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  1. Our previous studies of Alzheimer’s disease (AD) suggested that glutamine broadly improves cellular readiness to respond to stress and acts as a neuroprotectant both in vitro and in AD mouse models. We now exp...

    Authors: Jianmin Chen, Yanping Chen, Graham Vail, Heiman Chow, Yang Zhang, Lauren Louie, Jiali Li, Ronald P. Hart, Mark R. Plummer and Karl Herrup
    Citation: Molecular Neurodegeneration 2016 11:60
    Content type: Research article Published on:

    The Erratum to this article has been published in Molecular Neurodegeneration 2017 12:4

  2. Genome-wide association studies have identified BIN1 within the second most significant susceptibility locus in late-onset Alzheimer’s disease (AD). BIN1 undergoes complex alternative splicing to generate multipl...

    Authors: Pierre De Rossi, Virginie Buggia-Prévot, Benjamin L. L. Clayton, Jared B. Vasquez, Carson van Sanford, Robert J. Andrew, Ruben Lesnick, Alexandra Botté, Carole Deyts, Someya Salem, Eshaan Rao, Richard C. Rice, Angèle Parent, Satyabrata Kar, Brian Popko, Peter Pytel…
    Citation: Molecular Neurodegeneration 2016 11:59
    Content type: Research article Published on:

    The Correction to this article has been published in Molecular Neurodegeneration 2023 18:72

  3. We used lentiviral vectors (LVs) to generate a new SCA7 animal model overexpressing a truncated mutant ataxin-7 (MUT ATXN7) fragment in the mouse cerebellum, in order to characterize the specific neuropatholog...

    Authors: Sandro Alves, Thibaut Marais, Maria-Grazia Biferi, Denis Furling, Martina Marinello, Khalid El Hachimi, Nathalie Cartier, Merle Ruberg, Giovanni Stevanin, Alexis Brice, Martine Barkats and Annie Sittler
    Citation: Molecular Neurodegeneration 2016 11:58
    Content type: Research article Published on:

  5. Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease with death on average within 2–3 years of symptom onset. Mutations in superoxide dismutase 1 (SOD1) have been identified to cause ALS. ...

    Authors: Alexander McGown, Dame Pamela J. Shaw and Tennore Ramesh
    Citation: Molecular Neurodegeneration 2016 11:56
    Content type: Methodology Published on:

  6. Loss-of-function mutations in PINK1 and PARKIN are the most common causes of autosomal recessive Parkinson’s disease (PD). PINK1 is a mitochondrial serine/threonine kinase that plays a critical role in mitophagy,...

    Authors: Jaekwang Kim, Fabienne C. Fiesel, Krystal C. Belmonte, Roman Hudec, Wang-Xia Wang, Chaeyoung Kim, Peter T. Nelson, Wolfdieter Springer and Jungsu Kim
    Citation: Molecular Neurodegeneration 2016 11:55
    Content type: Research article Published on:

  7. The inflammatory myeloid cell activation is one of the hallmarks of experimental autoimmune encephalomyelitis (EAE), yet the in vivo role of the inflammatory myeloid cell activation in EAE has not been clearly...

    Authors: Min Jung Lee, So Jin Bing, Jonghee Choi, Minhee Jang, Gihyun Lee, Hyunkyoung Lee, Byung Soo Chang, Youngheun Jee, Sung Joong Lee and Ik-Hyun Cho
    Citation: Molecular Neurodegeneration 2016 11:54
    Content type: Research article Published on:

  8. Disease progression in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), as one of its animal models, is characterized by demyelination and neuronal damage in white and gray matter s...

    Authors: Reiner Schneider, Barbara Koop, Friederike Schröter, Jason Cline, Jens Ingwersen, Carsten Berndt, Hans-Peter Hartung, Orhan Aktas and Tim Prozorovski
    Citation: Molecular Neurodegeneration 2016 11:53
    Content type: Research article Published on:

  9. Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder worldwide. Clinically, AD is characterized by impairments of memory and cognitive functions. Accumulation of amyloid-β (Aβ) and neurofi...

