Antibody-mediated neuronal apoptosis: therapeutic implications for prion diseases

Immunology Letters
Mourad Tayebi, Simon Hawke

Abstract

Neuronal cell death is considered to be a hallmark in prion diseases. These disorders are believed to result from the post-translational conversion of a normal cell membrane sialoglycoprotein PrPC, composed primarily of alpha-helical structure, into a disease specific isoform, PrPSc that is rich in beta-sheet and partially proteinase-resistant. Recent in vivo studies indicate that prion replication can be inhibited by anti-PrP monoclonal antibodies that led to the indefinite delay in the development of prion disease. The recent report by Solforosi and colleagues has increased the need to understand pathway(s) leading to prion-associated apoptosis and neuronal death thought to be the cause of death in transmissible spongiform encephalopathy (TSE) individuals. Furthermore, these reports increased momentum about the use of antibody-based therapy in prion diseases, although great caution should be exerted when using anti-prion antibodies directly into the central nervous system (CNS) with special emphasis on refined strategies such as specific targeting of regions of the prion protein thought not to be involved in signalling pathways.

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Citations

May 9, 2007·Medical Microbiology and Immunology·Yin-Xia HuangXiao-Ping Dong
Feb 17, 2009·The Journal of General Virology·Mourad TayebiSimon Hawke
Mar 16, 2021·Frontiers in Aging Neuroscience·Allal BoutajangoutThomas Wisniewski

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis