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Journal articles on the topic 'Alpha-secretases'

Author: Grafiati

Published: 25 May 2024

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1

Nunan, Janelle, and David H. Small. "Proteolytic processing of the amyloid-beta protein precursor of Alzheimer's disease." Essays in Biochemistry 38 (October 1, 2002): 37–49. http://dx.doi.org/10.1042/bse0380037.

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The proteolytic processing of the amyloid-beta protein precursor plays a key role in the development of Alzheimer's disease. Cleavage of the amyloid-beta protein precursor may occur via two pathways, both of which involve the action of proteases called secretases. One pathway, involving beta- and gamma-secretase, liberates amyloid-beta protein, a protein associated with the neurodegeneration seen in Alzheimer's disease. The alternative pathway, involving alpha-secretase, precludes amyloid-beta protein formation. In this review, we describe the progress that has been made in identifying the secretases and their potential as therapeutic targets in the treatment or prevention of Alzheimer's disease.

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2

Luca, Monica Di. "Alpha beta-and gamma-secretases in alzheimer s disease." Frontiers in Bioscience S4, no. 3 (2012): 1126–50. http://dx.doi.org/10.2741/s322.

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3

Mezyk, Renata, Monika Bzowska, and Joanna Bereta. "Structure and functions of tumor necrosis factor-alpha converting enzyme." Acta Biochimica Polonica 50, no. 3 (September 30, 2003): 625–45. http://dx.doi.org/10.18388/abp.2003_3656.

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Tumor necrosis factor-alpha converting enzyme (TACE) is the first described and best characterized secretase. In this review the structure and the possible roles for TACE are summarized. The substrate specificity and the regulation of TACE activity as well as redundancy and possible cooperations of distinct secretases are also discussed.

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4

Kiesel, Violet A., and Silvia D. Stan. "Diallyl trisulfide, a chemopreventive agent from Allium vegetables, inhibits alpha-secretases in breast cancer cells." Biochemical and Biophysical Research Communications 484, no. 4 (March 2017): 833–38. http://dx.doi.org/10.1016/j.bbrc.2017.01.184.

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5

Singh, Som, Felix Yang, Andy Sivils, Victoria Cegielski, and Xiang-Ping Chu. "Amylin and Secretases in the Pathology and Treatment of Alzheimer’s Disease." Biomolecules 12, no. 7 (July 17, 2022): 996. http://dx.doi.org/10.3390/biom12070996.

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Alzheimer’s disease remains a prevailing neurodegenerative condition which has an array physical, emotional, and financial consequences to patients and society. In the past decade, there has been a greater degree of investigation on therapeutic small peptides. This group of biomolecules have a profile of fundamentally sound characteristics which make them an intriguing area for drug development. Among these biomolecules, there are four modulatory mechanisms of interest in this review: alpha-, beta-, gamma-secretases, and amylin. These protease-based biomolecules all have a contributory role in the amyloid cascade hypothesis. Moreover, the involvement of various biochemical pathways intertwines these peptides to have shared regulators (i.e., retinoids). Further clinical and translational investigation must occur to gain a greater understanding of its potential application in patient care. The aim of this narrative review is to evaluate the contemporary literature on these protease biomolecule modulators and determine its utility in the treatment of Alzheimer’s disease.

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6

Assaf, Naglaa, Marwa E. El-Shamarka, Neveen A. Salem, Yasser A. Khadrawy, and Nesrine S. El Sayed. "Neuroprotective effect of PPAR alpha and gamma agonists in a mouse model of amyloidogenesis through modulation of the Wnt/beta catenin pathway via targeting alpha- and beta-secretases." Progress in Neuro-Psychopharmacology and Biological Psychiatry 97 (March 2020): 109793. http://dx.doi.org/10.1016/j.pnpbp.2019.109793.

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7

Kim, Doo Yeon, Laura A. MacKenzie Ingano, Bryce W. Carey, Warren Pettingell, and Dora M. Kovacs. "P4-290 Voltage-gated sodium channel beta2 subunit is processed by alpha-, beta- and gamma-secretases, generating fragments elevated in AD brains." Neurobiology of Aging 25 (July 2004): S557—S558. http://dx.doi.org/10.1016/s0197-4580(04)81848-7.

