Total<i>Tau</i>Protein as Investigated by Cerebral Microdialysis Increases in Hypothermic Cardiac Arrest: A Pig Study

Schiefecker, Alois Josef; Putzer, Gabriel; Braun, Patrick; Martini, Judith; Strapazzon, Giacomo; Antunes, Ana; Mulino, Miriam; Pinggera, Daniel; Glodny, Bernhard; Brugger, Hermann; Paal, Peter; Mair, Peter; Pfausler, Bettina; Beer, Ronny; Humpel, Christian; Helbok, Raimund

doi:10.1089/ther.2020.0016

Cited by 18 publications

(20 citation statements)

References 32 publications

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“…To the best of our knowledge, one study has assessed that blood tau protein levels can be used as a predictor of the neurological prognosis of human neonatal asphyxia [22]. These data suggest that the hallmarks of Alzheimer's disease may begin during pre-or perinatal asphyxia and progress to full-blown disease later in life, so these conditions may contribute to the development of Alzheimer's disease, supporting the notion that environmental factors may cause or worsen symptoms of Alzheimer's disease [20,21,23]. It has been suggested that cerebral ischemia and neonatal hypoxia-ischemia may be causally related to Alzheimer's disease [24][25][26][27][28][29].…”

Section: Introductionmentioning

confidence: 82%

“…Perinatal asphyxia in mice causes delayed damage to the hippocampus and a significant deficit in spatial learning and memory [ 19 ]. Significantly higher levels of amyloid protein precursor, increased total tau protein and tau protein phosphorylation, decreased hypoxia-inducible factor, lower levels of amyloid-degrading neprilysin, increased amyloid deposition with activation of astrocytes and microglia in the brain have also been documented [ 20 , 21 ]. To the best of our knowledge, one study has assessed that blood tau protein levels can be used as a predictor of the neurological prognosis of human neonatal asphyxia [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

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Alzheimer’s Disease Associated Presenilin 1 and 2 Genes Dysregulation in Neonatal Lymphocytes Following Perinatal Asphyxia

Tarkowska

Furmaga-Jabłońska

Bogucki

et al. 2021

IJMS

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Perinatal asphyxia is mainly a brain disease leading to the development of neurodegeneration, in which a number of peripheral lesions have been identified; however, little is known about the expression of key genes involved in amyloid production by peripheral cells, such as lymphocytes, during the development of hypoxic-ischemic encephalopathy. We analyzed the gene expression of the amyloid protein precursor, β-secretase, presenilin 1 and 2 and hypoxia-inducible factor 1-α by RT-PCR in the lymphocytes of post-asphyxia and control neonates. In all examined periods after asphyxia, decreased expression of the genes of the amyloid protein precursor, β-secretase and hypoxia-inducible factor 1-α was noted in lymphocytes. Conversely, expression of presenilin 1 and 2 genes decreased on days 1–7 and 8–14 but increased after survival for more than 15 days. We believe that the expression of presenilin genes in lymphocytes could be a potential biomarker to determine the severity of the post-asphyxia neurodegeneration or to identify the underlying factors for brain neurodegeneration and get information about the time they occurred. This appears to be the first worldwide data on the role of the presenilin 1 and 2 genes associated with Alzheimer’s disease in the dysregulation of neonatal lymphocytes after perinatal asphyxia.

