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Page 17 of 20

  1. Nucleotide duplications in exon 4 of the ferritin light polypeptide (FTL) gene cause the autosomal dominant neurodegenerative disease neuroferritinopathy or hereditary ferritinopathy (HF). Pathologic examinati...

    Authors: Ana G Barbeito, Thierry Levade, Marie B Delisle, Bernardino Ghetti and Ruben Vidal

    Citation: Molecular Neurodegeneration 2010 5:50

    Content type: Research article

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  2. Tau hyperphosphorylation and aggregation to form intracellular neurofibrillar tangles is prevalent in a number of tauopathies. Thus there is current interest in the mechanisms involved in Tau clearance. It was...

    Authors: K Martin Chow, Hanjun Guan and Louis B Hersh

    Citation: Molecular Neurodegeneration 2010 5:48

    Content type: Research article

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  3. α-Synuclein aggregates in Lewy bodies and plays a central role in the pathogenesis of a group of neurodegenerative disorders, known as "Synucleinopathies", including Parkinson's disease. Parkin mutations resul...

    Authors: Preeti J Khandelwal, Sonya B Dumanis, Li Rebekah Feng, Kathleen Maguire-Zeiss, GW Rebeck, Hilal A Lashuel and Charbel EH Moussa

    Citation: Molecular Neurodegeneration 2010 5:47

    Content type: Research article

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  4. Although increasing evidence has indicated that brain insulin dysfunction is a risk factor for Alzheimer disease (AD), the underlying mechanisms by which insulin deficiency may impact the development of AD are...

    Authors: Xu Wang, Wei Zheng, Jing-Wei Xie, Tao Wang, Si-Ling Wang, Wei-Ping Teng and Zhan-You Wang

    Citation: Molecular Neurodegeneration 2010 5:46

    Content type: Research article

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  5. It has traditionally been thought that the pathological accumulation of tau in Alzheimer's disease and other tauopathies facilitates neurodegeneration, which in turn leads to cognitive impairment. However, rec...

    Authors: John C O'Leary III, Qingyou Li, Paul Marinec, Laura J Blair, Erin E Congdon, Amelia G Johnson, Umesh K Jinwal, John Koren III, Jeffrey R Jones, Clara Kraft, Melinda Peters, Jose F Abisambra, Karen E Duff, Edwin J Weeber, Jason E Gestwicki and Chad A Dickey

    Citation: Molecular Neurodegeneration 2010 5:45

    Content type: Research article

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  6. Apolipoprotein E (apoE) is a major cholesterol transport protein found in association with brain amyloid from Alzheimer's disease (AD) patients and the ε4 allele of apoE is a genetic risk factor for AD. Previous ...

    Authors: Sokreine Suon, Jie Zhao, Stephanie A Villarreal, Nikesh Anumula, Mali Liu, Linda M Carangia, John J Renger and Celina V Zerbinatti

    Citation: Molecular Neurodegeneration 2010 5:44

    Content type: Research article

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  7. The pathological hallmarks of Parkinson's disease (PD) include the presence of alpha-synuclein (α-syn) rich Lewy bodies and neurites and the loss of dopaminergic (DA) neurons of the substantia nigra (SN). Anim...

    Authors: James B Koprich, Tom H Johnston, M Gabriela Reyes, Xuan Sun and Jonathan M Brotchie

    Citation: Molecular Neurodegeneration 2010 5:43

    Content type: Research article

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  8. Overexpression of alpha-synuclein (α-SYN), a protein which plays an important role in the pathogenesis of Parkinson's disease (PD), triggers microglial activation and adaptive immune responses, and leads to ne...

    Authors: Shuwen Cao, Shaji Theodore and David G Standaert

    Citation: Molecular Neurodegeneration 2010 5:42

    Content type: Research article

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  9. Progranulin (PGRN) encoded by the GRN gene, is a secreted glycoprotein growth factor that has been implicated in many physiological and pathophysiological processes. PGRN haploinsufficiency caused by autosomal do...

