Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy
Recent years have seen remarkable progress in research into free radicals oxidative stress, particularly in the context of post-ischemic recirculation brain injury. Oxidative stress in post-ischemic tissues violates the integrity of the genome, causing DNA damage, death of neuronal, glial and vascul...
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| Format: | Article |
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MDPI AG
2022-01-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/11/1/146 |
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| author | Ryszard Pluta Jacek Kiś Sławomir Januszewski Mirosław Jabłoński Stanisław J. Czuczwar |
| author_facet | Ryszard Pluta Jacek Kiś Sławomir Januszewski Mirosław Jabłoński Stanisław J. Czuczwar |
| author_sort | Ryszard Pluta |
| collection | DOAJ |
| description | Recent years have seen remarkable progress in research into free radicals oxidative stress, particularly in the context of post-ischemic recirculation brain injury. Oxidative stress in post-ischemic tissues violates the integrity of the genome, causing DNA damage, death of neuronal, glial and vascular cells, and impaired neurological outcome after brain ischemia. Indeed, it is now known that DNA damage and repair play a key role in post-stroke white and gray matter remodeling, and restoring the integrity of the blood-brain barrier. This review will present one of the newly characterized mechanisms that emerged with genomic and proteomic development that led to brain ischemia to a new level of post-ischemic neuropathological mechanisms, such as the presence of amyloid plaques and the development of neurofibrillary tangles, which further exacerbate oxidative stress. Finally, we hypothesize that modified amyloid and the tau protein, along with the oxidative stress generated, are new key elements in the vicious circle important in the development of post-ischemic neurodegeneration in a type of Alzheimer’s disease proteinopathy. |
| first_indexed | 2024-03-10T01:59:50Z |
| format | Article |
| id | doaj.art-7426cbc9ffed41bdbd14be14311d91b4 |
| institution | Directory Open Access Journal |
| issn | 2076-3921 |
| language | English |
| last_indexed | 2024-03-10T01:59:50Z |
| publishDate | 2022-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj.art-7426cbc9ffed41bdbd14be14311d91b42023-11-23T12:48:04ZengMDPI AGAntioxidants2076-39212022-01-0111114610.3390/antiox11010146Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease ProteinopathyRyszard Pluta0Jacek Kiś1Sławomir Januszewski2Mirosław Jabłoński3Stanisław J. Czuczwar4Laboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, Pawińskiego 5 Str., 02-106 Warsaw, PolandDepartment of Urology, 1st Military Clinical Hospital with the Outpatient Clinic, Al. Racławickie 23, 20-049 Lublin, PolandLaboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, Pawińskiego 5 Str., 02-106 Warsaw, PolandDepartment of Rehabilitation and Orthopedics, Medical University of Lublin, Jaczewskiego 8 Str., 20-090 Lublin, PolandDepartment of Pathophysiology, Medical University of Lublin, Jaczewskiego 8b Str., 20-090 Lublin, PolandRecent years have seen remarkable progress in research into free radicals oxidative stress, particularly in the context of post-ischemic recirculation brain injury. Oxidative stress in post-ischemic tissues violates the integrity of the genome, causing DNA damage, death of neuronal, glial and vascular cells, and impaired neurological outcome after brain ischemia. Indeed, it is now known that DNA damage and repair play a key role in post-stroke white and gray matter remodeling, and restoring the integrity of the blood-brain barrier. This review will present one of the newly characterized mechanisms that emerged with genomic and proteomic development that led to brain ischemia to a new level of post-ischemic neuropathological mechanisms, such as the presence of amyloid plaques and the development of neurofibrillary tangles, which further exacerbate oxidative stress. Finally, we hypothesize that modified amyloid and the tau protein, along with the oxidative stress generated, are new key elements in the vicious circle important in the development of post-ischemic neurodegeneration in a type of Alzheimer’s disease proteinopathy.https://www.mdpi.com/2076-3921/11/1/146brain ischemiafree radicaloxidative stressreactive oxygen speciesreactive nitrogen speciesamyloid |
| spellingShingle | Ryszard Pluta Jacek Kiś Sławomir Januszewski Mirosław Jabłoński Stanisław J. Czuczwar Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy Antioxidants brain ischemia free radical oxidative stress reactive oxygen species reactive nitrogen species amyloid |
| title | Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy |
| title_full | Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy |
| title_fullStr | Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy |
| title_full_unstemmed | Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy |
| title_short | Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy |
| title_sort | cross talk between amyloid tau protein and free radicals in post ischemic brain neurodegeneration in the form of alzheimer s disease proteinopathy |
| topic | brain ischemia free radical oxidative stress reactive oxygen species reactive nitrogen species amyloid |
| url | https://www.mdpi.com/2076-3921/11/1/146 |
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