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8

Kron, Nicholas S., and Lynne A. Fieber. "Aplysia Neurons as a Model of Alzheimer’s Disease: Shared Genes and Differential Expression." Journal of Molecular Neuroscience 72, no. 2 (October 18, 2021): 287–302. http://dx.doi.org/10.1007/s12031-021-01918-3.

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AbstractAlthough Alzheimer’s disease (AD) is the most common form of dementia in the United States, development of therapeutics has proven difficult. Invertebrate alternatives to current mammalian AD models have been successfully employed to study the etiology of the molecular hallmarks of AD. The marine snail Aplysia californica offers a unique and underutilized system in which to study the physiological, behavioral, and molecular impacts of AD. Mapping of the Aplysia proteome to humans and cross-referencing with two databases of genes of interest in AD research identified 898 potential orthologs of interest in Aplysia. Included among these orthologs were alpha, beta and gamma secretases, amyloid-beta, and tau. Comparison of age-associated differential expression in Aplysia sensory neurons with that of late-onset AD in the frontal lobe identified 59 ortholog with concordant differential expression across data sets. The 21 concordantly upregulated genes suggested increased cellular stress and protein dyshomeostasis. The 47 concordantly downregulated genes included important components of diverse neuronal processes, including energy metabolism, mitochondrial homeostasis, synaptic signaling, Ca++ regulation, and cellular cargo transport. Compromised functions in these processes are known hallmarks of both human aging and AD, the ramifications of which are suggested to underpin cognitive declines in aging and neurodegenerative disease.

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9

Lopez Lloreda, Claudia, Sarah Chowdhury, Shivesh Ghura, Elena Alvarez-Periel, and Kelly Jordan-Sciutto. "HIV-Associated Insults Modulate ADAM10 and Its Regulator Sirtuin1 in an NMDA Receptor-Dependent Manner." Cells 11, no. 19 (September 22, 2022): 2962. http://dx.doi.org/10.3390/cells11192962.

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Neurologic deficits associated with human immunodeficiency virus (HIV) infection impact about 50% of persons with HIV (PWH). These disorders, termed HIV-associated neurocognitive disorders (HAND), possess neuropathologic similarities to Alzheimer’s disease (AD), including intra- and extracellular amyloid-beta (Aβ) peptide aggregates. Aβ peptide is produced through cleavage of the amyloid precursor protein (APP) by the beta secretase BACE1. However, this is precluded by cleavage of APP by the non-amyloidogenic alpha secretase, ADAM10. Previous studies have found that BACE1 expression was increased in the CNS of PWH with HAND as well as animal models of HAND. Further, BACE1 contributed to neurotoxicity. Yet in in vitro models, the role of ADAM10 and its potential regulatory mechanisms had not been examined. To address this, primary rat cortical neurons were treated with supernatants from HIV-infected human macrophages (HIV/MDMs). We found that HIV/MDMs decreased levels of both ADAM10 and Sirtuin1 (SIRT1), a regulator of ADAM10 that is implicated in aging and in AD. Both decreases were blocked with NMDA receptor antagonists, and treatment with NMDA was sufficient to induce reduction in ADAM10 and SIRT1 protein levels. Furthermore, decreases in SIRT1 protein levels were observed at an earlier time point than the decreases in ADAM10 protein levels, and the reduction in SIRT1 was reversed by proteasome inhibitor MG132. This study indicates that HIV-associated insults, particularly excitotoxicity, contribute to changes of APP secretases by downregulating levels of ADAM10 and its regulator.

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10

Yanagino, Kaori, and Naoyuki Miyashita. "Structure Prediction of the Transmembrane Region of Alpha- and Beta- Secretases using Replica-Exchange Molecular Dynamics Simulations, and the Interaction between Amyloid Precursor Protein and Them." Biophysical Journal 120, no. 3 (February 2021): 25a. http://dx.doi.org/10.1016/j.bpj.2020.11.414.

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11

Sharifulina, Svetlana, Andrey Khaitin, Valeria Guzenko, Yuliya Kalyuzhnaya, Valentina Dzreyan, Alexandr Logvinov, Natalia Dobaeva, et al. "Expression of Amyloid Precursor Protein, Caveolin-1, Alpha-, Beta-, and Gamma-Secretases in Penumbra Cells after Photothrombotic Stroke and Evaluation of Neuroprotective Effect of Secretase and Caveolin-1 Inhibitors." Biomedicines 10, no. 10 (October 20, 2022): 2655. http://dx.doi.org/10.3390/biomedicines10102655.

