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  1. The diagnostic guidelines of Alzheimer’s disease (AD) have recently been updated to include brain imaging and cerebrospinal fluid (CSF) biomarkers, with the aim of increasing the certainty of whether a patient...

    Authors: Christoffer Rosén, Oskar Hansson, Kaj Blennow and Henrik Zetterberg
    Citation: Molecular Neurodegeneration 2013 8:20
  2. Though the precise cause(s) of Alzheimer’s disease (AD) remain unknown, there is strong evidence that decreased clearance of β-amyloid (Aβ) from the brain can contribute to the disease. Therapeutic strategies ...

    Authors: Katherine D LaClair, Kebreten F Manaye, Dexter L Lee, Joanne S Allard, Alena V Savonenko, Juan C Troncoso and Philip C Wong
    Citation: Molecular Neurodegeneration 2013 8:18

    The Erratum to this article has been published in Molecular Neurodegeneration 2013 8:26

  3. Genetic studies have established a causative role for α-synuclein (αS) in Parkinson’s disease (PD), and the presence of αS aggregates in the form of Lewy body (LB) and Lewy neurite (LN) protein inclusions are ...

    Authors: Amanda N Sacino, Michael A Thomas, Carolina Ceballos-Diaz, Pedro E Cruz, Awilda M Rosario, Jada Lewis, Benoit I Giasson and Todd E Golde
    Citation: Molecular Neurodegeneration 2013 8:17
  4. Recent findings suggest that the pathological effects of apoE4, the most prevalent genetic risk factor for Alzheimer’s disease (AD), start many years before the onset of the disease and are already detectable ...

    Authors: Ori Liraz, Anat Boehm-Cagan and Daniel M Michaelson
    Citation: Molecular Neurodegeneration 2013 8:16
  5. Recent research in Alzheimer’s disease (AD) field has been focused on the potential role of the amyloid-β protein that is derived from the transmembrane amyloid precursor protein (APP) in directly mediating co...

    Authors: Jungsu Kim, Paramita Chakrabarty, Amanda Hanna, Amelia March, Dennis W Dickson, David R Borchelt, Todd Golde and Christopher Janus
    Citation: Molecular Neurodegeneration 2013 8:15
  6. Parkinson’s disease (PD) is a chronic neurodegenerative condition that is characterized by motor symptoms as a result of dopaminergic degeneration, particularly in the mesostriatal pathway. However, in recent ...

    Authors: Miguel M Carvalho, Filipa L Campos, Bárbara Coimbra, José M Pêgo, Carla Rodrigues, Rui Lima, Ana J Rodrigues, Nuno Sousa and António J Salgado
    Citation: Molecular Neurodegeneration 2013 8:14
  7. The APOE4 allele variant is the strongest known genetic risk factor for developing late-onset Alzheimer’s disease. The link between apolipoprotein E (apoE) and Alzheimer’s disease is likely due in large part to t...

    Authors: Jason D Ulrich, Jack M Burchett, Jessica L Restivo, Dorothy R Schuler, Philip B Verghese, Thomas E Mahan, Gary E Landreth, Joseph M Castellano, Hong Jiang, John R Cirrito and David M Holtzman
    Citation: Molecular Neurodegeneration 2013 8:13
  8. Sizing of GGGGCC hexanucleotide repeat expansions within the C9ORF72 locus, which account for approximately 10% of all amyotrophic lateral sclerosis (ALS) cases, is urgently required to answer fundamental questio...

    Authors: Vladimir L Buchman, Johnathan Cooper-Knock, Natalie Connor-Robson, Adrian Higginbottom, Janine Kirby, Olga D Razinskaya, Natalia Ninkina and Pamela J Shaw
    Citation: Molecular Neurodegeneration 2013 8:12
  9. The editors of Molecular Neurodegeneration would like to thank all the reviewers who have contributed to the journal in Volume 7 (2012).

    Authors: Guojun Bu and Huaxi Xu
    Citation: Molecular Neurodegeneration 2013 8:11
  10. P73 belongs to the p53 family of cell survival regulators with the corresponding locus Trp73 producing the N-terminally distinct isoforms, TAp73 and DeltaNp73. Recently, two studies have implicated the murine Trp...

    Authors: Badri Vardarajan, David Vergote, Fadel Tissir, Mark Logue, Jing Yang, Nathalie Daude, Kunie Ando, Ekaterina Rogaeva, Joseph Lee, Rong Cheng, Jean-Pierre Brion, Mahdi Ghani, Beipei Shi, Clinton T Baldwin, Satyabrata Kar, Richard Mayeux…
    Citation: Molecular Neurodegeneration 2013 8:10
  11. Tauopathies are characterized by intracellular deposition of the microtubule-associated protein tau as filamentous aggregates. The rTg4510 mouse conditionally expresses mutant human tau protein in various fore...

