Finnie, J.W.Jerrett, I.V.Manavis, J.2025-07-162025-07-162022Veterinary Research Communications, 2022; 46(1):289-2930165-73801573-7446https://hdl.handle.net/2440/146046The signature pathological feature of the pseudolaminar cerebrocortical necrosis found in polioencephalomalacia (PEM) of ruminants is the development of red (eosinophilic) neurons. These neurons are generally considered to be irredeemably injured but we have shown, for the first time, in ovine PEM cases, that most strongly express amyloid precursor protein (APP), which has a neuroprotective role in the brain. By contrast, neurons in unaffected cerebral cortices from control sheep were APP immunonegative. This finding suggests that, rather than being inevitably destined to die, some of these APP immunoreactive cortical neurons may survive and regain structural and functional integrity.en© The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.Polioencephalomalacia; Sheep; Red neurons; Amyloid precursor protein immunolabelling; NeuroprotectionAmyloid beta-Protein PrecursorAnimalsEncephalomalaciaNecrosisNeuronsSheepSheep DiseasesRed neurons in ovine polioencephalomalacia (cerebrocortical necrosis) are strongly amyloid precursor protein immunopositiveJournal article10.1007/s11259-022-09888-62024-08-07600159Finnie, J.W. [0000-0003-2277-1693]Manavis, J. [0000-0001-7381-7781] [0000-0003-1268-561X]