Discrepancy in Expression of β-Secretase and Amyloid-β Protein Precursor in Alzheimer-Related Genes in the Rat Medial Temporal Lobe Cortex Following Transient Global Brain Ischemia

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.

doi:10.3233/jad-151102

Cited by 46 publications

(62 citation statements)

References 58 publications

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“…There is convincing evidence that hypoxic insults increase the expression and activity level of BACE1 not only in cultured neuronal cells but also in the affected brain regions (Sun et al 2006;Zhang et al 2007;Guglielmotto et al 2009;Li et al 2009). Global ischemia and stroke also augmented the expression of BACE1 (Zhiyou et al 2009;Pluta et al 2013aPluta et al , 2016bKocki et al 2015). In addition, hypoxia enhanced the expression of BACE1 in brain capillary endothelial cells (Bulbarelli et al 2012).…”

Section: Hypoxia Induces Expression Of B-secretasementioning

confidence: 94%

Hypoxia/ischemia activate processing of Amyloid Precursor Protein: impact of vascular dysfunction in the pathogenesis of Alzheimer's disease

Salminen

Kauppinen

Kaarniranta

2017

Journal of Neurochemistry

153

124

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Alzheimer's disease (AD) is associated with deficiencies in cerebrovascular functions, e.g. reduced cerebral blood flow and capillary amyloid angiopathy, both of which are evident during the early phase of AD, thus local hypoxia/ischemia could augment the pathogenesis of AD. There is abundant literature revealing that exposures to hypoxia/ischemia increase the amyloidogenic processing of amyloid-b precursor protein (APP) leading to the accumulation of amyloid-b peptides in brain. This hypoxia-induced response has been attributed to a significant increase in the activities of b-and csecretases, whereas a-secretase activity decreases in hypoxia. Recent studies have indicated that hypoxia-inducible factor-1a (HIF-1a) stimulates the transcription of the bsecretase 1 (BACE1) gene through the hypoxia-response element in the BACE1 promoter. Moreover, HIF-1a protein can directly interact with the c-secretase complex and increase its activity in a non-transcriptional manner. Hypoxia/ischemia also trigger endoplasmic reticulum stress and impair autophagy in brain, which consequently can stimulate the expression of presenilin 1 (PS1) and activate c-secretase. Subsequently, PS1 protein can stabilize HIF-1a protein and in addition, APP intracellular domain peptide is able to induce the expression of HIF-1a. The activation of b-and c-secretases is an evolutionarily conserved hypoxia response, e.g. it is also present in zebrafish. Given that b-and c-secretases have many substrates in addition to APP, one could postulate that AD pathology is a byproduct of the rescue process mediated by these two aspartyl proteinases under hypoxic/ischemic conditions. We will review the recent evidence indicating that vascular dysfunctions can provoke AD pathology by activating b-and c-secretases.

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Section: Hypoxia Induces Expression Of B-secretasementioning

confidence: 94%

Hypoxia/ischemia activate processing of Amyloid Precursor Protein: impact of vascular dysfunction in the pathogenesis of Alzheimer's disease

Salminen

Kauppinen

Kaarniranta

2017

Journal of Neurochemistry

153

124

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“…Because the accumulation of amyloid and tau protein is not the cause of Alzheimer's disease pathogenesis, as found in the NIA-AA Research Framework: towards the biological definition of Alzheimer's disease [114], it is understandable that advanced study is necessary in this area. Ultimately, the experimental models of ischemia-reperfusion brain damage used in the study of Alzheimer's disease seem to be a useful new approach to clarifying the role of folding proteins and their genes in neurodegenerative diseases such as cerebral ischemia and sporadic Alzheimer's disease [15,16,[27][28][29][30]34,35,[115][116][117][118][119].…”

Section: Discussionmentioning

confidence: 99%

“…The dangerous and regular damage of the brain after ischemia-reperfusion is the progressive and delayed dementia of the Alzheimer's disease type [2,4,6,[17][18][19][20][21][22][23][24][25]. Previous brain damage associated with ischemia and reperfusion may further increase the likelihood of developing dementia associated with Alzheimer's disease, increasing the extent of post-ischemic changes, through the proteomic and genomic cascade associated with Alzheimer's disease [26][27][28][29][30][31][32][33][34][35][36][37]. Based on the above observations, it has been suggested that the history of cerebral ischemia in humans and animals is associated with the subsequent development of sporadic Alzheimer's disease [1,7,12,[15][16][17][26][27][28][29][30][31][32][33][34][35][36][38][39][40][41]…”

