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

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  1. Microglia, the resident immune cells of the brain, play a critical role in numerous diseases, but are a minority cell type and difficult to genetically manipulate in vivo with viral vectors and other approache...

    Authors: Mika P. Cadiz, Tanner D. Jensen, Jonathon P. Sens, Kuixi Zhu, Won-Min Song, Bin Zhang, Mark Ebbert, Rui Chang and John D. Fryer
    Citation: Molecular Neurodegeneration 2022 17:26
  2. Across neurodegenerative diseases, common mechanisms may reveal novel therapeutic targets based on neuronal protection, repair, or regeneration, independent of etiology or site of disease pathology. To address...

    Authors: Lauren K. Wareham, Shane A. Liddelow, Sally Temple, Larry I. Benowitz, Adriana Di Polo, Cheryl Wellington, Jeffrey L. Goldberg, Zhigang He, Xin Duan, Guojun Bu, Albert A. Davis, Karthik Shekhar, Anna La Torre, David C. Chan, M. Valeria Canto-Soler, John G. Flanagan…
    Citation: Molecular Neurodegeneration 2022 17:23
  3. Epidemiological studies suggest a link between the melanoma-related pigmentation gene melanocortin 1 receptor (MC1R) and risk of Parkinson’s disease (PD). We previously showed that MC1R signaling can facilitate n...

    Authors: Waijiao Cai, Pranay Srivastava, Danielle Feng, Yue Lin, Charles R. Vanderburg, Yuehang Xu, Pamela Mclean, Matthew P. Frosch, David E. Fisher, Michael A. Schwarzschild and Xiqun Chen
    Citation: Molecular Neurodegeneration 2022 17:16
  4. Transactive response DNA binding protein of 43 kDa (TDP-43) is an intranuclear protein encoded by the TARDBP gene that is involved in RNA splicing, trafficking, stabilization, and thus, the regulation of gene exp...

    Authors: Axel Meneses, Shunsuke Koga, Justin O’Leary, Dennis W. Dickson, Guojun Bu and Na Zhao
    Citation: Molecular Neurodegeneration 2021 16:84
  5. Synucleinopathies are clinically and pathologically heterogeneous disorders characterized by pathologic aggregates of α-synuclein in neurons and glia, in the form of Lewy bodies, Lewy neurites, neuronal cytopl...

    Authors: Shunsuke Koga, Hiroaki Sekiya, Naveen Kondru, Owen A. Ross and Dennis W. Dickson
    Citation: Molecular Neurodegeneration 2021 16:83
  6. A detailed understanding of the pathological processes involved in genetic frontotemporal dementia is critical in order to provide the patients with an optimal future treatment. Protein levels in CSF have the ...

    Authors: Sofia Bergström, Linn Öijerstedt, Julia Remnestål, Jennie Olofsson, Abbe Ullgren, Harro Seelaar, John C. van Swieten, Matthis Synofzik, Raquel Sanchez-Valle, Fermin Moreno, Elizabeth Finger, Mario Masellis, Carmela Tartaglia, Rik Vandenberghe, Robert Laforce, Daniela Galimberti…
    Citation: Molecular Neurodegeneration 2021 16:79
  7. Parkinson’s disease is a disabling neurodegenerative movement disorder characterized by dopaminergic neuron loss induced by α-synuclein oligomers. There is an urgent need for disease-modifying therapies for Pa...

    Authors: Kevin S. Chen, Krystal Menezes, Jarlath B. Rodgers, Darren M. O’Hara, Nhat Tran, Kazuko Fujisawa, Seiya Ishikura, Shahin Khodaei, Hien Chau, Anna Cranston, Minesh Kapadia, Grishma Pawar, Susan Ping, Aldis Krizus, Alix Lacoste, Scott Spangler…
    Citation: Molecular Neurodegeneration 2021 16:77
  8. Mitochondrial dysfunction is a feature of neurodegenerative diseases, including Alzheimer’s disease (AD). Changes in the mitochondrial DNA copy number (mtDNAcn) and increased mitochondrial DNA mutation burden ...

    Authors: Hans-Ulrich Klein, Caroline Trumpff, Hyun-Sik Yang, Annie J. Lee, Martin Picard, David A. Bennett and Philip L. De Jager
    Citation: Molecular Neurodegeneration 2021 16:75
  9. Microtubule-associated protein tau is abnormally aggregated in neuronal and glial cells in a range of neurodegenerative diseases that are collectively referred to as tauopathies. Multiple studies have suggeste...

