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159 result(s) for 'mayo clinic' within Molecular Neurodegeneration

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  1. Human apolipoprotein E (apoE) exists in three major isoforms: apoE2, apoE3 and apoE4. In the brain, apoE is produced mostly by astrocytes and transports cholesterol to neurons via apoE receptors. Among the gen...

    Authors: Jin Hu, Chia-Chen Liu, Xiao-Fen Chen, Yun-wu Zhang, Huaxi Xu and Guojun Bu
    Citation: Molecular Neurodegeneration 2015 10:6
  2. Loss of function COQ2 mutations results in primary CoQ10 deficiency. Recently, recessive mutations of the COQ2 gene have been identified in two unrelated Japanese families with multiple system atrophy (MSA). It h...

    Authors: Kotaro Ogaki, Shinsuke Fujioka, Michael G Heckman, Sruti Rayaprolu, Alexandra I Soto-Ortolaza, Catherine Labbé, Ronald L Walton, Oswaldo Lorenzo-Betancor, Xue Wang, Yan Asmann, Rosa Rademakers, Neill Graff-Radford, Ryan Uitti, William P Cheshire, Zbigniew K Wszolek, Dennis W Dickson…
    Citation: Molecular Neurodegeneration 2014 9:44
  3. The accumulation of α-synuclein aggregates is the hallmark of Parkinson’s disease, and more generally of synucleinopathies. The accumulation of tau aggregates however is classically found in the brains of pati...

    Authors: Simon Moussaud, Daryl R Jones, Elisabeth L Moussaud-Lamodière, Marion Delenclos, Owen A Ross and Pamela J McLean
    Citation: Molecular Neurodegeneration 2014 9:43
  4. Hexanucleotide repeat expansions in chromosome 9 open reading frame 72 (C9ORF72) are causative for frontotemporal dementia (FTD) and motor neuron disease (MND). Substantial phenotypic heterogeneity has been descr...

    Authors: Marka van Blitterswijk, Bianca Mullen, Aleksandra Wojtas, Michael G Heckman, Nancy N Diehl, Matthew C Baker, Mariely DeJesus-Hernandez, Patricia H Brown, Melissa E Murray, Ging-Yuek R Hsiung, Heather Stewart, Anna M Karydas, Elizabeth Finger, Andrew Kertesz, Eileen H Bigio, Sandra Weintraub…
    Citation: Molecular Neurodegeneration 2014 9:38
  5. The ingestion of a high-fat diet (HFD) and the resulting obese state can exert a multitude of stressors on the individual including anxiety and cognitive dysfunction. Though many studies have shown that exerci...

    Authors: Silvia S Kang, Patricio R Jeraldo, Aishe Kurti, Margret E Berg Miller, Marc D Cook, Keith Whitlock, Nigel Goldenfeld, Jeffrey A Woods, Bryan A White, Nicholas Chia and John D Fryer
    Citation: Molecular Neurodegeneration 2014 9:36
  6. Although genome wide studies have associated single nucleotide polymorphisms (SNP)s near PICALM with Alzheimer’s disease (AD), the mechanism underlying this association is unclear. PICALM is involved in clathrin-...

    Authors: Ishita Parikh, Christopher Medway, Steven Younkin, David W Fardo and Steven Estus
    Citation: Molecular Neurodegeneration 2014 9:32
  7. The editors of Molecular Neurodegeneration would like to thank all the reviewers who have contributed to the journal in Volume 8 (2013).

    Authors: Guojun Bu and Huaxi Xu
    Citation: Molecular Neurodegeneration 2014 9:9
  8. Recent genome-wide association studies (GWAS) of late-onset Alzheimer’s disease (LOAD) have identified single nucleotide polymorphisms (SNPs) which show significant association at the well-known APOE locus and at...

    Authors: Christopher W Medway, Samer Abdul-Hay, Tynickwa Mims, Li Ma, Gina Bisceglio, Fanggeng Zou, Shane Pankratz, Sigrid B Sando, Jan O Aasly, Maria Barcikowska, Joanna Siuda, Zbigniew K Wszolek, Owen A Ross, Minerva Carrasquillo, Dennis W Dickson, Neill Graff-Radford…
    Citation: Molecular Neurodegeneration 2014 9:11
  9. Cross-breeding of transgenic mice is commonly used to assess gene-gene interactions, particularly in the context of disease. Strain background changes can influence the phenotype of mouse models and can confou...

    Authors: Rachel M Bailey, John Howard, Joshua Knight, Naruhiko Sahara, Dennis W Dickson and Jada Lewis
    Citation: Molecular Neurodegeneration 2014 9:8
  10. The β-amyloid (Aβ) peptide has been postulated to be a key determinant in the pathogenesis of Alzheimer’s disease (AD). Aβ is produced through sequential cleavage of the β-amyloid precursor protein (APP) by β-...