    Authors: Babykumari P Chitramuthu, David C Baranowski, Denis G Kay, Andrew Bateman and Hugh PJ Bennett

    Citation: Molecular Neurodegeneration 2010 5:41

    Content type: Research article

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  10. Retrograde transport of several transmembrane proteins from endosomes to the trans-Golgi network (TGN) occurs via Rab 5-containing endosomes, mediated by clathrin and the recently characterized retromer comple...

    Authors: Sandra I Vieira, Sandra Rebelo, Hermann Esselmann, Jens Wiltfang, James Lah, Rachel Lane, Scott A Small, Sam Gandy, Edgar F da Cruz e Silva and Odete AB da Cruz e Silva

    Citation: Molecular Neurodegeneration 2010 5:40

    Content type: Research article

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  11. Active and passive immunotherapy in both amyloid-beta precursor protein (APP) transgenic mice and Alzheimer's Disease (AD) patients have resulted in remarkable reductions in amyloid plaque accumulation, althou...

    Authors: Chera L Maarouf, Ian D Daugs, Tyler A Kokjohn, Walter M Kalback, R Lyle Patton, Dean C Luehrs, Eliezer Masliah, James AR Nicoll, Marwan N Sabbagh, Thomas G Beach, Eduardo M Castaño and Alex E Roher

    Citation: Molecular Neurodegeneration 2010 5:39

    Content type: Research article

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  12. Mutations in presenilin-1 (Psen1) cause familial Alzheimer's disease (FAD). Both hypoxia and ischemia have been implicated in the pathological cascade that leads to amyloid deposition in AD. Here we investigated ...

    Authors: Rita De Gasperi, Miguel A Gama Sosa, Stella Dracheva and Gregory A Elder

    Citation: Molecular Neurodegeneration 2010 5:38

    Content type: Research article

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  13. The BACE1 gene encodes the beta-site APP-cleaving enzyme 1 and has been associated with Alzheimer's disease (AD). BACE1 is the most important β-secretase responsible for the generation of Alzheimer-associated amy...

    Authors: Annica Sjölander, Henrik Zetterberg, Ulf Andreasson, Lennart Minthon and Kaj Blennow

    Citation: Molecular Neurodegeneration 2010 5:37

    Content type: Short report

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  14. Cholesterol content of cerebral membranes is tightly regulated by elaborate mechanisms that balance the level of cholesterol synthesis, uptake and efflux. Among the conventional regulatory elements, a recent r...

    Authors: Afia Akram, James Schmeidler, Pavel Katsel, Patrick R Hof and Vahram Haroutunian

    Citation: Molecular Neurodegeneration 2010 5:36

    Content type: Research article

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  15. X11-family proteins, including X11, X11-like (X11L) and X11-like 2 (X11L2), bind to the cytoplasmic domain of amyloid β-protein precursor (APP) and regulate APP metabolism. Both X11 and X11L are expressed spec...

    Authors: Maho Kondo, Maki Shiono, Genzo Itoh, Norio Takei, Takahide Matsushima, Masahiro Maeda, Hidenori Taru, Saori Hata, Tohru Yamamoto, Yuhki Saito and Toshiharu Suzuki

    Citation: Molecular Neurodegeneration 2010 5:35

    Content type: Research article

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  16. Alleles of apolipoprotein E (APOE) are the major genetic risk factor for late onset Alzheimer's Disease (LOAD). Recently, an APOE splice variant that retains intron 3 (APOE-I3) was identified. To gain insight int...

    Authors: Laura S Dieter and Steven Estus

    Citation: Molecular Neurodegeneration 2010 5:34

    Content type: Research article

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  17. Inclusions of TAR DNA binding protein-43 (TDP-43) are the defining histopathological feature of several neurodegenerative diseases collectively referred to as TDP-43 proteinopathies. These diseases are charact...

    Authors: Yong-Jie Zhang, Tania F Gendron, Ya-Fei Xu, Li-Wen Ko, Shu-Hui Yen and Leonard Petrucelli

    Citation: Molecular Neurodegeneration 2010 5:33

    Content type: Research article

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  18. Pericytes are integral members of the neurovascular unit. Using mouse models lacking endothelial-secreted platelet derived growth factor-B (PDGF-B) or platelet derived growth factor receptor beta (PDGFRβ) on p...