    Authors: Ramon Velazquez, Darren M. Shaw, Antonella Caccamo and Salvatore Oddo
    Citation: Molecular Neurodegeneration 2016 11:52
    Content type: Research article Published on:

  10. Apolipoprotein E (ApoE) is a major lipid carrier that supports lipid transport and injury repair in the brain. The APOE ε4 allele is associated with depression, mild cognitive impairment (MCI) and dementia; howev...

    Authors: Lan-yan Lin, Jing Zhang, Xiao-man Dai, Nai-an Xiao, Xi-lin Wu, Zhen Wei, Wen-ting Fang, Yuan-gui Zhu and Xiao-chun Chen
    Citation: Molecular Neurodegeneration 2016 11:51
    Content type: Research article Published on:

  11. Alzheimer’s disease (AD) is an incurable and debilitating chronic progressive neurodegenerative disorder which is the leading cause of dementia worldwide. AD is a heterogeneous and multifactorial disorder, his...

    Authors: Syed Faraz Kazim and Khalid Iqbal
    Citation: Molecular Neurodegeneration 2016 11:50
    Content type: Review Published on:

  12. α-synucleinopathy emerges quite early in olfactory structures such as the olfactory bulb and anterior olfactory nucleus (OB/AON) in Parkinson's disease. This may contribute to smell impairments years before th...

    Authors: Daniel M. Mason, Negin Nouraei, Deepti B. Pant, Kristin M. Miner, Daniel F. Hutchison, Kelvin C. Luk, John F. Stolz and Rehana K. Leak
    Citation: Molecular Neurodegeneration 2016 11:49
    Content type: Short report Published on:

    The Erratum to this article has been published in Molecular Neurodegeneration 2016 11:57

  13. Immunization against amyloid-β (Aβ) peptides deposited in Alzheimer’s disease (AD) has shown considerable therapeutic effect in animal models however, the translation into human Alzheimer’s patients is challen...

    Authors: Holger Cynis, Jeffrey L. Frost, Helen Crehan and Cynthia A. Lemere
    Citation: Molecular Neurodegeneration 2016 11:48
    Content type: Review Published on:

  14. Neurons are highly polarized cells in which asymmetric axonal-dendritic distribution of proteins is crucial for neuronal function. Loss of polarized distribution of the axonal protein tau is an early sign of A...

    Authors: Peter Dongmin Sohn, Tara E. Tracy, Hye-In Son, Yungui Zhou, Renata E. P. Leite, Bruce L. Miller, William W. Seeley, Lea T. Grinberg and Li Gan
    Citation: Molecular Neurodegeneration 2016 11:47
    Content type: Research article Published on:

  15. Progranulin (PGRN) is a secreted growth factor important for neuronal survival and may do so, in part, by regulating lysosome homeostasis. Mutations in the PGRN gene (GRN) are a common cause of frontotemporal lob...

    Authors: Christopher J. Holler, Georgia Taylor, Zachary T. McEachin, Qiudong Deng, William J. Watkins, Kathryn Hudson, Charles A. Easley, William T. Hu, Chadwick M. Hales, Wilfried Rossoll, Gary J. Bassell and Thomas Kukar
    Citation: Molecular Neurodegeneration 2016 11:46
    Content type: Research article Published on:

  16. The aggregation of amyloid-β (Aβ) into insoluble plaques is a hallmark pathology of Alzheimer’s disease (AD). Previous work has shown increasing serotonin levels with selective serotonin re-uptake inhibitor (S...

    Authors: Jonathan R. Fisher, Clare E. Wallace, Danielle L. Tripoli, Yvette I. Sheline and John R. Cirrito
    Citation: Molecular Neurodegeneration 2016 11:45
    Content type: Research article Published on:

  17. To date, there are no effective disease-modifying treatments for Alzheimer’s disease (AD). In order to develop new therapeutics for stages where they are most likely to be effective, it is important to identif...

    Authors: Claire S. Harwell and Michael P. Coleman
    Citation: Molecular Neurodegeneration 2016 11:44
    Content type: Methodology Published on:

  18. Pathological Golgi fragmentation represents a constant pre-clinical feature of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS) but its molecular mechanisms remain hitherto unclear.

    Authors: Sarah Bellouze, Gilbert Baillat, Dorothée Buttigieg, Pierre de la Grange, Catherine Rabouille and Georg Haase
    Citation: Molecular Neurodegeneration 2016 11:43
    Content type: Research article Published on:

  19. Authors: Philipp A. Jaeger, Kurt M. Lucin, Markus Britschgi, Badri Vardarajan, Ruo-Pan Huang, Elizabeth D. Kirby, Rachelle Abbey, Bradley F. Boeve, Adam L. Boxer, Lindsay A. Farrer, NiCole Finch, Neill R. Graff-Radford, Elizabeth Head, Matan Hofree, Ruochun Huang, Hudson Johns…
    Citation: Molecular Neurodegeneration 2016 11:42
    Content type: Erratum Published on:

    The original article was published in Molecular Neurodegeneration 2016 11:31

  21. Authors: Jia Luo, Sue H. Lee, Lawren VandeVrede, Zhihui Qin, Manel Ben Aissa, John Larson, Andrew F. Teich, Ottavio Arancio, Yohan D’Souza, Ahmed Elharram, Kevin Koster, Leon M. Tai, Mary Jo LaDu, Brian M. Bennett and Gregory R. J. Thatcher
    Citation: Molecular Neurodegeneration 2016 11:40
    Content type: Erratum Published on:

    The original article was published in Molecular Neurodegeneration 2016 11:35

  22. Alzheimer's disease (AD) is the most common cause of dementia in those over the age of 65. While a numerous of disease-causing genes and risk factors have been identified, the exact etiological mechanisms of A...

    Authors: Juan Yang, Song Li, Xi-Biao He, Cheng Cheng and Weidong Le
    Citation: Molecular Neurodegeneration 2016 11:39
    Content type: Review Published on:

  23. Despite the clear physical association between activated astrocytes and amyloid-β (Aβ) plaques, the importance of astrocytes and their therapeutic potential in Alzheimer’s disease remain elusive. Soluble Aβ ag...

    Authors: Sofia Söllvander, Elisabeth Nikitidou, Robin Brolin, Linda Söderberg, Dag Sehlin, Lars Lannfelt and Anna Erlandsson
    Citation: Molecular Neurodegeneration 2016 11:38
    Content type: Research article Published on:

  24. The accumulation, aggregation and deposition of amyloid-β (Aβ) peptides in the brain are central to the pathogenesis of Alzheimer’s disease (AD). Alzheimer’s disease risk increases significantly in individuals...

    Authors: Yuan Fu, Jing Zhao, Yuka Atagi, Henrietta M. Nielsen, Chia-Chen Liu, Honghua Zheng, Mitsuru Shinohara, Takahisa Kanekiyo and Guojun Bu
    Citation: Molecular Neurodegeneration 2016 11:37
    Content type: Research article Published on:

  25. Mutations in the progranulin gene (GRN) are the most common cause of frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). TDP-43 pathology is characterized by the hyperphosphorylation of the prote...

    Authors: Carolina Alquezar, Irene G. Salado, Ana de la Encarnación, Daniel I. Pérez, Fermín Moreno, Carmen Gil, Adolfo López de Munain, Ana Martínez and Ángeles Martín-Requero
    Citation: Molecular Neurodegeneration 2016 11:36
    Content type: Research article Published on:

  26. Clinical failures singularly targeting amyloid-β pathology indicate a critical need for alternative Alzheimer’s disease (AD) therapeutic strategies. The mixed pathology reported in a large population of AD pat...

    Authors: Jia Luo, Sue H. Lee, Lawren VandeVrede, Zhihui Qin, Manel Ben Aissa, John Larson, Andrew F. Teich, Ottavio Arancio, Yohan D’Souza, Ahmed Elharram, Kevin Koster, Leon M. Tai, Mary Jo LaDu, Brian M. Bennett and Gregory R. J. Thatcher
    Citation: Molecular Neurodegeneration 2016 11:35
    Content type: Research article Published on:

    The Erratum to this article has been published in Molecular Neurodegeneration 2016 11:40

  27. Apoptosis takes place in naturally occurring neuronal death, but also in aging, neurodegenerative disorders, and traumatic brain injuries. Caspase 3 (Casp3) is the most important effector protease in apoptosis...