    Authors: Shangtong Jiang, Yanfang Li, Xian Zhang, Guojun Bu, Huaxi Xu and Yun-wu Zhang
    Citation: Molecular Neurodegeneration 2014 9:6
  11. The APOE4 allele of apolipoprotein E (apoE) is the greatest genetic risk factor for Alzheimer’s disease (AD) compared to APOE2 and APOE3. Amyloid-β (Aβ), particularly in a soluble oligomeric form (oAβ), is consid...

    Authors: Leon M Tai, Shipra Mehra, Varsha Shete, Steve Estus, G William Rebeck, Guojun Bu and Mary Jo LaDu
    Citation: Molecular Neurodegeneration 2014 9:2
  12. Mutations in the gene encoding superoxide dismutase 1 (SOD1) account for about 20% of the cases of familial amyotrophic lateral sclerosis (fALS). It is well established that mutations in SOD1, associated with ...

    Authors: David A Qualls, Mercedes Prudencio, Brittany LT Roberts, Keith Crosby, Hilda Brown and David R Borchelt
    Citation: Molecular Neurodegeneration 2013 8:46
  13. A rare variant in the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) gene has been reported to be a genetic risk factor for Alzheimer’s disease by two independent groups (Odds ratio between 2.9-4.5). Gi...

    Authors: Sruti Rayaprolu, Bianca Mullen, Matt Baker, Timothy Lynch, Elizabeth Finger, William W Seeley, Kimmo J Hatanpaa, Catherine Lomen-Hoerth, Andrew Kertesz, Eileen H Bigio, Carol Lippa, Keith A Josephs, David S Knopman, Charles L White III, Richard Caselli, Ian R Mackenzie…
    Citation: Molecular Neurodegeneration 2013 8:19
  14. 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
  15. 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
  16. 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
  17. 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
  18. 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
  19. 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
  20. 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
  21. 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
  22. 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
  23. Transgenic mice expressing disease-associated proteins have become standard tools for studying human neurological disorders. Transgenes are often expressed using promoters chosen to drive continuous high-level...

    Authors: Shaefali P Rodgers, Heather A Born, Pritam Das and Joanna L Jankowsky
    Citation: Molecular Neurodegeneration 2012 7:28
  24. Mutations in the LRRK2 gene are the most common cause of genetic Parkinson’s disease. Although the mechanisms behind the pathogenic effects of LRRK2 mutations are still not clear, data emerging from in vitro and

    Authors: Kelly M Hinkle, Mei Yue, Bahareh Behrouz, Justus C Dächsel, Sarah J Lincoln, Erin E Bowles, Joel E Beevers, Brittany Dugger, Beate Winner, Iryna Prots, Caroline B Kent, Kenya Nishioka, Wen-Lang Lin, Dennis W Dickson, Christopher J Janus, Matthew J Farrer…
    Citation: Molecular Neurodegeneration 2012 7:25
  25. Glutathione S-transferase omega-1 and 2 genes (GSTO1, GSTO2), residing within an Alzheimer and Parkinson disease (AD and PD) linkage region, have diverse functions including mitigation of oxidative stress and may...

    Authors: Mariet Allen, Fanggeng Zou, High Seng Chai, Curtis S Younkin, Richard Miles, Asha A Nair, Julia E Crook, V Shane Pankratz, Minerva M Carrasquillo, Christopher N Rowley, Thuy Nguyen, Li Ma, Kimberly G Malphrus, Gina Bisceglio, Alexandra I Ortolaza, Ryan Palusak…
    Citation: Molecular Neurodegeneration 2012 7:13
  26. The form(s) of amyloid-β peptide (Aβ) associated with the pathology characteristic of Alzheimer's disease (AD) remains unclear. In particular, the neurotoxicity of intraneuronal Aβ accumulation is an issue of ...

    Authors: Katherine L Youmans, Leon M Tai, Takahisa Kanekiyo, W Blaine Stine Jr, Sara-Claude Michon, Evelyn Nwabuisi-Heath, Arlene M Manelli, Yifan Fu, Sean Riordan, William A Eimer, Lester Binder, Guojun Bu, Chunjiang Yu, Dean M Hartley and Mary Jo LaDu
    Citation: Molecular Neurodegeneration 2012 7:8
  27. Atypical expression of cell cycle regulatory proteins has been implicated in Alzheimer's disease (AD), but the molecular mechanisms by which they induce neurodegeneration are not well understood. We examined t...

    Authors: Monique Judge, Lisa Hornbeck, Huntington Potter and Jaya Padmanabhan
    Citation: Molecular Neurodegeneration 2011 6:80
  28. Abnormal distribution, modification and aggregation of transactivation response DNA-binding protein 43 (TDP-43) are the hallmarks of multiple neurodegenerative diseases, especially frontotemporal lobar degener...