    Authors: Dah-eun Chloe Chung, Shanu Roemer, Leonard Petrucelli and Dennis W. Dickson
    Citation: Molecular Neurodegeneration 2021 16:57
  10. Human tauopathies including Alzheimer’s disease (AD) are characterized by alterations in the post-translational modification (PTM) pattern of Tau, which parallel the formation of insoluble Tau aggregates, neur...

    Authors: Maria Bichmann, Nuria Prat Oriol, Ebru Ercan-Herbst, David C. Schöndorf, Borja Gomez Ramos, Vera Schwärzler, Marie Neu, Annabelle Schlüter, Xue Wang, Liang Jin, Chenqi Hu, Yu Tian, Janina S. Ried, Per Haberkant, Laura Gasparini and Dagmar E. Ehrnhoefer
    Citation: Molecular Neurodegeneration 2021 16:46
  11. Passive immunotherapies targeting Aβ continue to be evaluated as Alzheimer’s disease (AD) therapeutics, but there remains debate over the mechanisms by which these immunotherapies work. Besides the amount of p...

    Authors: Yona Levites, Cory Funk, Xue Wang, Paramita Chakrabarty, Karen N. McFarland, Baxter Bramblett, Veronica O’Neal, Xufei Liu, Thomas Ladd, Max Robinson, Mariet Allen, Minerva M. Carrasquillo, Dennis Dickson, Pedro Cruz, Danny Ryu, Hong-Dong Li…
    Citation: Molecular Neurodegeneration 2021 16:32
  12. An amendment to this paper has been published and can be accessed via the original article.

    Authors: Kevin Clayton, Jean Christophe Delpech, Shawn Herron, Naotoshi Iwahara, Maria Ericsson, Takashi Saito, Takaomi C. Saido, Seiko Ikezu and Tsuneya Ikezu
    Citation: Molecular Neurodegeneration 2021 16:24

    The original article was published in Molecular Neurodegeneration 2021 16:18

  13. Recent studies suggest that microglia contribute to tau pathology progression in Alzheimer’s disease. Amyloid plaque accumulation transforms microglia, the primary innate immune cells in the brain, into neurod...

    Authors: Kevin Clayton, Jean Christophe Delpech, Shawn Herron, Naotoshi Iwahara, Maria Ericsson, Takashi Saito, Takaomi C. Saido, Seiko Ikezu and Tsuneya Ikezu
    Citation: Molecular Neurodegeneration 2021 16:18

    The Correction to this article has been published in Molecular Neurodegeneration 2021 16:24

  14. The most common mutation in the Leucine-rich repeat kinase 2 gene (LRRK2), G2019S, causes familial Parkinson’s Disease (PD) and renders the encoded protein kinase hyperactive. While targeting LRRK2 activity is...

    Authors: Jillian H. Kluss, Melissa Conti Mazza, Yan Li, Claudia Manzoni, Patrick A. Lewis, Mark R. Cookson and Adamantios Mamais
    Citation: Molecular Neurodegeneration 2021 16:17
  15. Genome-wide association studies have established clusterin (CLU) as a genetic modifier for late-onset Alzheimer’s disease (AD). Both protective and risk alleles have been identified which may be associated wit...

    Authors: Fading Chen, Dan B. Swartzlander, Anamitra Ghosh, John D. Fryer, Baiping Wang and Hui Zheng
    Citation: Molecular Neurodegeneration 2021 16:5
  16. Accumulation of amyloid-β (Aβ) peptide in the brain is a pathological hallmark of Alzheimer’s disease (AD). The clusterin (CLU) gene confers a risk for AD and CLU is highly upregulated in AD patients, with the co...

    Authors: Aleksandra M. Wojtas, Jonathon P. Sens, Silvia S. Kang, Kelsey E. Baker, Taylor J. Berry, Aishe Kurti, Lillian Daughrity, Karen R. Jansen-West, Dennis W. Dickson, Leonard Petrucelli, Guojun Bu, Chia-Chen Liu and John D. Fryer
    Citation: Molecular Neurodegeneration 2020 15:71
  17. Late-onset Alzheimer’s disease (LOAD) is the most common form of dementia worldwide. To date, animal models of Alzheimer’s have focused on rare familial mutations, due to a lack of frank neuropathology from mo...