    Authors: Laura Lossi, Carolina Cocito, Silvia Alasia and Adalberto Merighi
    Citation: Molecular Neurodegeneration 2016 11:34
    Content type: Methodology Published on:

  28. A certain number of mutations in the Microtubule-Associated Protein Tau (MAPT) gene have been identified in individuals with high risk to develop neurodegenerative diseases, collectively called tauopathies. The m...

    Authors: Ghulam Jeelani Pir, Bikash Choudhary, Eckhard Mandelkow and Eva-Maria Mandelkow
    Citation: Molecular Neurodegeneration 2016 11:33
    Content type: Research article Published on:

  29. Tauopathy is characterized by neurofibrillary tangles composed of insoluble hyperphosphorylated tau protein. Currently, cellular models that mimic neurofibrillary tangles in vitro are lacking. Previous studies...

    Authors: Yin Xu, Heidi Martini-Stoica and Hui Zheng
    Citation: Molecular Neurodegeneration 2016 11:32
    Content type: Methodology Published on:

  30. Biological pathways that significantly contribute to sporadic Alzheimer’s disease are largely unknown and cannot be observed directly. Cognitive symptoms appear only decades after the molecular disease onset, ...

    Authors: Philipp A. Jaeger, Kurt M. Lucin, Markus Britschgi, Badri Vardarajan, Ruo-Pan Huang, Elizabeth D. Kirby, Rachelle Abbey, Bradley F. Boeve, Adam L. Boxer, Lindsay A. Farrer, NiCole Finch, Neill R. Graff-Radford, Elizabeth Head, Matan Hofree, Ruochun Huang, Hudson Johns…
    Citation: Molecular Neurodegeneration 2016 11:31
    Content type: Research article Published on:

    The Erratum to this article has been published in Molecular Neurodegeneration 2016 11:42

  31. The c-Jun N-terminal kinase (JNK) signaling pathway plays an important role in neuronal pathophysiology. Using JNK inhibitors, we examined involvement of the JNK pathway in cultured rat retinal ganglion cell (...

    Authors: Byung-Jin Kim, Sean M. Silverman, Yang Liu, Robert J. Wordinger, Iok-Hou Pang and Abbot F. Clark
    Citation: Molecular Neurodegeneration 2016 11:30
    Content type: Research article Published on:

  32. Most sequencing studies in Parkinson’s disease (PD) have focused on either a particular gene, primarily in familial and early onset PD samples, or on screening single variants in sporadic PD cases. To date, th...

    Authors: Bruno A. Benitez, Albert A. Davis, Sheng Chih Jin, Laura Ibanez, Sara Ortega-Cubero, Pau Pastor, Jiyoon Choi, Breanna Cooper, Joel S. Perlmutter and Carlos Cruchaga
    Citation: Molecular Neurodegeneration 2016 11:29
    Content type: Research article Published on:

  33. α-Synuclein (α-Syn), a pathological hallmark of Parkinson’s disease (PD), has been recognized to induce the production of interleukin-1β in a process that depends, at least in vitro, on nod-like receptor prote...

    Authors: Yan Zhou, Ming Lu, Ren-Hong Du, Chen Qiao, Chun-Yi Jiang, Ke-Zhong Zhang, Jian-Hua Ding and Gang Hu
    Citation: Molecular Neurodegeneration 2016 11:28
    Content type: Research article Published on:

  34. Huntington’s disease (HD) is an incurable hereditary neurodegenerative disorder, which manifests itself as a loss of GABAergic medium spiny (GABA MS) neurons in the striatum and caused by an expansion of the C...