    Authors: Pablo D Perez, Gabrielle Hall, Tetsuya Kimura, Yan Ren, Rachel M Bailey, Jada Lewis, Marcelo Febo and Naruhiko Sahara
    Citation: Molecular Neurodegeneration 2013 8:9
  12. Alzheimer’s Disease (AD) is a progressive neurodegenerative disease, especially affecting the hippocampus. Impairment of cognitive and memory functions is associated with amyloid β-peptide-induced oxidative st...

    Authors: Francesca Fanelli, Sara Sepe, Marcello D’Amelio, Cinzia Bernardi, Loredana Cristiano, AnnaMaria Cimini, Francesco Cecconi, Maria Paola Ceru' and Sandra Moreno
    Citation: Molecular Neurodegeneration 2013 8:8
  13. Histone deacetylase (HDAC) inhibitors have been demonstrated to be beneficial in animal models of neurodegenerative diseases. Such results were mainly associated with the epigenetic modulation caused by HDACs,...

    Authors: Claudia Simões-Pires, Vincent Zwick, Alessandra Nurisso, Esther Schenker, Pierre-Alain Carrupt and Muriel Cuendet
    Citation: Molecular Neurodegeneration 2013 8:7
  14. Lewy bodies (LB) are a neuropathological hallmark of Parkinson’s disease (PD) and other synucleinopathies. The role their formation plays in disease pathogenesis is not well understood, in part because studies...

    Authors: Emily N Cronin-Furman, M Kathleen Borland, Kristen E Bergquist, James P Bennett Jr and Patricia A Trimmer
    Citation: Molecular Neurodegeneration 2013 8:6
  15. Aggregation of the α-Synuclein (α-Syn) protein, amyloid fibril formation and progressive neurodegeneration are the neuropathological hallmarks of Parkinson's Disease (PD). However, a detailed mechanism of α-Sy...

    Authors: Alireza Roostaee, Simon Beaudoin, Antanas Staskevicius and Xavier Roucou
    Citation: Molecular Neurodegeneration 2013 8:5
  16. Neurodegenerative diseases including Parkinson’s and Alzheimer’s diseases progress slowly and steadily over years or decades. They show significant between-subject variation in progress and clinical symptoms, ...

    Authors: Takuya Hayashi, Masamitsu Shimazawa, Hiroshi Watabe, Takayuki Ose, Yuta Inokuchi, Yasushi Ito, Hajime Yamanaka, Shin-ichi Urayama, Yasuyoshi Watanabe, Hideaki Hara and Hirotaka Onoe
    Citation: Molecular Neurodegeneration 2013 8:4
  17. Accumulation of β-amyloid (Aβ) and cholinergic deficiency are two prominent features of Alzheimer’s disease (AD). To understand how Aβ-induced dysfunction of the nicotinic system may contribute to cognitive im...

    Authors: Guo-Jun Chen, Zhe Xiong and Zhen Yan
    Citation: Molecular Neurodegeneration 2013 8:3
  18. Although the mechanism of neuron loss in Alzheimer’s disease (AD) is enigmatic, it is associated with cerebral accumulation of Aβ42. The 5XFAD mouse model of amyloid deposition expresses five familial AD (FAD) mu...

    Authors: William A Eimer and Robert Vassar
    Citation: Molecular Neurodegeneration 2013 8:2
  19. A proline-to-serine substitution at position-56 (P56S) of vesicle-associated membrane protein-associated protein B (VAPB) causes a form of dominantly inherited motor neuron disease (MND), including typical and...

    Authors: Linghua Qiu, Tao Qiao, Melissa Beers, Weijia Tan, Hongyan Wang, Bin Yang and Zuoshang Xu
    Citation: Molecular Neurodegeneration 2013 8:1
  20. A hallmark of Alzheimer’s disease is the presence of senile plaques in human brain primarily containing the amyloid peptides Aβ42 and Aβ40. Many drug discovery efforts have focused on decreasing the production of...