    Authors: Christoph Preuss, Ravi Pandey, Erin Piazza, Alexander Fine, Asli Uyar, Thanneer Perumal, Dylan Garceau, Kevin P. Kotredes, Harriet Williams, Lara M. Mangravite, Bruce T. Lamb, Adrian L. Oblak, Gareth R. Howell, Michael Sasner, Benjamin A. Logsdon and Gregory W. Carter
    Citation: Molecular Neurodegeneration 2020 15:67
  18. Investigations of apolipoprotein E (APOE) gene, the major genetic risk modifier for Alzheimer’s disease (AD), have yielded significant insights into the pathogenic mechanism. Among the three common coding variant...

    Authors: Zonghua Li, Francis Shue, Na Zhao, Mitsuru Shinohara and Guojun Bu
    Citation: Molecular Neurodegeneration 2020 15:63
  19. An amendment to this paper has been published and can be accessed via the original article.

    Authors: Xue Wang, Mariet Allen, Shaoyu Li, Zachary S. Quicksall, Tulsi A. Patel, Troy P. Carnwath, Joseph S. Reddy, Minerva M. Carrasquillo, Sarah J. Lincoln, Thuy T. Nguyen, Kimberly G. Malphrus, Dennis W. Dickson, Julia E. Crook, Yan W. Asmann and Nilüfer Ertekin-Taner
    Citation: Molecular Neurodegeneration 2020 15:54

    The original article was published in Molecular Neurodegeneration 2020 15:38

  20. Large-scale brain bulk-RNAseq studies identified molecular pathways implicated in Alzheimer’s disease (AD), however these findings can be confounded by cellular composition changes in bulk-tissue. To identify ...

    Authors: Xue Wang, Mariet Allen, Shaoyu Li, Zachary S. Quicksall, Tulsi A. Patel, Troy P. Carnwath, Joseph S. Reddy, Minerva M. Carrasquillo, Sarah J. Lincoln, Thuy T. Nguyen, Kimberly G. Malphrus, Dennis W. Dickson, Julia E. Crook, Yan W. Asmann and Nilüfer Ertekin-Taner
    Citation: Molecular Neurodegeneration 2020 15:38

    The Correction to this article has been published in Molecular Neurodegeneration 2020 15:54

  21. An amendment to this paper has been published and can be accessed via the original article.

    Authors: Xiaoqiang Tang, Arturo Toro, T. G. Sahana, Junli Gao, Jessica Chalk, Björn Oskarsson and Ke Zhang
    Citation: Molecular Neurodegeneration 2020 15:37

    The original article was published in Molecular Neurodegeneration 2020 15:34

  22. Ever since a GGGGCC hexanucleotide repeat expansion mutation in C9ORF72 was identified as the most common cause of familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), three competing b...

    Authors: Xiaoqiang Tang, Arturo Toro, Sahana T.G., Junli Gao, Jessica Chalk, Björn E. Oskarsson and Ke Zhang
    Citation: Molecular Neurodegeneration 2020 15:34

    The Correction to this article has been published in Molecular Neurodegeneration 2020 15:37

  23. Frontotemporal lobar degeneration (FTLD) is a devastating and progressive disorder, and a common cause of early onset dementia. Progranulin (PGRN) haploinsufficiency due to autosomal dominant mutations in the ...

    Authors: Jonathan Frew, Alireza Baradaran-Heravi, Aruna D. Balgi, Xiujuan Wu, Tyler D. Yan, Steve Arns, Fahimeh S. Shidmoossavee, Jason Tan, James B. Jaquith, Karen R. Jansen-West, Francis C. Lynn, Fen-Biao Gao, Leonard Petrucelli, Howard H. Feldman, Ian R. Mackenzie, Michel Roberge…
    Citation: Molecular Neurodegeneration 2020 15:21
  24. The C9ORF72 hexanucleotide repeat expansion is the most common known genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two fatal age-related neurodegenerative diseases. Th...

