Abstract
A number of unexpected pathophysiological connections linking different neurodegenerative diseases have emerged over the past decade. An example is provided by prion and Alzheimer’s diseases. Despite being distinct pathologies, these disorders share several neurotoxic mechanisms, including accumulation of misfolded protein isoforms, stress of the protein synthesis machinery, and activation of a neurotoxic signaling mediated by the cellular prion protein. Here, in addition to reviewing these mechanisms, we will discuss the potential therapeutic interventions for prion and Alzheimer’s diseases that are arising from the comprehension of their common neurodegenerative pathways.
Acknowledgments
This study was supported by a Young Investigator Award from the Italian Ministry of Health, to EB (GR-2010-2312769). SRE was supported by a grant from the E-Rare Joint Transnational Call (E-Rare-2). EB is an Assistant Telethon Scientist at the Dulbecco Telethon Institute (TCP14009, Fondazione Telethon, Italy).
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Artikel in diesem Heft
- Frontmatter
- Reviews
- Dynamic organization of the mitochondrial protein import machinery
- Common therapeutic strategies for prion and Alzheimer’s diseases
- IL-1 family cytokines in cancer immunity – a matter of life and death
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Epigenetic regulation of KLK7 gene expression in pancreatic and cervical cancer cells
- Molecular Medicine
- Regulation of glycosylphosphatidylinositol-anchored proteins and GPI-phospholipase D in a c-Myc transgenic mouse model of hepatocellular carcinoma and human HCC
- Biological characteristics of renal cancer cells after CTP-mediated cancer suppressor gene NPRL2 protein treatment
- Cell Biology and Signaling
- Hepatitis B virus surface protein-induced hPIAS1 transcription requires TAL1, E47, MYOG, NFI, and MAPK signal pathways
- Inhibition of interleukin-3- and interferon- α-induced JAK/STAT signaling by the synthetic α-X-2′,3,4,4′-tetramethoxychalcones α-Br-TMC and α-CF3-TMC
- Vitamin C promotes pluripotency of human induced pluripotent stem cells via the histone demethylase JARID1A
Artikel in diesem Heft
- Frontmatter
- Reviews
- Dynamic organization of the mitochondrial protein import machinery
- Common therapeutic strategies for prion and Alzheimer’s diseases
- IL-1 family cytokines in cancer immunity – a matter of life and death
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Epigenetic regulation of KLK7 gene expression in pancreatic and cervical cancer cells
- Molecular Medicine
- Regulation of glycosylphosphatidylinositol-anchored proteins and GPI-phospholipase D in a c-Myc transgenic mouse model of hepatocellular carcinoma and human HCC
- Biological characteristics of renal cancer cells after CTP-mediated cancer suppressor gene NPRL2 protein treatment
- Cell Biology and Signaling
- Hepatitis B virus surface protein-induced hPIAS1 transcription requires TAL1, E47, MYOG, NFI, and MAPK signal pathways
- Inhibition of interleukin-3- and interferon- α-induced JAK/STAT signaling by the synthetic α-X-2′,3,4,4′-tetramethoxychalcones α-Br-TMC and α-CF3-TMC
- Vitamin C promotes pluripotency of human induced pluripotent stem cells via the histone demethylase JARID1A