Section: Introductionmentioning

confidence: 99%

“…Previous brain damage associated with ischemia and reperfusion may further increase the likelihood of developing dementia associated with Alzheimer's disease, increasing the extent of post-ischemic changes, through the proteomic and genomic cascade associated with Alzheimer's disease [26][27][28][29][30][31][32][33][34][35][36][37]. Based on the above observations, it has been suggested that the history of cerebral ischemia in humans and animals is associated with the subsequent development of sporadic Alzheimer's disease [1,7,12,[15][16][17][26][27][28][29][30][31][32][33][34][35][36][38][39][40][41][42][43][44][45][46]. In this review, we focus first on identifying the response of the tau protein gene and its product to ischemia-reperfusion brain damage.…”

Section: Introductionmentioning

confidence: 99%

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Proteomic and Genomic Changes in Tau Protein, Which Are Associated with Alzheimer’s Disease after Ischemia-Reperfusion Brain Injury

Ułamek-Kozioł

Czuczwar

Januszewski

et al. 2020

IJMS

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Recent evidence suggests that transient ischemia of the brain with reperfusion in humans and animals is associated with the neuronal accumulation of neurotoxic molecules associated with Alzheimer’s disease, such as all parts of the amyloid protein precursor and modified tau protein. Pathological changes in the amyloid protein precursor and tau protein at the protein and gene level due to ischemia may lead to dementia of the Alzheimer’s disease type after ischemic brain injury. Some studies have demonstrated increased tau protein immunoreactivity in neuronal cells after brain ischemia-reperfusion injury. Recent research has presented many new tau protein functions, such as neural activity control, iron export, protection of genomic DNA integrity, neurogenesis and long-term depression. This review discusses the potential mechanisms of tau protein in the brain after ischemia, including oxidative stress, apoptosis, autophagy, excitotoxicity, neurological inflammation, endothelium, angiogenesis and mitochondrial dysfunction. In addition, attention was paid to the role of tau protein in damage to the neurovascular unit. Tau protein may be at the intersection of many regulatory mechanisms in the event of major neuropathological changes in ischemic stroke. Data show that brain ischemia activates neuronal changes and death in the hippocampus in a manner dependent on tau protein, thus determining a new and important way to regulate the survival and/or death of post-ischemic neurons. Meanwhile, the association between tau protein and ischemic stroke has not been well discussed. In this review, we aim to update the knowledge about the proteomic and genomic changes in tau protein following ischemia-reperfusion injury and the connection between dysfunctional tau protein and ischemic stroke pathology. Finally we present the positive correlation between tau protein dysfunction and the development of sporadic Alzheimer’s disease type of neurodegeneration.

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“…In the CA1 region of the hippocampus and temporal cortex, the expression of the amyloid protein precursor gene was below the control value within 2 days after ischemia (79,80). In the above areas, 7 and 30 days after cerebral ischemia-reperfusion, the expression of the amyloid protein precursor gene was above the control value (79,80). The expression of the β-secretase gene increased above the control value following brain ischemia injury in the CA1 area of the hippocampus 2 to 7 days after recirculation (79).…”

Section: Ca1 Area Of the Hippocampus And Medial Temporal Cortexmentioning

confidence: 99%

Common Proteomic and Genomic Contribution to Ischemic Brain Damage and Alzheimer’s Disease

Pluta

Ułamek-Kozioł

Januszewski

et al. 2019

Alzheimer’s Disease

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Ischemic brain damage is associated with the deposition of folding proteins, such as all fragments of the amyloid protein precursor and tau protein, in the intra-and extracellular spaces of neurons. In this chapter, we summarize the protein changes associated with Alzheimer' s disease and their gene expression (amyloid protein precursor and tau protein) after cerebral ischemia and their role in the ischemic etiology of Alzheimer' s disease. Recent advances in understanding the ischemic etiology of Alzheimer' s disease have revealed dysregulation of amyloid protein precursors, β-secretase, presenilin 1 and 2, autophagy, mitophagy, apoptosis, and tau protein genes after ischemic brain injury. However, reduced expression of mRNA of the α-secretase in cerebral ischemia causes neurons to be less resistant to injury. In this chapter, we present the latest evidence that Alzheimer' s diseaserelated proteins and their genes play a key role in brain damage with ischemiareperfusion and that ischemic episode is an essential and leading provider of Alzheimer' s disease development. Understanding the underlying processes of linking Alzheimer' s disease-related proteins and their genes in brain ischemia

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Discrepancy in Expression of β-Secretase and Amyloid-β Protein Precursor in Alzheimer-Related Genes in the Rat Medial Temporal Lobe Cortex Following Transient Global Brain Ischemia

Cited by 46 publications

References 58 publications

Hypoxia/ischemia activate processing of Amyloid Precursor Protein: impact of vascular dysfunction in the pathogenesis of Alzheimer's disease

Hypoxia/ischemia activate processing of Amyloid Precursor Protein: impact of vascular dysfunction in the pathogenesis of Alzheimer's disease

Proteomic and Genomic Changes in Tau Protein, Which Are Associated with Alzheimer’s Disease after Ischemia-Reperfusion Brain Injury

Common Proteomic and Genomic Contribution to Ischemic Brain Damage and Alzheimer’s Disease

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