    Authors: Kathryn Rogers, Kevin M Felsenstein, Lori Hrdlicka, Zhiming Tu, Faris Albayya, Winnie Lee, Sarah Hopp, Mary-Jo Miller, Darcie Spaulding, Zhiyong Yang, Hilliary Hodgdon, Scott Nolan, Melody Wen, Don Costa, Jean-Francois Blain, Emily Freeman…
    Citation: Molecular Neurodegeneration 2012 7:61
  21. Mutations in either Aβ Precursor protein (APP) or genes that regulate APP processing, such as BRI2/ITM2B and PSEN1/PSEN2, cause familial dementias. Although dementias due to APP/PSEN1/PSEN2 mutations are classifi...

    Authors: Robert Tamayev, Nsikan Akpan, Ottavio Arancio, Carol M Troy and Luciano D’Adamio
    Citation: Molecular Neurodegeneration 2012 7:60
  22. Axonal pathology might constitute one of the earliest manifestations of Alzheimer disease. Axonal dystrophies were observed in Alzheimer’s patients and transgenic models at early ages. These axonal dystrophies...

    Authors: Manuel Torres, Sebastian Jimenez, Raquel Sanchez-Varo, Victoria Navarro, Laura Trujillo-Estrada, Elisabeth Sanchez-Mejias, Irene Carmona, Jose Carlos Davila, Marisa Vizuete, Antonia Gutierrez and Javier Vitorica
    Citation: Molecular Neurodegeneration 2012 7:59
  23. The accumulation of amyloid beta (Aβ) oligomers or fibrils is thought to be one of the main causes of synaptic and neuron loss, believed to underlie cognitive dysfunction in Alzheimer’s disease (AD). Neuron lo...

    Authors: Hannah Brautigam, John W Steele, David Westaway, Paul E Fraser, Peter H St George-Hyslop, Sam Gandy, Patrick R Hof and Dara L Dickstein
    Citation: Molecular Neurodegeneration 2012 7:58
  24. The definitive indicator of Alzheimer’s disease (AD) pathology is the profuse accumulation of amyloid-ß (Aß) within the brain. Various in vitro and cell-based models have been proposed for high throughput drug sc...

    Authors: Gawain McColl, Blaine R Roberts, Tara L Pukala, Vijaya B Kenche, Christine M Roberts, Christopher D Link, Timothy M Ryan, Colin L Masters, Kevin J Barnham, Ashley I Bush and Robert A Cherny
    Citation: Molecular Neurodegeneration 2012 7:57
  25. Recent studies suggest that the chemotactic G-protein-coupled-receptor (GPCR) formyl-peptide-receptor-like-1 (FPRL1) and the receptor-for-advanced-glycation-end-products (RAGE) play an important role in the in...

    Authors: Alexander Slowik, Julika Merres, Anne Elfgen, Sandra Jansen, Fabian Mohr, Christoph J Wruck, Thomas Pufe and Lars-Ove Brandenburg
    Citation: Molecular Neurodegeneration 2012 7:55
  26. Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective loss of upper and lower motor neurons, a cell type that is intrinsically more vulnerable than other cell ...

    Authors: Anaïs Aulas, Stéphanie Stabile and Christine Vande Velde
    Citation: Molecular Neurodegeneration 2012 7:1

    The Erratum to this article has been published in Molecular Neurodegeneration 2015 10:45

  27. Mutations in the gene encoding the RNA-binding protein fused in sarcoma (FUS) can cause familial and sporadic amyotrophic lateral sclerosis (ALS) and rarely frontotemproal dementia (FTD). FUS accumulates in ne...

    Authors: Christophe Verbeeck, Qiudong Deng, Mariely DeJesus-Hernandez, Georgia Taylor, Carolina Ceballos-Diaz, Jannet Kocerha, Todd Golde, Pritam Das, Rosa Rademakers, Dennis W Dickson and Thomas Kukar
    Citation: Molecular Neurodegeneration 2012 7:53
  28. Alzheimer’s disease (AD) is a complex age-related pathology, the etiology of which has not been firmly delineated. Among various histological stigmata, AD-affected brains display several cellular dysfunctions ...

    Authors: Linda Chami and Frédéric Checler
    Citation: Molecular Neurodegeneration 2012 7:52
  29. Friedreich’s ataxia (FRDA) is a neurodegenerative disease caused by deficiency of the mitochondrial iron chaperone frataxin (Fxn). FRDA has no cure, but disease-modifying strategies to increase frataxin are un...

    Authors: Carolina Franco, Silvia Fernández and Ignacio Torres-Alemán
    Citation: Molecular Neurodegeneration 2012 7:51
  30. One of the best-characterized causative factors of Alzheimer’s disease (AD) is the generation of amyloid-β peptide (Aβ). AD subjects are at high risk of epileptic seizures accompanied by aberrant neuronal exci...

