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Authors: Pluta, Ryszard | Ułamek-Kozioł, Marzena | Januszewski, Sławomir | Czuczwar, Stanisław J.

Article Type: Review Article

Abstract: Brain ischemia comprises blood-brain barrier, glial, and neuronal cells. The blood–brain barrier controls permeability of different substances and the composition of the neuronal cells ‘milieu’, which is required for their physiological functioning. Recent evidence indicates that brain ischemia itself and ischemic blood-brain barrier dysfunction is associated with the accumulation of neurotoxic molecules within brain tissue, e.g., different parts of amyloid-β protein precursor and changed pathologically tau protein. All these changes due to ischemia can initiate and progress neurodegeneration of the Alzheimer’s disease-type. This review presents brain ischemia and ischemic blood-brain barrier as a trigger for tau protein alterations. Thus, we …hypothesize that the changes in pattern of phosphorylation of tau protein are critical to microtubule function especially in neurons, and contribute to the neurodegeneration following brain ischemia-reperfusion episodes with Alzheimer’s disease phenotype. Show more

Keywords: Blood-brain barrier, brain ischemia, dementia, experimental, gene expression, human, neurodegeneration, neuronal death, stroke, tau protein

DOI: 10.3233/JAD-180772

Citation: Journal of Alzheimer's Disease, vol. 66, no. 2, pp. 429-437, 2018

Authors: Ułamek-Kozioł, Marzena | Czuczwar, Stanisław J. | Kocki, Janusz | Januszewski, Sławomir | Bogucki, Jacek | Bogucka-Kocka, Anna | Pluta, Ryszard

Article Type: Research Article

Abstract:  There is currently no knowledge about the expression profile of the autophagy (BECN1 ), mitophagy (BNIP3 ), and apoptosis (CASP3 ) genes in the CA3 region of the hippocampus after cerebral ischemia. In addition, it is unknown whether genes for BECN1 , BNIP3 , and CASP3 have any effect on the neuronal death in the CA3 area of the hippocampus due to ischemia. In this study, for the first time, we present, by means of a quantitative PCR protocol with reverse transcriptase, the expression of BECN1 and CASP3 genes in the neuronal CA3 region of the hippocampus with the co-expression …of the mitochondrial BNIP3 gene, which genes are associated with Alzheimer’s disease, in the ischemic model of Alzheimer’s disease in the rat. The present study showed that after ischemia, the CASP3 gene was significantly expressed within 7–30 days, the BECN1 gene was significantly overexpressed on the thirtieth day, and the BINP3 gene was lowered below control values during post-ischemic follow-up period. The caspase-dependent neuronal death in the CA3 region of the hippocampus after ischemia is not accompanied by overexpression of the BNIP3 gene. Our data may therefore suggest a new insight into the BNIP3 gene in the regulation of neuronal mitophagy in neurodegeneration in the CA3 region of the hippocampus after ischemia. This indicates no involvement of the BNIP3 gene along with the CASP3 gene in the CA3 region of the hippocampus in delayed neuronal death after brain ischemia. Show more

Keywords: Alzheimer’s disease, apoptosis, autophagy, brain ischemia, cardiac arrest, genes, mitophagy

DOI: 10.3233/JAD-190966

Citation: Journal of Alzheimer's Disease, vol. 72, no. 4, pp. 1279-1286, 2019

Authors: Ułamek-Kozioł, Marzena | Kocki, Janusz | Bogucka-Kocka, Anna | Petniak, Alicja | Gil-Kulik, Paulina | Januszewski, Sławomir | Bogucki, Jacek | Jabłoński, Mirosław | Furmaga-Jabłońska, Wanda | Brzozowska, Judyta | Czuczwar, Stanisław J. | Pluta, Ryszard

Article Type: Research Article

Abstract: Ischemic brain damage is a pathological incident that is often linked with medial temporal lobe cortex injury and finally its atrophy. Post-ischemic brain injury associates with poor prognosis since neurons of selectively vulnerable ischemic brain areas are disappearing by apoptotic program of neuronal death. Autophagy has been considered, after brain ischemia, as a guardian against neurodegeneration. Consequently, we have examined changes in autophagy (BECN 1), mitophagy (BNIP 3), and apoptotic (caspase 3) genes in the medial temporal lobe cortex with the use of quantitative reverse-transcriptase PCR following transient 10-min global brain ischemia in rats with survival 2, 7, and 30 …days. The intense significant overexpression of BECN 1 gene was noted on the 2nd day, while on days 7–30 the expression of this gene was still upregulated. BNIP 3 gene was downregulated on the 2nd day, but on days 7–30 post-ischemia, there was a significant reverse tendency. Caspase 3 gene, associated with apoptotic neuronal death, was induced in the same way as BNIP 3 gene after brain ischemia. Thus, the demonstrated changes indicate that the considerable dysregulation of expression of BECN 1, BNIP 3, and caspase 3 genes may be connected with a response of neuronal cells in medial temporal lobe cortex to transient complete brain ischemia. Show more