    Authors: Evgeny D. Nekrasov, Vladimir A. Vigont, Sergey A. Klyushnikov, Olga S. Lebedeva, Ekaterina M. Vassina, Alexandra N. Bogomazova, Ilya V. Chestkov, Tatiana A. Semashko, Elena Kiseleva, Lyubov A. Suldina, Pavel A. Bobrovsky, Olga A. Zimina, Maria A. Ryazantseva, Anton Yu. Skopin, Sergey N. Illarioshkin, Elena V. Kaznacheyeva…
    Citation: Molecular Neurodegeneration 2016 11:27
    Content type: Research article Published on:

  35. Glaucoma is a complex, multifactorial disease characterised by the loss of retinal ganglion cells and their axons leading to a decrease in visual function. The earliest events that damage retinal ganglion cell...

    Authors: Pete A. Williams, James R. Tribble, Keating W. Pepper, Stephen D. Cross, B Paul Morgan, James E. Morgan, Simon W. M. John and Gareth R. Howell
    Citation: Molecular Neurodegeneration 2016 11:26
    Content type: Research article Published on:

  36. Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms. The cause of the motor symptoms is the loss of dopaminergic neurons in the substantia nigra with...

    Authors: Milena Pinto, Nadee Nissanka, Susana Peralta, Roberta Brambilla, Francisca Diaz and Carlos T. Moraes
    Citation: Molecular Neurodegeneration 2016 11:25
    Content type: Research article Published on:

  37. C1q represents the initiating protein of the classical complement cascade, however recent findings indicate pathway independent roles such as developmental pruning of retinal ganglion cell (RGC) axons. Further...

    Authors: Sean M. Silverman, Byung-Jin Kim, Garreth R. Howell, Joselyn Miller, Simon W. M. John, Robert J. Wordinger and Abbot F. Clark
    Citation: Molecular Neurodegeneration 2016 11:24
    Content type: Research article Published on:

  38. Interleukin-1 beta (IL-1β) and its key regulator, the inflammasome, are suspected to play a role in the neuroinflammation observed in Alzheimer’s disease (AD); no conclusive data are nevertheless available in ...

    Authors: Marina Saresella, Francesca La Rosa, Federica Piancone, Martina Zoppis, Ivana Marventano, Elena Calabrese, Veronica Rainone, Raffaello Nemni, Roberta Mancuso and Mario Clerici
    Citation: Molecular Neurodegeneration 2016 11:23
    Content type: Research article Published on:

  39. Increasing evidence suggests a potential therapeutic benefit of vitamin D supplementation against Alzheimer’s disease (AD). Although studies have shown improvements in cognitive performance and decreases in ma...

    Authors: Véréna Landel, Pascal Millet, Kévin Baranger, Béatrice Loriod and François Féron
    Citation: Molecular Neurodegeneration 2016 11:22
    Content type: Research article Published on:

  40. In frontotemporal dementia (FTD) there is a critical lack in the understanding of biological and molecular mechanisms involved in disease pathogenesis. The heterogeneous genetic features associated with FTD su...

    Authors: Raffaele Ferrari, Paola Forabosco, Jana Vandrovcova, Juan A. Botía, Sebastian Guelfi, Jason D. Warren, Parastoo Momeni, Michael E. Weale, Mina Ryten and John Hardy
    Citation: Molecular Neurodegeneration 2016 11:21
    Content type: Research article Published on:

  41. Authors: Wendy E. Heywood, Daniela Galimberti, Emily Bliss, Ernestas Sirka, Ross W. Paterson, Nadia K. Magdalinou, Miryam Carecchio, Emma Reid, Amanda Heslegrave, Chiara Fenoglio, Elio Scarpini, Jonathan M. Schott, Nick C. Fox, John Hardy, Kailash P. Bhatia, Simon Heales…
    Citation: Molecular Neurodegeneration 2016 11:20
    Content type: Erratum Published on:

    The original article was published in Molecular Neurodegeneration 2015 10:64

  42. The metalloprotease meprin β cleaves the Alzheimer’s Disease (AD) relevant amyloid precursor protein (APP) as a β-secretase reminiscent of BACE-1, however, predominantly generating N-terminally truncated Aβ2-x...