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Section: Introductionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Alzheimer’s Disease Associated Presenilin 1 and 2 Genes Dysregulation in Neonatal Lymphocytes Following Perinatal Asphyxia

Tarkowska

Furmaga-Jabłońska

Bogucki

et al. 2021

IJMS

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“…Another study showed that the altered tau protein blocks the movement of organelles, neurofilaments, amyloid protein precursor vesicles, and increases oxidative stress in the neuronal body, axons, and dendrites, leading to the accumulation of the amyloid protein precursor in neuronal cells [ 50 ]. In addition, the levels of total tau protein, which were tested using brain microdialysis, increased in the brain following ischemia induced by cardiac arrest [ 51 ].…”

Section: Post-ischemic Tau Protein Accumulation In the Brainmentioning

confidence: 99%

The Many Faces of Post-Ischemic Tau Protein in Brain Neurodegeneration of the Alzheimer’s Disease Type

Pluta

Czuczwar

Januszewski

et al. 2021

Cells

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Recent data suggest that post-ischemic brain neurodegeneration in humans and animals is associated with the modified tau protein in a manner typical of Alzheimer’s disease neuropathology. Pathological changes in the tau protein, at the gene and protein level due to cerebral ischemia, can lead to the development of Alzheimer’s disease-type neuropathology and dementia. Some studies have shown increased tau protein staining and gene expression in neurons following ischemia-reperfusion brain injury. Recent studies have found the tau protein to be associated with oxidative stress, apoptosis, autophagy, excitotoxicity, neuroinflammation, blood-brain barrier permeability, mitochondrial dysfunction, and impaired neuronal function. In this review, we discuss the interrelationship of these phenomena with post-ischemic changes in the tau protein in the brain. The tau protein may be at the intersection of many pathological mechanisms due to severe neuropathological changes in the brain following ischemia. The data indicate that an episode of cerebral ischemia activates the damage and death of neurons in the hippocampus in a tau protein-dependent manner, thus determining a novel and important mechanism for the survival and/or death of neuronal cells following ischemia. In this review, we update our understanding of proteomic and genomic changes in the tau protein in post-ischemic brain injury and present the relationship between the modified tau protein and post-ischemic neuropathology and present a positive correlation between the modified tau protein and a post-ischemic neuropathology that has characteristics of Alzheimer’s disease-type neurodegeneration.

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“…Data suggest that the hallmarks of AD may also occur during PA, leading to the development of full-blown AD later in life. Thus, PA may contribute to the development of AD, supporting the thesis that environmental factors influence the development of neurodegenerative diseases (61,98,99). Whether this constitutes the etiological basis of neurodegenerative disorders, such as AD in adulthood, still needs to be verified by conducting additional experiments as well as clinical and epidemiological observations (18).…”

Section: Discussionmentioning

confidence: 87%

Hypoxic-Ischemic Brain Injury after Perinatal Asphyxia as a Possible Factor in the Pathology of Alzheimer’s Disease

Tarkowska

2021

Cerebral Ischemia

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Perinatal asphyxia is a common pathological condition occurring worldwide in approximately 4 million newborns annually. The result of this phenomenon is multi-organ damage and the development of chronic hypoxic encephalopathy. It is currently believed that an episode of cerebral hypoxia/ischemia may be one of the major factors responsible for the development of Alzheimer's disease-type dementia and/or Alzheimer's disease. It cannot be ruled out that hypoxia in the perinatal period may be a trigger factor for the development of Alzheimer's disease in adulthood. The data from scientific research indicate a possible relationship between hypoxia in the earliest stages of life and the occurrence of long-lasting genetic and biochemical changes leading to the development of neurodegeneration in Alzheimer's disease-type.

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TotalTauProtein as Investigated by Cerebral Microdialysis Increases in Hypothermic Cardiac Arrest: A Pig Study

Cited by 18 publications

References 32 publications

Alzheimer’s Disease Associated Presenilin 1 and 2 Genes Dysregulation in Neonatal Lymphocytes Following Perinatal Asphyxia

Alzheimer’s Disease Associated Presenilin 1 and 2 Genes Dysregulation in Neonatal Lymphocytes Following Perinatal Asphyxia

The Many Faces of Post-Ischemic Tau Protein in Brain Neurodegeneration of the Alzheimer’s Disease Type

Hypoxic-Ischemic Brain Injury after Perinatal Asphyxia as a Possible Factor in the Pathology of Alzheimer’s Disease

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