Keywords: Alzheimer’s disease, BECN 1, BNIP 3, brain ischemia, caspase 3, genes, rat, selective vulnerability, temporal cortex

DOI: 10.3233/JAD-160387

Citation: Journal of Alzheimer's Disease, vol. 54, no. 1, pp. 113-121, 2016

Authors: Kocki, Janusz | Ułamek-Kozioł, Marzena | Bogucka-Kocka, Anna | Januszewski, Sławomir | Jabłoński, Mirosław | Gil-Kulik, Paulina | Brzozowska, Judyta | Petniak, Alicja | Furmaga-Jabłońska, Wanda | Bogucki, Jacek | Czuczwar, Stanisław J. | Pluta, Ryszard

Article Type: Research Article

Abstract: The interaction between brain ischemia and Alzheimer’s disease (AD) has been intensively investigated recently. Nevertheless, we have not yet understood the nature and mechanisms of the ischemic episodes triggering the onset of AD and how they influence its slow progression. The assumed connection between brain ischemia and the accumulation of amyloid-β (Aβ) peptide awaits to be clearly explained. In our research, we employed a rat cardiac arrest model to study the changes in gene expression of amyloid-β protein precursor (AβPP) and its cleaving enzymes, β- and γ -secretases (including presenilins) in hippocampal CA1 sector, following transient 10-min global brain ischemia. …The quantitative reverse-transcriptase PCR assay demonstrated that the expression of all above genes that contribute to Aβ peptide generation was dysregulated during 30 days in postischemic hippocampal CA1 area. It suggests that studied Aβ peptide generation-related genes can be involved in AβPP metabolism, following global brain ischemia and will be useful to identify the molecular mechanisms underpinning that cerebral ischemia might be an etiological cause of AD via dysregulation of AβPP and its cleaving enzymes, β- and γ -secretases genes, and subsequently, it may increase Aβ peptide production and promote the gradual and slow development of AD neuropathology. Our data demonstrate that brain ischemia activates delayed neuronal death in hippocampus in an AβPP-dependent manner, thus defining a new and important mode of ischemic cell death. Show more

Keywords: Alzheimer’s disease, amyloid-β protein precursor, β-secretase, brain ischemia, CA1 area, dementia, γ-secretase, genes, hippocampus, presenilin 1 and 2

DOI: 10.3233/JAD-150299

Citation: Journal of Alzheimer's Disease, vol. 47, no. 4, pp. 1047-1056, 2015

Authors: Pluta, Ryszard | Kocki, Janusz | Ułamek-Kozioł, Marzena | Petniak, Alicja | Gil-Kulik, Paulina | Januszewski, Sławomir | Bogucki, Jacek | Jabłoński, Mirosław | Brzozowska, Judyta | Furmaga-Jabłońska, Wanda | Bogucka-Kocka, Anna | Czuczwar, Stanisław J.

Article Type: Research Article

Abstract: Brain ischemia may be causally related with Alzheimer’s disease. Presumably, β-secretase and amyloid-β protein precursor gene expression changes may be associated with Alzheimer’s disease neuropathology. Consequently, we have examined quantitative changes in both β-secretase and amyloid-β protein precursor genes in the medial temporal lobe cortex with the use of quantitative rtPCR analysis following 10-min global brain ischemia in rats with survival of 2, 7, and 30 days. The greatest significant overexpression of β-secretase gene was noted on the 2nd day, while on days 7–30 the expression of this gene was only modestly downregulated. Amyloid-β protein precursor gene was downregulated on …the 2nd day, but on days 7–30 postischemia, there was a significant reverse tendency. Thus, the demonstrated alterations indicate that the considerable changes of expression of β-secretase and amyloid-β protein precursor genes may be connected with a response of neurons in medial temporal lobe cortex to transient global brain ischemia. Finally, the ischemia-induced gene changes may play a key role in a late and slow onset of Alzheimer-type pathology. Show more

Keywords: Alzheimer’s disease, amyloid-β protein precursor, β-secretase, brain ischemia, dementia, temporal cortex

DOI: 10.3233/JAD-151102

Citation: Journal of Alzheimer's Disease, vol. 51, no. 4, pp. 1023-1031, 2016