    Authors: Ethan A Winkler, Robert D Bell and Berislav V Zlokovic

    Citation: Molecular Neurodegeneration 2010 5:32

    Content type: Research article

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  19. BACE1 is a key enzyme in the generation of the Aβ peptide that plays a central role in the pathogenesis of Alzheimer's disease. While BACE1 is an attractive therapeutic target, its normal physiological functio...

    Authors: Brian D Hitt, Thomas C Jaramillo, Dane M Chetkovich and Robert Vassar

    Citation: Molecular Neurodegeneration 2010 5:31

    Content type: Research article

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  20. Alzheimer's disease (AD) is a progressive neurodegenerative disease, characterised by the formation of insoluble amyloidogenic plaques and neurofibrillary tangles. Beta amyloid (Aβ) peptide is one of the main ...

    Authors: Lana Shabala, Claire Howells, Adrian K West and Roger S Chung

    Citation: Molecular Neurodegeneration 2010 5:30

    Content type: Research article

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  21. Age-related decline of neuronal function is associated with age-related structural changes. In the central nervous system, age-related decline of cognitive performance is thought to be caused by synaptic loss ...

    Authors: Haiyan Shen, Jonathan I Matsui, Debin Lei, Lirong Han, Kevin K Ohlemiller and Jianxin Bao

    Citation: Molecular Neurodegeneration 2010 5:28

    Content type: Research article

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  22. The pathogenesis of HIV-associated dementia (HAD) is poorly understood. To date, detailed proteomic fingerprinting directly from autopsied brain tissues of HAD and HIV non-dementia patients has not been perfor...

    Authors: Li Zhou, Eve Diefenbach, Ben Crossett, Sieu L Tran, Thomas Ng, Helen Rizos, Rejane Rua, Bin Wang, Amit Kapur, Kaushal Gandhi, Bruce J Brew and Nitin K Saksena

    Citation: Molecular Neurodegeneration 2010 5:27

    Content type: Research article

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  23. Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a CAG repeat expansion within the huntingtin gene. Mutant huntingtin protein misfolds and accumulates within neurons where it med...

    Authors: Jonathan H Fox, Teal Connor, Vanita Chopra, Kate Dorsey, Jibrin A Kama, Dorothee Bleckmann, Claudia Betschart, Daniel Hoyer, Stefan Frentzel, Marian DiFiglia, Paolo Paganetti and Steven M Hersch

    Citation: Molecular Neurodegeneration 2010 5:26

    Content type: Research article

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  24. Up to the 1950s, there was an ongoing debate about the diversity of hereditary optic neuropathies, in particular as to whether all inherited optic atrophies can be ascribed to Leber's hereditary optic neuropat...

    Authors: Nico Fuhrmann, Simone Schimpf, York Kamenisch, Beate Leo-Kottler, Christiane Alexander, Georg Auburger, Eberhart Zrenner, Bernd Wissinger and Marcel V Alavi

    Citation: Molecular Neurodegeneration 2010 5:25

    Content type: Research article

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  25. Hsp90 is a molecular chaperone with important roles in regulating pathogenic transformation. In addition to its well-characterized functions in malignancy, recent evidence from several laboratories suggests a ...

    Authors: Wenjie Luo, Weilin Sun, Tony Taldone, Anna Rodina and Gabriela Chiosis

    Citation: Molecular Neurodegeneration 2010 5:24

    Content type: Review

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  26. The extent to which the effect of risk factors on cognitive ageing is dependent on APOE ε4 remains unclear. The objective of this study is to examine whether APOE ε4 allele modifies the association between hea...

    Authors: Séverine Sabia, Mika Kivimaki, Meena Kumari, Martin J Shipley and Archana Singh-Manoux

    Citation: Molecular Neurodegeneration 2010 5:23

    Content type: Short report

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  27. Studies have implicated reduced levels of brain-derived neurotrophic factor (BDNF) in the pathogenesis of Huntington's disease. Mutant huntingtin (Htt) protein was previously reported to decrease BDNF gene tra...