    Authors: Nadja S. Andrade, Melina Ramic, Rustam Esanov, Wenjun Liu, Mathew J. Rybin, Gabriel Gaidosh, Abbas Abdallah, Samuel Del’Olio, Tyler C. Huff, Nancy T. Chee, Sadhana Anatha, Tania F. Gendron, Claes Wahlestedt, Yanbin Zhang, Michael Benatar, Christian Mueller…
    Citation: Molecular Neurodegeneration 2020 15:13
  25. All samples were obtained through the ALS Center at Mayo Clinic Florida. Our primary cohort included 75 unrelated...C9orf72 repeat, 33 patients who did not possess this expansion, and 20 control subjects without ...

    Authors: Jazmyne L. Jackson, NiCole A. Finch, Matthew C. Baker, Jennifer M. Kachergus, Mariely DeJesus-Hernandez, Kimberly Pereira, Elizabeth Christopher, Mercedes Prudencio, Michael G. Heckman, E. Aubrey Thompson, Dennis W. Dickson, Jaimin Shah, Björn Oskarsson, Leonard Petrucelli, Rosa Rademakers and Marka van Blitterswijk
    Citation: Molecular Neurodegeneration 2020 15:7
  26. Misfolding and aggregation of the presynaptic protein alpha-synuclein (αsyn) is a hallmark of Parkinson’s disease (PD) and related synucleinopathies. Although predominantly localized in the cytosol, a body of ...

    Authors: Jae-Hyeon Park, Jeremy D. Burgess, Ayman H. Faroqi, Natasha N. DeMeo, Fabienne C. Fiesel, Wolfdieter Springer, Marion Delenclos and Pamela J. McLean
    Citation: Molecular Neurodegeneration 2020 15:5
  27. New genetic and genomic resources have identified multiple genetic risk factors for late-onset Alzheimer’s disease (LOAD) and characterized this common dementia at the molecular level. Experimental studies in ...

    Authors: Ravi S. Pandey, Leah Graham, Asli Uyar, Christoph Preuss, Gareth R. Howell and Gregory W. Carter
    Citation: Molecular Neurodegeneration 2019 14:50
  28. Alzheimer’s disease is a progressive neurodegenerative disease most often associated with memory deficits and cognitive decline, although less common clinical presentations are increasingly recognized. The car...

    Authors: Michael A. DeTure and Dennis W. Dickson
    Citation: Molecular Neurodegeneration 2019 14:32
  29. Low frequency coding variants in TREM2 are associated with Alzheimer disease (AD) risk and cerebrospinal fluid (CSF) TREM2 protein levels are different between AD cases and controls. Similarly, TREM2 risk variant...

    Authors: Jorge L. Del-Aguila, Bruno A. Benitez, Zeran Li, Umber Dube, Kathie A. Mihindukulasuriya, John P. Budde, Fabiana H. G. Farias, Maria Victoria Fernández, Laura Ibanez, Shan Jiang, Richard J. Perrin, Nigel J. Cairns, John C. Morris, Oscar Harari and Carlos Cruchaga
    Citation: Molecular Neurodegeneration 2019 14:18
  30. A G4C2 hexanucleotide repeat expansion in the noncoding region of C9orf72 is the major genetic cause of frontotemporal dementia and amyotrophic lateral sclerosis (c9FTD/ALS). Putative disease mechanisms underlyin...

    Authors: Jeannie Chew, Casey Cook, Tania F. Gendron, Karen Jansen-West, Giulia del Rosso, Lillian M. Daughrity, Monica Castanedes-Casey, Aishe Kurti, Jeannette N. Stankowski, Matthew D. Disney, Jeffrey D. Rothstein, Dennis W. Dickson, John D. Fryer, Yong-Jie Zhang and Leonard Petrucelli
    Citation: Molecular Neurodegeneration 2019 14:9
  31. Activation of microglia, the resident immune cells of the central nervous system, is a prominent pathological hallmark of Alzheimer’s disease (AD). However, the gene expression changes underlying microglia act...

    Authors: Hong Wang, Yupeng Li, John W. Ryder, Justin T. Hole, Philip J. Ebert, David C. Airey, Hui-Rong Qian, Benjamin Logsdon, Alice Fisher, Zeshan Ahmed, Tracey K. Murray, Annalisa Cavallini, Suchira Bose, Brian J. Eastwood, David A. Collier, Jeffrey L. Dage…
    Citation: Molecular Neurodegeneration 2018 13:65
  32. Rare coding variants ABI3_rs616338-T and PLCG2_rs72824905-G were identified as risk or protective factors, respectively, for Alzheimer’s disease (AD).

