Guo JL, Covell DJ, Daniels JP, Iba M, Stieber A, Zhang B, Riddle DM, Kwong LK, Xu Y, Trojanowski JQ, Lee VM: Distinct alpha-synuclein strains differentially promote tau inclusions in neurons. Cell. 2013, 154 (1): 103-17. 10.1016/j.cell.2013.05.057. doi:10.1016/j.cell.2013.05.057, PubMed PMID: 23827677; PubMed Central PMCID: PMC3820001CrossRefPubMed
16.
Zurück zum Zitat Lau P, Bossers K, Janky R, Salta E, Frigerio CS, Barbash S, Rothman R, Sierksma AS, Thathiah A, Greenberg D, Papadopoulou AS, Achsel T, Ayoubi T, Soreq H, Verhaagen J, Swaab DF, Aerts S, De Strooper B: Alteration of the microRNA network during the progression of Alzheimer's disease. EMBO Mol Med. 2013, 5 (10): 1613-34. 10.1002/emmm.201201974. doi:10.1002/emmm.201201974, PubMed PMID: 24014289, PubMed Central PMCID: PMC3799583PubMedCentralCrossRefPubMed Lau P, Bossers K, Janky R, Salta E, Frigerio CS, Barbash S, Rothman R, Sierksma AS, Thathiah A, Greenberg D, Papadopoulou AS, Achsel T, Ayoubi T, Soreq H, Verhaagen J, Swaab DF, Aerts S, De Strooper B: Alteration of the microRNA network during the progression of Alzheimer's disease. EMBO Mol Med. 2013, 5 (10): 1613-34. 10.1002/emmm.201201974. doi:10.1002/emmm.201201974, PubMed PMID: 24014289, PubMed Central PMCID: PMC3799583PubMedCentralCrossRefPubMed
17.
Zurück zum Zitat Duplan E, Giaime E, Viotti J, Sevalle J, Corti O, Brice A, Ariga H, Qi L, Checler F, da Alves Costa C: ER-stress-associated functional link between Parkin and DJ-1 via a transcriptional cascade involving the tumor suppressor p53 and the spliced X-box binding protein XBP-1. J Cell Sci. 2013, 126 (Pt 9): 2124-33.CrossRefPubMed Duplan E, Giaime E, Viotti J, Sevalle J, Corti O, Brice A, Ariga H, Qi L, Checler F, da Alves Costa C: ER-stress-associated functional link between Parkin and DJ-1 via a transcriptional cascade involving the tumor suppressor p53 and the spliced X-box binding protein XBP-1. J Cell Sci. 2013, 126 (Pt 9): 2124-33.CrossRefPubMed
18.
Zurück zum Zitat Wang X, Zhao Y, Zhang X, Badie H, Zhou Y, Mu Y, Loo LS, Cai L, Thompson RC, Yang B, Chen Y, Johnson PF, Wu C, Bu G, Mobley WC, Zhang D, Gage FH, Ranscht B, Zhang YW, Lipton SA, Hong W, Xu H: Loss of sorting nexin 27 contributes to excitatory synaptic dysfunction by modulating glutamate receptor recycling in Down's syndrome. Nat Med. 2013, 19 (4): 473-80. 10.1038/nm.3117. doi:10.1038/nm.3117, PubMed PMID: 23524343; PubMed Central PMCID: PMC3911880PubMedCentralCrossRefPubMed Wang X, Zhao Y, Zhang X, Badie H, Zhou Y, Mu Y, Loo LS, Cai L, Thompson RC, Yang B, Chen Y, Johnson PF, Wu C, Bu G, Mobley WC, Zhang D, Gage FH, Ranscht B, Zhang YW, Lipton SA, Hong W, Xu H: Loss of sorting nexin 27 contributes to excitatory synaptic dysfunction by modulating glutamate receptor recycling in Down's syndrome. Nat Med. 2013, 19 (4): 473-80. 10.1038/nm.3117. doi:10.1038/nm.3117, PubMed PMID: 23524343; PubMed Central PMCID: PMC3911880PubMedCentralCrossRefPubMed
19.
Zurück zum Zitat Buggia-Prevot V, Fernandez CG, Riordan S, Vetrivel KS, Roseman J, Waters J, Bindokas VP, Vassar R, Thinakaran G: Axonal BACE1 dynamics and targeting in hippocampal neurons: a role for Rab11 GTPase. Mol Neurodegener. 2014, 9 (1): 1-10.1186/1750-1326-9-1. doi:10.1186/1750-1326-9-1, PubMed PMID: 24386896; PubMed Central PMCID: PMC4031619PubMedCentralCrossRefPubMed Buggia-Prevot V, Fernandez CG, Riordan S, Vetrivel KS, Roseman J, Waters J, Bindokas VP, Vassar R, Thinakaran G: Axonal BACE1 dynamics and targeting in hippocampal neurons: a role for Rab11 GTPase. Mol Neurodegener. 2014, 9 (1): 1-10.1186/1750-1326-9-1. doi:10.1186/1750-1326-9-1, PubMed PMID: 24386896; PubMed Central PMCID: PMC4031619PubMedCentralCrossRefPubMed
20.
Zurück zum Zitat Buggia-Prevot V, Fernandez CG, Udayar V, Vetrivel KS, Elie A, Roseman J, Sasse VA, Lefkow M, Meckler X, Bhattacharyya S, George M, Kar S, Bindokas VP, Parent AT, Rajendran L, Band H, Vassar R, Thinakaran G: A function for EHD family proteins in unidirectional retrograde dendritic transport of BACE1 and Alzheimer's disease Abeta production. Cell Rep. 2013, 5 (6): 1552-63. 10.1016/j.celrep.2013.12.006. doi:10.1016/j.celrep.2013.12.006, PubMed PMID: 24373286; PubMed Central PMCID: PMC3932704PubMedCentralCrossRefPubMed Buggia-Prevot V, Fernandez CG, Udayar V, Vetrivel KS, Elie A, Roseman J, Sasse VA, Lefkow M, Meckler X, Bhattacharyya S, George M, Kar S, Bindokas VP, Parent AT, Rajendran L, Band H, Vassar R, Thinakaran G: A function for EHD family proteins in unidirectional retrograde dendritic transport of BACE1 and Alzheimer's disease Abeta production. Cell Rep. 2013, 5 (6): 1552-63. 10.1016/j.celrep.2013.12.006. doi:10.1016/j.celrep.2013.12.006, PubMed PMID: 24373286; PubMed Central PMCID: PMC3932704PubMedCentralCrossRefPubMed
Metadaten
Titel
Molecular neurodegeneration: basic biology and disease pathways
verfasst von
Robert Vassar
Hui Zheng
Publikationsdatum
01.12.2014
Verlag
BioMed Central
Erschienen in
Molecular Neurodegeneration / Ausgabe 1/2014
Elektronische ISSN: 1750-1326
DOI
https://doi.org/10.1186/1750-1326-9-34

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