    Authors: Yuhki Saito, Tsuyoshi Inoue, Gang Zhu, Naoki Kimura, Motohiro Okada, Masaki Nishimura, Nobuyuki Kimura, Shigeo Murayama, Sunao Kaneko, Ryuichi Shigemoto, Keiji Imoto and Toshiharu Suzuki
    Citation: Molecular Neurodegeneration 2012 7:50
  31. Parkinson's disease (PD) is a multifactorial disease where environmental factors act on genetically predisposed individuals. Although only 5% of PD manifestations are associated with specific mutations, majori...

    Authors: Paula Desplats, Pruthul Patel, Kori Kosberg, Michael Mante, Christina Patrick, Edward Rockenstein, Masayo Fujita, Makoto Hashimoto and Eliezer Masliah
    Citation: Molecular Neurodegeneration 2012 7:49
  32. Macroautophagy is an evolutionarily conserved mechanism for bulk intracellular degradation of proteins and organelles. Pathological studies have implicated macroautophagy defects in human neurodegenerative dis...

    Authors: Keiichi Inoue, Joanne Rispoli, Hanoch Kaphzan, Eric Klann, Emily I Chen, Jongpil Kim, Masaaki Komatsu and Asa Abeliovich
    Citation: Molecular Neurodegeneration 2012 7:48
  33. The transcription factor NFκB is an important mediator of cell survival and inflammation in the immune system. In the central nervous system (CNS), NFκB signaling has been implicated in regulating neuronal sur...

    Authors: Hong Lian, David J Shim, Samson SK Gaddam, Jennifer Rodriguez-Rivera, Brittany R Bitner, Robia G Pautler, Claudia S Robertson and Hui Zheng
    Citation: Molecular Neurodegeneration 2012 7:47
  34. Proteases that degrade the amyloid ß-protein (Aß) have emerged as key players in the etiology and potential treatment of Alzheimer’s disease (AD), but it is unlikely that all such proteases have been identifie...

    Authors: Samer O Abdul-Hay, Tomoko Sahara, Melinda McBride, Dongcheul Kang and Malcolm A Leissring
    Citation: Molecular Neurodegeneration 2012 7:46
  35. Dopaminergic (DA) neurons in the ventral midbrain selectively degenerate in Parkinson’s disease (PD) in part because their oxidative environment in the substantia nigra (SN) may render them vulnerable to neuro...

    Authors: Terina N Martinez, Xi Chen, Sibali Bandyopadhyay, Alfred H Merrill and Malú G Tansey
    Citation: Molecular Neurodegeneration 2012 7:45
  36. Amyotrophic lateral sclerosis (ALS) is a fatal disorder involving the degeneration and loss of motor neurons. The mechanisms of motor neuron loss in ALS are unknown and there are no effective treatments. Defec...

    Authors: Stacey A Sakowski, J Simon Lunn, Angela S Busta, Sang Su Oh, Grettel Zamora-Berridi, Madeline Palmer, Andrew A Rosenberg, Stephen G Philip, James J Dowling and Eva L Feldman
    Citation: Molecular Neurodegeneration 2012 7:44
  37. Huntington's Disease (HD) is a fatal hereditary neurodegenerative disease caused by the accumulation of mutant huntingtin protein (Htt) containing an expanded polyglutamine (polyQ) tract. Activation of the cha...

    Authors: Peter O Bauer, Roman Hudec, Anand Goswami, Masaru Kurosawa, Gen Matsumoto, Katsuhiko Mikoshiba and Nobuyuki Nukina
    Citation: Molecular Neurodegeneration 2012 7:43
  38. Aggregation of alpha-synuclein (αsyn) and resulting cytotoxicity is a hallmark of sporadic and familial Parkinson’s disease (PD) as well as dementia with Lewy bodies, with recent evidence implicating oligomeri...

    Authors: Karin M Danzer, Lisa R Kranich, Wolfgang P Ruf, Ozge Cagsal-Getkin, Ashley R Winslow, Liya Zhu, Charles R Vanderburg and Pamela J McLean
    Citation: Molecular Neurodegeneration 2012 7:42
  39. The multifunctional glycoprotein clusterin has been associated with late-onset Alzheimer’s disease (AD). Further investigation to define the role of clusterin in AD phenotypes would be aided by the development...

    Authors: Junjun Chen, Meiyao Wang and Illarion V Turko
    Citation: Molecular Neurodegeneration 2012 7:41
  40. Mutations or deletions in DJ-1/PARK7 gene are causative for recessive forms of early onset Parkinson’s disease (PD). Wild-type DJ-1 has cytoprotective roles against cell death through multiple pathways. The mo...