    Authors: Olivia J Conway, Minerva M Carrasquillo, Xue Wang, Jenny M Bredenberg, Joseph S Reddy, Samantha L Strickland, Curtis S Younkin, Jeremy D Burgess, Mariet Allen, Sarah J Lincoln, Thuy Nguyen, Kimberly G Malphrus, Alexandra I Soto, Ronald L Walton, Bradley F Boeve, Ronald C Petersen…
    Citation: Molecular Neurodegeneration 2018 13:53
  33. Many neurodegenerative diseases are caused by nucleotide repeat expansions, but most expansions, like the C9orf72 ‘GGGGCC’ (G4C2) repeat that causes approximately 5–7% of all amyotrophic lateral sclerosis (ALS) a...

    Authors: Mark T. W. Ebbert, Stefan L. Farrugia, Jonathon P. Sens, Karen Jansen-West, Tania F. Gendron, Mercedes Prudencio, Ian J. McLaughlin, Brett Bowman, Matthew Seetin, Mariely DeJesus-Hernandez, Jazmyne Jackson, Patricia H. Brown, Dennis W. Dickson, Marka van Blitterswijk, Rosa Rademakers, Leonard Petrucelli…
    Citation: Molecular Neurodegeneration 2018 13:46
  34. Progressive supranuclear palsy (PSP) is a parkinsonian neurodegenerative tauopathy affecting brain regions involved in motor function, including the basal ganglia, diencephalon and brainstem. While PSP is larg...

    Authors: Monica Y. Sanchez-Contreras, Naomi Kouri, Casey N. Cook, Daniel J. Serie, Michael G. Heckman, NiCole A. Finch, Richard J. Caselli, Ryan J. Uitti, Zbigniew K. Wszolek, Neill Graff-Radford, Leonard Petrucelli, Li-San Wang, Gerard D. Schellenberg, Dennis W. Dickson, Rosa Rademakers and Owen A. Ross
    Citation: Molecular Neurodegeneration 2018 13:37
  35. Single nucleotide polymorphisms (SNPs) inherited as one of two common haplotypes at the transmembrane protein 106B (TMEM106B) locus are associated with the risk of multiple neurodegenerative diseases, including f...

    Authors: Yingxue Ren, Marka van Blitterswijk, Mariet Allen, Minerva M. Carrasquillo, Joseph S. Reddy, Xue Wang, Thomas G. Beach, Dennis W. Dickson, Nilüfer Ertekin-Taner, Yan W. Asmann and Rosa Rademakers
    Citation: Molecular Neurodegeneration 2018 13:35
  36. Loss of function mutations in progranulin (GRN) are a major cause of frontotemporal dementia (FTD). Progranulin is a secreted glycoprotein that localizes to lysosomes and is critical for proper lysosomal function...

    Authors: Andrew E. Arrant, Alexandra M. Nicholson, Xiaolai Zhou, Rosa Rademakers and Erik D. Roberson
    Citation: Molecular Neurodegeneration 2018 13:32
  37. Extracellular aggregation of the amyloid-β (Aβ) peptide into toxic multimers is a key event in Alzheimer’s disease (AD) pathogenesis. Aβ aggregation is concentration-dependent, with higher concentrations of Aβ...

    Authors: Jane C. Hettinger, Hyo Lee, Guojun Bu, David M. Holtzman and John R. Cirrito
    Citation: Molecular Neurodegeneration 2018 13:22
  38. TREM2 is an innate immune receptor specifically expressed in microglia. Coding variations in TREM2 have been reported to increase the risk for Alzheimer’s disease (AD) and other neurodegenerative diseases. Whi...

    Authors: Li Zhong, Zongqi Wang, Daxin Wang, Zhe Wang, Yuka A. Martens, Linbei Wu, Ying Xu, Kai Wang, Jianguo Li, Ruizhi Huang, Dan Can, Huaxi Xu, Guojun Bu and Xiao-Fen Chen
    Citation: Molecular Neurodegeneration 2018 13:15
  39. Early onset Parkinson’s disease is caused by variants in PINK1, parkin, and DJ-1. PINK1 and parkin operate in pathways that preserve mitochondrial integrity, but the function of DJ-1 and how it relates to PINK1 a...