    Authors: Bin Ma, Brady P Culver, Gabriele Baj, Enrico Tongiorgi, Moses V Chao and Naoko Tanese

    Citation: Molecular Neurodegeneration 2010 5:22

    Content type: Research article

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  28. Parkinson's disease (PD) involves the selective damage of dopaminergic neuron cells resulting from the accumulation and fibril formation of alpha-synuclein. Recently, it has been shown that not only full-lengt...

    Authors: Jihoon Kim, Ryuichi Harada, Masaki Kobayashi, Natsuki Kobayashi and Koji Sode

    Citation: Molecular Neurodegeneration 2010 5:20

    Content type: Research article

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  29. One pathological hallmark of Alzheimer's disease (AD) is amyloid plaques, composed primarily of amyloid-β peptide (Aβ). Over-production or diminished clearance of the 42 amino acid form of Aβ (Aβ42) in the bra...

    Authors: Chunjiang Yu, Evelyn Nwabuisi-Heath, Kevin Laxton and Mary Jo LaDu

    Citation: Molecular Neurodegeneration 2010 5:19

    Content type: Research article

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  30. Huntington's disease (HD) is a neurodegenerative disorder caused by a polyglutamine (polyQ) expansion in Huntingtin protein (Htt). PolyQ expansion in Httexp causes selective degeneration of striatal medium spi...

    Authors: Hongyu Wang, Xi Chen, Yuemei Li, Tie-Shan Tang and Ilya Bezprozvanny

    Citation: Molecular Neurodegeneration 2010 5:18

    Content type: Research article

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  31. Cultured spinal motor neurons are a valuable tool to study basic mechanisms of development, axon growth and pathfinding, and, importantly, to analyze the pathomechanisms underlying motor neuron diseases. Howev...

    Authors: Claudia Fallini, Gary J Bassell and Wilfried Rossoll

    Citation: Molecular Neurodegeneration 2010 5:17

    Content type: Methodology

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  32. Apolipoprotein E (apoE) is postulated to affect brain Aβ levels through multiple mechanisms--by altering amyloid precursor protein (APP) processing, Aβ degradation, and Aβ clearance. We previously showed that ...

    Authors: S Sakura Minami, Antoinette Cordova, John R Cirrito, Joseph A Tesoriero, Lenard W Babus, Gary C Davis, Sivanesan Dakshanamurthy, R Scott Turner, Daniel TS Pak, G William Rebeck, Mikell Paige and Hyang-Sook Hoe

    Citation: Molecular Neurodegeneration 2010 5:16

    Content type: Research article

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  33. Evidence indicates that soluble forms of amyloid-β (Aβ) are vasoactive, which may contribute to cerebrovascular dysfunction noted in patients with Alzheimer's Disease and cerebral amyloid angiopathy. The effec...

    Authors: Hans H Dietrich, Chuanxi Xiang, Byung H Han, Gregory J Zipfel and David M Holtzman

    Citation: Molecular Neurodegeneration 2010 5:15

    Content type: Research article

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  34. Microglia cells are the brain counterpart of macrophages and function as the first defense in the brain. Although they are neuroprotective in the young brain, microglia cells may be primed to react abnormally ...

    Authors: Xiao-Guang Luo, Jian-Qing Ding and Sheng-Di Chen

    Citation: Molecular Neurodegeneration 2010 5:12

    Content type: Review

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  35. Alzheimer's disease (AD) is characterized by protein aggregates, i.e. senile plaques and neurofibrillary tangles. The ubiquitin-proteasome system has been proposed a role in proteolytic removal of these protein a...

    Authors: Madeleine Zetterberg, Annica Sjölander, Malin von Otter, Mona Seibt Palmér, Sara Landgren, Lennart Minthon, Anders Wallin, Niels Andreasen, Kaj Blennow and Henrik Zetterberg

    Citation: Molecular Neurodegeneration 2010 5:11

    Content type: Short report

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  36. Alpha-synuclein is a presynaptic protein with a proposed role in neurotransmission and dopamine homeostasis. Abnormal accumulation of α-synuclein aggregates in dopaminergic neurons of the substantia nigra is d...