    Authors: Haigang Ren, Kai Fu, Chenchen Mu, Xuechu Zhen and Guanghui Wang
    Citation: Molecular Neurodegeneration 2012 7:40
  41. Alzheimer’s disease (AD) is the leading cause of dementia among the elderly. Disease modifying therapies targeting Aβ that are in development have been proposed to be more effective if treatment was initiated ...

    Authors: Pritam Das, Christophe Verbeeck, Lisa Minter, Paramita Chakrabarty, Kevin Felsenstein, Thomas Kukar, Ghulam Maharvi, Abdul Fauq, Barbara A Osborne and Todd E Golde
    Citation: Molecular Neurodegeneration 2012 7:39
  42. The intracellular deposition of misfolded proteins is a common neuropathological hallmark of most neurodegenerative disorders. Increasing evidence suggests that these pathogenic proteins may spread to neighbor...

    Authors: Masatoshi Konno, Takafumi Hasegawa, Toru Baba, Emiko Miura, Naoto Sugeno, Akio Kikuchi, Fabienne C Fiesel, Tsutomu Sasaki, Masashi Aoki, Yasuto Itoyama and Atsushi Takeda
    Citation: Molecular Neurodegeneration 2012 7:38
  43. It is well established that vaccination of humans and transgenic animals against fibrillar Aβ prevents amyloid accumulation in plaques and preserves cognitive function in transgenic mouse models. However, auto...

    Authors: Suhail Rasool, Ricardo Albay III, Hilda Martinez-Coria, Leonid Breydo, Jessica Wu, Saskia Milton, Sunit Misra, Andy Tran, Anna Pensalfini, Frank Laferla, Rakez Kayed and Charles G Glabe
    Citation: Molecular Neurodegeneration 2012 7:37
  44. Pro-inflammatory stimuli, including cytokines like Interleukin-1β, Interleukin-6 and Interferon-γ, in the brain have been proposed to exacerbate existing Alzheimer’s disease (AD) neuropathology by increasing a...

    Authors: Paramita Chakrabarty, Li Tianbai, Amanda Herring, Carolina Ceballos-Diaz, Pritam Das and Todd E Golde
    Citation: Molecular Neurodegeneration 2012 7:36
  45. Fibrillar amyloid-like deposits and co-deposits of tau and α-synuclein are found in several common neurodegenerative diseases. Recent evidence indicates that small oligomers are the most relevant toxic aggrega...

    Authors: Georg Nübling, Benedikt Bader, Johannes Levin, Jenna Hildebrandt, Hans Kretzschmar and Armin Giese
    Citation: Molecular Neurodegeneration 2012 7:35
  46. Among the essential biological roles of bone marrow-derived cells, secretion of many soluble factors is included and these small molecules can act upon specific receptors present in many tissues including the ...

    Authors: Victor Tulio Ribeiro-Resende, Alvaro Carrier-Ruiz, Robertha M R Lemes, Ricardo A M Reis and Rosalia Mendez-Otero
    Citation: Molecular Neurodegeneration 2012 7:34
  47. Progranulin (PGRN), a widely secreted growth factor, is involved in multiple biological functions, and mutations located within the PGRN gene (GRN) are a major cause of frontotemporal lobar degeneration with TDP-...

    Authors: Jennifer Gass, Wing C Lee, Casey Cook, Nicole Finch, Caroline Stetler, Karen Jansen-West, Jada Lewis, Christopher D Link, Rosa Rademakers, Anders Nykjær and Leonard Petrucelli
    Citation: Molecular Neurodegeneration 2012 7:33
  48. Alzheimer’s disease (AD) is the most frequently diagnosed neurodegenerative disorder affecting humans, with advanced age being the most prominent risk factor for developing AD. Despite intense research efforts...

    Authors: Carole J Proctor, Ilse Sanet Pienaar, Joanna L Elson and Thomas BL Kirkwood
    Citation: Molecular Neurodegeneration 2012 7:32
  49. The Aβ peptide that accumulates in Alzheimer’s disease (AD) is derived from amyloid precursor protein (APP) following proteolysis by β- and γ-secretases. Substantial evidence indicates that alterations in APP ...

    Authors: Julie Brodeur, Caroline Thériault, Mélissa Lessard-Beaudoin, Alexandre Marcil, Sophie Dahan and Christine Lavoie
    Citation: Molecular Neurodegeneration 2012 7:31