<i>Trans</i>- and <i>Cis</i>-Phosphorylated Tau Protein: New Pieces of the Puzzle in the Development of Neurofibrillary Tangles in Post-Ischemic Brain Neurodegeneration of the Alzheimer’s Disease-like Type
Recent evidence indicates that experimental brain ischemia leads to dementia with an Alzheimer’s disease-like type phenotype and genotype. Based on the above evidence, it was hypothesized that brain ischemia may contribute to the development of Alzheimer’s disease. Brain ischemia and Alzheimer’s dis...
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MDPI AG
2024-03-01
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author | Ryszard Pluta Stanisław J. Czuczwar |
author_facet | Ryszard Pluta Stanisław J. Czuczwar |
author_sort | Ryszard Pluta |
collection | DOAJ |
description | Recent evidence indicates that experimental brain ischemia leads to dementia with an Alzheimer’s disease-like type phenotype and genotype. Based on the above evidence, it was hypothesized that brain ischemia may contribute to the development of Alzheimer’s disease. Brain ischemia and Alzheimer’s disease are two diseases characterized by similar changes in the hippocampus that are closely related to memory impairment. Following brain ischemia in animals and humans, the presence of amyloid plaques in the extracellular space and intracellular neurofibrillary tangles was revealed. The phenomenon of tau protein hyperphosphorylation is a similar pathological feature of both post-ischemic brain injury and Alzheimer’s disease. In Alzheimer’s disease, the phosphorylated Thr231 motif in tau protein has two distinct <i>trans</i> and <i>cis</i> conformations and is the primary site of tau protein phosphorylation in the pre-entanglement cascade and acts as an early precursor of tau protein neuropathology in the form of neurofibrillary tangles. Based on the latest publication, we present a similar mechanism of the formation of neurofibrillary tangles after brain ischemia as in Alzheimer’s disease, established on <i>trans</i>- and <i>cis</i>-phosphorylation of tau protein, which ultimately influences the development of tauopathy. |
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language | English |
last_indexed | 2024-04-24T18:12:59Z |
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publisher | MDPI AG |
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series | International Journal of Molecular Sciences |
spelling | doaj.art-eedadab19e174d48bd754277f6903abf2024-03-27T13:44:59ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672024-03-01256309110.3390/ijms25063091<i>Trans</i>- and <i>Cis</i>-Phosphorylated Tau Protein: New Pieces of the Puzzle in the Development of Neurofibrillary Tangles in Post-Ischemic Brain Neurodegeneration of the Alzheimer’s Disease-like TypeRyszard Pluta0Stanisław J. Czuczwar1Department of Pathophysiology, Medical University of Lublin, 20-090 Lublin, PolandDepartment of Pathophysiology, Medical University of Lublin, 20-090 Lublin, PolandRecent evidence indicates that experimental brain ischemia leads to dementia with an Alzheimer’s disease-like type phenotype and genotype. Based on the above evidence, it was hypothesized that brain ischemia may contribute to the development of Alzheimer’s disease. Brain ischemia and Alzheimer’s disease are two diseases characterized by similar changes in the hippocampus that are closely related to memory impairment. Following brain ischemia in animals and humans, the presence of amyloid plaques in the extracellular space and intracellular neurofibrillary tangles was revealed. The phenomenon of tau protein hyperphosphorylation is a similar pathological feature of both post-ischemic brain injury and Alzheimer’s disease. In Alzheimer’s disease, the phosphorylated Thr231 motif in tau protein has two distinct <i>trans</i> and <i>cis</i> conformations and is the primary site of tau protein phosphorylation in the pre-entanglement cascade and acts as an early precursor of tau protein neuropathology in the form of neurofibrillary tangles. Based on the latest publication, we present a similar mechanism of the formation of neurofibrillary tangles after brain ischemia as in Alzheimer’s disease, established on <i>trans</i>- and <i>cis</i>-phosphorylation of tau protein, which ultimately influences the development of tauopathy.https://www.mdpi.com/1422-0067/25/6/3091brain ischemiaAlzheimer’s diseasecardiac arresttau proteinhyperphosphorylation<i>cis</i>-phosphorylated tau protein |
spellingShingle | Ryszard Pluta Stanisław J. Czuczwar <i>Trans</i>- and <i>Cis</i>-Phosphorylated Tau Protein: New Pieces of the Puzzle in the Development of Neurofibrillary Tangles in Post-Ischemic Brain Neurodegeneration of the Alzheimer’s Disease-like Type International Journal of Molecular Sciences brain ischemia Alzheimer’s disease cardiac arrest tau protein hyperphosphorylation <i>cis</i>-phosphorylated tau protein |
title | <i>Trans</i>- and <i>Cis</i>-Phosphorylated Tau Protein: New Pieces of the Puzzle in the Development of Neurofibrillary Tangles in Post-Ischemic Brain Neurodegeneration of the Alzheimer’s Disease-like Type |
title_full | <i>Trans</i>- and <i>Cis</i>-Phosphorylated Tau Protein: New Pieces of the Puzzle in the Development of Neurofibrillary Tangles in Post-Ischemic Brain Neurodegeneration of the Alzheimer’s Disease-like Type |
title_fullStr | <i>Trans</i>- and <i>Cis</i>-Phosphorylated Tau Protein: New Pieces of the Puzzle in the Development of Neurofibrillary Tangles in Post-Ischemic Brain Neurodegeneration of the Alzheimer’s Disease-like Type |
title_full_unstemmed | <i>Trans</i>- and <i>Cis</i>-Phosphorylated Tau Protein: New Pieces of the Puzzle in the Development of Neurofibrillary Tangles in Post-Ischemic Brain Neurodegeneration of the Alzheimer’s Disease-like Type |
title_short | <i>Trans</i>- and <i>Cis</i>-Phosphorylated Tau Protein: New Pieces of the Puzzle in the Development of Neurofibrillary Tangles in Post-Ischemic Brain Neurodegeneration of the Alzheimer’s Disease-like Type |
title_sort | i trans i and i cis i phosphorylated tau protein new pieces of the puzzle in the development of neurofibrillary tangles in post ischemic brain neurodegeneration of the alzheimer s disease like type |
topic | brain ischemia Alzheimer’s disease cardiac arrest tau protein hyperphosphorylation <i>cis</i>-phosphorylated tau protein |
url | https://www.mdpi.com/1422-0067/25/6/3091 |
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