scholarly journals Late phase cell cycle proteins in Alzheimer’s disease: a possible target for therapy?

2016 ◽  
Vol 3 (1) ◽  
Author(s):  
Vladan Bajic ◽  
Vladimir B. Bajic ◽  
Lada Zivkovic ◽  
Thomas Arendt ◽  
George Perry ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Late Phase ◽  
Phase Cell ◽  
Cell Cycle Proteins

P3-319: Elevated expression of cell cycle proteins in very early stages of Alzheimer's disease

2008 ◽  
Vol 4 ◽  
pp. T615-T615
Author(s):  
Juan C. Troncoso ◽  
Miguel A. Riudavets ◽  
Marcelo Schultz ◽  
Gustavo Sevlever ◽  
Gay Rudow ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Cell Cycle Proteins ◽  
Early Stages ◽  
Elevated Expression

scholarly journals Overexpression of Cell Cycle Proteins of Peripheral Lymphocytes in Patients with Alzheimer's Disease

2016 ◽  
Vol 13 (1) ◽  
pp. 127 ◽  
Author(s):  
Hyeran Kim ◽  
Young-Ah Kwon ◽  
Inn Sook Ahn ◽  
Sangha Kim ◽  
Seonwoo Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Cell Cycle Proteins ◽  
Peripheral Lymphocytes

scholarly journals Microglial derived tumor necrosis factor-α drives Alzheimer's disease-related neuronal cell cycle events

2014 ◽  
Vol 62 ◽  
pp. 273-285 ◽  
Author(s):  
Kiran Bhaskar ◽  
Nicole Maphis ◽  
Guixiang Xu ◽  
Nicholas H. Varvel ◽  
Olga N. Kokiko-Cochran ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Neuronal Cell ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Pathogenic tau disrupts the cellular program that maintains neuronal identity

2021 ◽  
Author(s):  
Adrian Beckmann ◽  
Paulino Ramirez ◽  
Maria Gamez ◽  
William J. Ray ◽  
Bess Frost
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Formation ◽  
Therapeutic Approaches ◽  
Nuclear Pleomorphism ◽  
Mesenchymal Transition ◽  
Neuronal Identity ◽  
Cell Cycle Activation

AbstractNeurons in human Alzheimer’s disease acquire phenotypes that are also present in various cancers, including over-stabilization of the cytoskeleton, nuclear pleomorphism, decondensation of constitutive heterochromatin, and aberrant activation of the cell cycle. Unlike in cancer, in which cell cycle activation drives tumor formation, activation of the cell cycle in post-mitotic neurons is sufficient to induce neuronal death. Multiple lines of evidence suggest that abortive cell cycle activation is a consequence of pathogenic forms of tau, a protein that drives neurodegeneration in Alzheimer’s disease and related “tauopathies.” We have combined network analysis of human Alzheimer’s disease and mouse tauopathy with mechanistic studies in Drosophila to discover that pathogenic forms of tau drive abortive cell cycle activation by disrupting the cellular program that maintains neuronal identity. Mechanistically, we identify Moesin, a prognostic biomarker for cancer and mediator of the epithelial-mesenchymal transition (EMT), as a major effector of tau-induced neurotoxicity. We find that aberrant activation of Moesin in neurons acts through the actin cytoskeleton to dysregulate the cellular program that maintains neuronal identity. Our study identifies mechanistic parallels between tauopathy and cancer and sets the stage for novel therapeutic approaches.

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