    Authors: Mong-Lin Yang, Linda Hasadsri, Wendy S Woods and Julia M George

    Citation: Molecular Neurodegeneration 2010 5:9

    Content type: Research article

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  37. Mitochondrial dysfunction, oxidative damage and the accumulation of somatic mutations in mitochondrial DNA (mtDNA) have been associated with certain neurodegenerative disorders. Previous studies have also prov...

    Authors: Johanna Krüger, Reetta Hinttala, Kari Majamaa and Anne M Remes

    Citation: Molecular Neurodegeneration 2010 5:8

    Content type: Research article

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  38. Recent evidence suggests that glycogen synthase kinase-3β (GSK3β) is implicated in both sporadic and familial forms of Alzheimer's disease. The transcription factor, p53 also plays a role and has been linked t...

    Authors: Carole J Proctor and Douglas A Gray

    Citation: Molecular Neurodegeneration 2010 5:7

    Content type: Research article

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  39. Prion diseases are disorders of protein conformation in which PrPC, the normal cellular conformer, is converted to an abnormal, protease-resistant conformer rPrPSc. Approximately 80% of rPrPSc accumulates in neur...

    Authors: Stephen J DeArmond and Krystyna Bajsarowicz

    Citation: Molecular Neurodegeneration 2010 5:6

    Content type: Review

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  40. Septal cholinergic neurons account for most of the cholinergic innervations of the hippocampus, playing a key role in the regulation of hippocampal synaptic activity. Disruption of the septo-hippocampal pathwa...

    Authors: Oscar M Lazo, Jocelyn C Mauna, Claudia A Pissani, Nibaldo C Inestrosa and Francisca C Bronfman

    Citation: Molecular Neurodegeneration 2010 5:5

    Content type: Research article

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  41. The presence of amyloid-β (Aβ) deposits in selected brain regions is a hallmark of Alzheimer's disease (AD). The amyloid deposits have "chaperone molecules" which play critical roles in amyloid formation and t...

    Authors: Margarita C Dinamarca, Juan P Sagal, Rodrigo A Quintanilla, Juan A Godoy, Macarena S Arrázola and Nibaldo C Inestrosa

    Citation: Molecular Neurodegeneration 2010 5:4

    Content type: Research article

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  42. Soluble amyloid-β (Aβ;) oligomers have been recognized to be early and key intermediates in Alzheimer's disease (AD)-related synaptic dysfunction. Aβ oligomers block hippocampal long-term potentiation (LTP) an...

    Authors: Waldo Cerpa, Ginny G Farías, Juan A Godoy, Marco Fuenzalida, Christian Bonansco and Nibaldo C Inestrosa

    Citation: Molecular Neurodegeneration 2010 5:3

    Content type: Research article

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  43. Alzheimer's disease (AD) is associated with deposition of amyloid β (Aβ) in the brain, which is reflected by low concentration of the Aβ1-42 peptide in the cerebrospinal fluid (CSF). There are at least 15 addi...

    Authors: Erik Portelius, Ulf Andreasson, John M Ringman, Katharina Buerger, Jonny Daborg, Peder Buchhave, Oskar Hansson, Andreas Harmsen, Mikael K Gustavsson, Eric Hanse, Douglas Galasko, Harald Hampel, Kaj Blennow and Henrik Zetterberg

    Citation: Molecular Neurodegeneration 2010 5:2

    Content type: Research article

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  44. The low-density lipoprotein receptor related protein 1 (LRP1) has been implicated in Alzheimer's disease (AD) but its signalling has not been fully evaluated. There is good evidence that the cytoplasmic domain...

    Authors: Yuji Kajiwara, Sonia Franciosi, Nagahide Takahashi, Lisa Krug, James Schmeidler, Kevin Taddei, Vahram Haroutunian, Ulrik Fried, Michelle Ehrlich, Ralph N Martins, Samuel Gandy and Joseph D Buxbaum

    Citation: Molecular Neurodegeneration 2010 5:1

    Content type: Research article

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