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  1. Generation of the amyloid β (Aβ) peptide of Alzheimer's disease (AD) is differentially regulated through the intracellular trafficking of the amyloid β precursor protein (APP) within the secretory and endocyti...

    Authors: Rachel F Lane, Joshua W Gatson, Scott A Small, Michelle E Ehrlich and Sam Gandy
    Citation: Molecular Neurodegeneration 2010 5:62
  2. The voltage-gated sodium channel β2 subunit (Navβ2) is a physiological substrate of BACE1 (β-site APP cleaving enzyme) and γ-secretase, two proteolytic enzymes central to Alzheimer's disease pathogenesis. Prev...

    Authors: Manuel T Gersbacher, Doo Yeon Kim, Raja Bhattacharyya and Dora M Kovacs
    Citation: Molecular Neurodegeneration 2010 5:61
  3. Although the cerebellum is considered to be predominantly involved in fine motor control, emerging evidence documents its participation in language, impulsive behavior and higher cognitive functions. While the...

    Authors: Jianmin Chen, Mark L Cohen, Alan J Lerner, Yan Yang and Karl Herrup
    Citation: Molecular Neurodegeneration 2010 5:60
  4. Our previous work indicated that novel analogs of choline have cytoprotective effects in vitro that might be useful in neurodegenerative conditions such as Alzheimer's disease (AD). Furthermore, two lead compound...

    Authors: Roongpetch Keowkase, Marwa Aboukhatwa, Bao-Ling Adam, J Warren Beach, Alvin V Terry Jr, Jerry J Buccafussco and Yuan Luo
    Citation: Molecular Neurodegeneration 2010 5:59
  5. The mutation in Huntington's disease is a polyglutamine expansion near the N-terminus of huntingtin. Huntingtin expressed in immortalized neurons is cleaved near the N-terminus to form N-terminal polypeptides ...

    Authors: Kimberly B Kegel, Ellen Sapp, Jonathan Alexander, Patrick Reeves, Dorothee Bleckmann, Linsday Sobin, Nicholas Masso, Antonio Valencia, Hyunkyung Jeong, Dimitri Krainc, James Palacino, Daniel Curtis, Rainer Kuhn, Claudia Betschart, Miguel Sena-Esteves, Neil Aronin…
    Citation: Molecular Neurodegeneration 2010 5:58
  6. Age-related neurodegenerative diseases share a number of important pathological features, such as accumulation of misfolded proteins as amyloid oligomers and fibrils. Recent evidence suggests that soluble amyl...

    Authors: Rakez Kayed, Isabel Canto, Leonid Breydo, Suhail Rasool, Tamas Lukacsovich, Jessica Wu, Ricardo Albay III, Anna Pensalfini, Stephen Yeung, Elizabeth Head, J Lawrence Marsh and Charles Glabe
    Citation: Molecular Neurodegeneration 2010 5:57
  7. Accumulation of filamentous α-synuclein as Lewy bodies is a hallmark of Parkinson's disease. To identify the mechanisms involved in α-synuclein assembly and determine whether the assemblies are cytotoxic, we d...

    Authors: Peizhou Jiang, Ming Gan, Abdul Shukkur Ebrahim, Wen-Lang Lin, Heather L Melrose and Shu-Hui C Yen
    Citation: Molecular Neurodegeneration 2010 5:56
  8. The pathogenesis of Parkinson's disease (PD) and dementia with Lewy bodies (DLB) is associated with the accumulation of aggregated forms of the α-synuclein (αSN) protein. An early event in the neuropathology o...

    Authors: Clive Bate, Steve Gentleman and Alun Williams
    Citation: Molecular Neurodegeneration 2010 5:55
  9. Thiamine (vitamin B1) deficiency (TD) causes mild impairment of oxidative metabolism and region-selective neuronal loss in the central nervous system (CNS). TD in animals has been used to model aging-associate...

    Authors: Shuchen Lee, Guang Yang, Yue Yong, Ying Liu, Liyun Zhao, Jing Xu, Xiaomin Zhang, Yanjie Wan, Chun Feng, Zhiqin Fan, Yong Liu, Jia Luo and Zun-Ji Ke
    Citation: Molecular Neurodegeneration 2010 5:54
  10. Age-related functional decline of the nervous system is consistently observed, though cellular and molecular events responsible for this decline remain largely unknown. One of the most prevalent age-related fu...

    Authors: Benjamin Fu, Colleen Le Prell, Dwayne Simmons, Debin Lei, Angela Schrader, Amelia B Chen and Jianxin Bao
    Citation: Molecular Neurodegeneration 2010 5:53
  11. Transactive response DNA-binding protein 43 (TDP-43) is the pathological protein found in frontotemporal lobar degeneration with ubiquitin positive inclusions and in amyotrophic lateral sclerosis. In diseased ...

    Authors: Antonella Caccamo, Andrea Magrí and Salvatore Oddo
    Citation: Molecular Neurodegeneration 2010 5:51
  12. 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
  13. The phosphatase PTEN governs the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway which is arguably the most important pro-survival pathway in neurons. Recently, PTEN has also been implicated in multiple...

    Authors: Young-Don Kwak, Tao Ma, Shiyong Diao, Xue Zhang, Yaomin Chen, Janet Hsu, Stuart A Lipton, Eliezer Masliah, Huaxi Xu and Francesca-Fang Liao
    Citation: Molecular Neurodegeneration 2010 5:49
  14. 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
  15. 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
  16. 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
  17. 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
  18. 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
  19. 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
  20. 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
  21. 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
  22. 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
  23. 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
  24. 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
  25. 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
  26. 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
  27. 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
  28. 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
  29. 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
  30. 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
  31. 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
  32. 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
  33. 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
  34. 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
  35. 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
  36. 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
  37. 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
  38. 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
  39. 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
  40. 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
  41. 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
  42. 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
  43. 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
  44. 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
  45. 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