    Authors: Ya-Fei Xu, Yong-Jie Zhang, Wen-Lang Lin, Xiangkun Cao, Caroline Stetler, Dennis W Dickson, Jada Lewis and Leonard Petrucelli
    Citation: Molecular Neurodegeneration 2011 6:73
  29. Recent genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNP)s that are essentially unequivocally associated with peripheral cholesterol. Since the alleles of the APOE gene, ...

    Authors: Christopher R Simmons, Fanggeng Zou, Steven G Younkin and Steven Estus
    Citation: Molecular Neurodegeneration 2011 6:62
  30. A recently published genome-wide association study (GWAS) of late-onset Alzheimer's disease (LOAD) revealed genome-wide significant association of variants in or near MS4A4A, CD2AP, EPHA1 and CD33. Meta-analyses ...

    Authors: Minerva M Carrasquillo, Olivia Belbin, Talisha A Hunter, Li Ma, Gina D Bisceglio, Fanggeng Zou, Julia E Crook, V Shane Pankratz, Sigrid B Sando, Jan O Aasly, Maria Barcikowska, Zbigniew K Wszolek, Dennis W Dickson, Neill R Graff-Radford, Ronald C Petersen, Peter Passmore…
    Citation: Molecular Neurodegeneration 2011 6:54
  31. Rheumatoid arthritis (RA) and Alzheimer's disease (AD) are inversely associated. To test the hypothesis that genetic elements associated with increased RA risk are associated with decreased AD risk, we evaluat...

    Authors: Christopher R Simmons, Fanggeng Zou, Steven G Younkin and Steven Estus
    Citation: Molecular Neurodegeneration 2011 6:33
  32. Fibrillar amyloid β (fAβ) peptide is the major component of Aβ plaques in the brains of Alzheimer's disease (AD) patients. Inflammatory mediators have previously been proposed to be drivers of Aβ pathology in ...

    Authors: Paramita Chakrabarty, Amanda Herring, Carolina Ceballos-Diaz, Pritam Das and Todd E Golde
    Citation: Molecular Neurodegeneration 2011 6:16
  33. 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
  34. 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
  35. 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
  36. 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
  37. Variations in sortilin-related receptor (SORL1) expression and function have been implicated in Alzheimers Disease (AD). Here, to gain insights into SORL1, we evaluated SORL1 expression and splicing as a funct...

    Authors: Karrie E Grear, I-Fang Ling, James F Simpson, Jennifer L Furman, Christopher R Simmons, Shawn L Peterson, Frederick A Schmitt, William R Markesbery, Qiang Liu, Julia E Crook, Steven G Younkin, Guojun Bu and Steven Estus
    Citation: Molecular Neurodegeneration 2009 4:46
  38. Insulin-degrading enzyme (IDE) is a widely studied zinc-metalloprotease implicated in the pathogenesis of type 2 diabetes mellitus, Alzheimer disease (AD) and varicella zoster virus infection. Despite more tha...

    Authors: Anthony DelleDonne, Naomi Kouri, Lael Reinstatler, Tomoko Sahara, Lilin Li, Ji Zhao, Dennis W Dickson, Nilufer Ertekin-Taner and Malcolm A Leissring
    Citation: Molecular Neurodegeneration 2009 4:39
  39. Correction to Nural H, He P, Beach T, Sue L, Xia W, Shen Y. Disassembled DJ-1 high molecular weight complex in cortex mitochondria from Parkinson's disease patients Molecular Neurodegeneration 2009, 4:23.

    Authors: Zhenyu Zhong, Hikmet Nural, Ping He, Gina Civarella, Thomas Beach, Lucia Sue, Charles Adler, Holly Shill, John Caviness, Weiming Xia and Yong Shen
    Citation: Molecular Neurodegeneration 2009 4:30

    The original article was published in Molecular Neurodegeneration 2009 4:23

  40. The γ-secretase complex is a major therapeutic target for the prevention and treatment of Alzheimer's disease. Previous studies have shown that treatment of young APP mice with specific inhibitors of γ-secreta...

    Authors: Monica Garcia-Alloza, Meenakshi Subramanian, Diana Thyssen, Laura A Borrelli, Abdul Fauq, Pritam Das, Todd E Golde, Bradley T Hyman and Brian J Bacskai
    Citation: Molecular Neurodegeneration 2009 4:19
  41. Since the identification of tau as the main component of neurofibrillary tangles in Alzheimer's disease and related tauopathies, and the discovery that mutations in the tau gene cause frontotemporal dementia, ...

    Authors: Tania F Gendron and Leonard Petrucelli
    Citation: Molecular Neurodegeneration 2009 4:13