    Authors: Caroline Schönherr, Jessica Bien, Simone Isbert, Rielana Wichert, Johannes Prox, Hermann Altmeppen, Sathish Kumar, Jochen Walter, Stefan F. Lichtenthaler, Sascha Weggen, Markus Glatzel, Christoph Becker-Pauly and Claus U. Pietrzik
    Citation: Molecular Neurodegeneration 2016 11:19
    Content type: Research article Published on:

  43. Prions and amyloid-β (Aβ) oligomers trigger neurodegeneration by hijacking a poorly understood cellular signal mediated by the prion protein (PrP) at the plasma membrane. In early zebrafish embryos, PrP-1-depe...

    Authors: Emily Sempou, Emiliano Biasini, Alejandro Pinzón-Olejua, David A. Harris and Edward Málaga-Trillo
    Citation: Molecular Neurodegeneration 2016 11:18
    Content type: Research article Published on:

  44. While many biological studies can be performed on cell-based systems, the investigation of molecular pathways related to complex human dysfunctions – e.g. neurodegenerative diseases – often requires long-term ...

    Authors: Matteo Cornaglia, Gopalan Krishnamani, Laurent Mouchiroud, Vincenzo Sorrentino, Thomas Lehnert, Johan Auwerx and Martin A. M. Gijs
    Citation: Molecular Neurodegeneration 2016 11:17
    Content type: Methodology Published on:

  45. Alzheimer disease (AD) and other tauopathies develop cerebral intracellular inclusions of hyperphosphorylated tau. Epidemiological and experimental evidence suggests a clear link between type 2 diabetes mellit...

    Authors: Erica Barini, Odetta Antico, Yingjun Zhao, Francesco Asta, Valter Tucci, Tiziano Catelani, Roberto Marotta, Huaxi Xu and Laura Gasparini
    Citation: Molecular Neurodegeneration 2016 11:16
    Content type: Research article Published on:

  47. A unique feature of the pathological change after spinal cord injury (SCI) is the progressive enlargement of lesion area, which usually results in cavity formation and is accompanied by reactive astrogliosis a...

    Authors: Hong Fan, Kun Zhang, Lequn Shan, Fang Kuang, Kun Chen, Keqing Zhu, Heng Ma, Gong Ju and Ya-Zhou Wang
    Citation: Molecular Neurodegeneration 2016 11:14
    Content type: Research article Published on:

  48. Parkinson’s disease (PD) is a motor disease associated with the degeneration of dopaminergic neurons of the substantia nigra pars compacta. p53 is a major neuronal pro-apoptotic factor that is at the center of gr...

    Authors: Eric Duplan, Cécile Giordano, Frédéric Checler and Cristine Alves da Costa
    Citation: Molecular Neurodegeneration 2016 11:13
    Content type: Research article Published on:

  49. Deep brain stimulation (DBS) of the subthalamic nucleus (STN) or the internal segment of the globus pallidus (GPi) has been established as a highly effective symptomatic therapy for Parkinson’s disease (PD). A...

    Authors: Affif Zaccaria, Ali Bouamrani, Stephan Chabardès, Michèle El Atifi, Eric Seigneuret, Johannes A. Lobrinus, Michel Dubois-Dauphin, François Berger and Pierre R. Burkhard
    Citation: Molecular Neurodegeneration 2016 11:12
    Content type: Methodology Published on:

  50. Prion diseases are characterized by the accumulation in the central nervous system of an abnormally folded isoform of the prion protein, named PrPSc. Aggregation of PrPSc into oligomers and fibrils is critically ...

    Authors: Thibaut Imberdis, Adeline Ayrolles-Torro, Alysson Duarte Rodrigues, Joan Torrent, Maria Teresa Alvarez-Martinez, Gabor G. Kovacs, Jean-Michel Verdier, Mike Robitzer and Véronique Perrier
    Citation: Molecular Neurodegeneration 2016 11:11
    Content type: Research article Published on:
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  • ISSN: 1750-1326 (electronic)

Molecular Neurodegeneration

ISSN: 1750-1326