    Authors: David N. Hauser, Adamantios Mamais, Melissa M. Conti, Christopher T. Primiani, Ravindran Kumaran, Allissa A. Dillman, Rebekah G. Langston, Alexandra Beilina, Joseph H. Garcia, Alberto Diaz-Ruiz, Michel Bernier, Fabienne C. Fiesel, Xu Hou, Wolfdieter Springer, Yan Li, Rafael de Cabo…
    Citation: Molecular Neurodegeneration 2017 12:70
  40. Haploinsufficiency of GRN, the gene encoding progranulin (PGRN), causes frontotemporal lobar degeneration (FTLD), the second most common cause of early-onset dementia. Receptor-mediated lysosomal targeting has...

    Authors: Chris W. Lee, Jeannette N. Stankowski, Jeannie Chew, Casey N. Cook, Ying-Wai Lam, Sandra Almeida, Yari Carlomagno, Kwok-Fai Lau, Mercedes Prudencio, Fen-Biao Gao, Matthew Bogyo, Dennis W. Dickson and Leonard Petrucelli
    Citation: Molecular Neurodegeneration 2017 12:55
  41. Amyotrophic Lateral Sclerosis (ALS) is a fatal and progressive neurodegenerative disorder with identified genetic causes representing a significant minority of all cases. A GGGGCC hexanucleotide repeat expansi...

    Authors: Rustam Esanov, Gabriela Toro Cabrera, Nadja S. Andrade, Tania F. Gendron, Robert H. Brown Jr., Michael Benatar, Claes Wahlestedt, Christian Mueller and Zane Zeier
    Citation: Molecular Neurodegeneration 2017 12:46
  42. Prionoid transmission of α-synuclein (αSyn) aggregates along neuroanatomically connected projections is posited to underlie disease progression in α-synucleinopathies. Here, we specifically wanted to study whe...

    Authors: Zachary A. Sorrentino, Mieu M.T. Brooks, Vincent Hudson III, Nicola J. Rutherford, Todd E. Golde, Benoit I. Giasson and Paramita Chakrabarty
    Citation: Molecular Neurodegeneration 2017 12:40
  43. Mitochondrial dysfunction has been linked to the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Functional studies of mitochondrial bioenergetics have focused...

    Authors: Hibiki Kawamata, Pablo Peixoto, Csaba Konrad, Gloria Palomo, Kirsten Bredvik, Meri Gerges, Federica Valsecchi, Leonard Petrucelli, John M. Ravits, Anatoly Starkov and Giovanni Manfredi
    Citation: Molecular Neurodegeneration 2017 12:37
  44. Mutations in PINK1 and PARKIN are the most common causes of recessive early-onset Parkinson’s disease (EOPD). Together, the mitochondrial ubiquitin (Ub) kinase PINK1 and the cytosolic E3 Ub ligase PARKIN direct a...

    Authors: Maya Ando, Fabienne C. Fiesel, Roman Hudec, Thomas R. Caulfield, Kotaro Ogaki, Paulina Górka-Skoczylas, Dariusz Koziorowski, Andrzej Friedman, Li Chen, Valina L. Dawson, Ted M. Dawson, Guojun Bu, Owen A. Ross, Zbigniew K. Wszolek and Wolfdieter Springer
    Citation: Molecular Neurodegeneration 2017 12:32
  45. Alzheimer’s disease (AD)-linked protein, presenilin 1 (PS1), is present at the synapse, and the knock-out of presenilin in mice leads to synaptic dysfunction. On the other hand, synaptic activity was shown to ...

    Authors: Katarzyna Marta Zoltowska, Masato Maesako, Iryna Lushnikova, Shuko Takeda, Laura J. Keller, Galina Skibo, Bradley T. Hyman and Oksana Berezovska
    Citation: Molecular Neurodegeneration 2017 12:15
  46. APOE genotype is the foremost genetic factor modulating β-amyloid (Aβ) deposition and risk of sporadic Alzheimer’s disease (AD). Here we investigated how APOE genotype influences respo...

    Authors: Joanna E Pankiewicz, Jairo Baquero-Buitrago, Sandrine Sanchez, Jennifer Lopez-Contreras, Jungsu Kim, Patrick M. Sullivan, David M. Holtzman and Martin J. Sadowski
    Citation: Molecular Neurodegeneration 2017 12:12