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Our studies reveal changes in the expression of the main participants in the processing of amyloid precursor protein (APP) in neurons and astrocytes after photothrombotic stroke (PTS). Here we show the increase in the level of N- and C-terminal fragments of APP in the cytoplasm of ischemic penumbra cells at 24 h after PTS and their co-immunoprecipitation with caveolin-1. The ADAM10 α-secretase level decreased in the rat brain cortex on the first day after PTS. Levels of γ-secretase complex proteins presenilin-1 and nicastrin were increased in astrocytes, but not in neurons, in the penumbra after PTS. Inhibitory analysis showed that these changes lead to neuronal death and activation of astrocytes in the early recovery period after PTS. The caveolin-1 inhibitor daidzein shifted APP processing towards Aβ synthesis, which caused astroglial activation. γ-secretase inhibitor DAPT down-regulated glial fibrillary acidic protein (GFAP) in astrocytes, prevented mouse cerebral cortex cells from PTS-induced apoptosis, and reduced the infarction volume. Thus, new generation γ-secretase inhibitors may be considered as potential agents for the treatment of stroke.

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12

Stan, Silvia, and Minna Abtahi. "Mechanisms of Action of Diallyl Trisulfide in Breast Ductal Carcinoma In Situ Cells." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 353. http://dx.doi.org/10.1093/cdn/nzaa044_052.

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Abstract Objectives Breast ductal carcinoma in situ (DCIS) is an early stage, localized form of breast cancer that can progress to an invasive breast cancer phenotype. Diallyl trisulfide is a bioactive organosulfur compound derived from Allium vegetables that has been shown to have anticancer effects in various cancer models. We have previously shown that diallyl trisulfide inhibits alpha secretases and Notch signaling pathway components in breast cancer cells. The objective of this study was to investigate the mechanisms of action of diallyl trisulfide in breast DCIS cells, with a primary focus on characterizing the induction of apoptosis in breast DCIS cells. Methods Breast DCIS cells SUM102PT [ER(−) and PR(+)] and SUM225CWN [ER(−) and PR(−)] were used in this study. Clonogenic assay was used to determine the colony formation ability of DCIS cells exposed to diallyl trisulfide. Apoptosis was quantified using a cell death detection ELISAPLUS kit from Roche according to the manufacturer's instructions. Western immunoblotting was used to determine the effect of diallyl trisulfide on apoptosis molecular markers. Results Diallyl trisulfide, a bioactive compound derived from Allium vegetables, induced a dose-dependent reduction in colony formation ability of breast DCIS cells. Diallyl trisulfide inhibited DCIS cell growth by inducing apoptosis as shown by a dose-dependent increase in DNA fragmentation as determined by ELISA assay. Induction of apoptosis was more pronounced in SUM102PT cells than in SUM225CWN cells at similar concentrations of diallyl trisulfide. Induction of apoptosis was characterized by a dose-dependent increase in cleaved PARP, cleaved caspase 3, and cleaved caspase 7. Expression levels of anti-apoptotic proteins Bcl2 and p-Bcl2 were decreased in DCIS cells exposed to diallyl trisulfide in a dose-dependent manner. Conclusions Diallyl trisulfide inhibits growth and induces apoptosis in breast DCIS cells. This study supports further investigation of diallyl trisulfide as a potential chemopreventive agent for breast DCIS. Funding Sources This work was supported by the USDA National Institute of Food and Agriculture, Hatch project NEV00765. Core facility used for research was supported by NIH grant P20 GM103650.

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13

Buniatian, Gayane Hrachia, Ute Schwinghammer, Roman Tremmel, Holger Cynis, Thomas S. Weiss, Ralf Weiskirchen, Volker M. Lauschke, et al. "Consequences of Amyloid‐β Deficiency for the Liver." Advanced Science, March 2, 2024. http://dx.doi.org/10.1002/advs.202307734.

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AbstractThe hepatic content of amyloid beta (Aβ) decreases drastically in human and rodent cirrhosis highlighting the importance of understanding the consequences of Aβ deficiency in the liver. This is especially relevant in view of recent advances in anti‐Aβ therapies for Alzheimer's disease (AD). Here, it is shown that partial hepatic loss of Aβ in transgenic AD mice immunized with Aβ antibody 3D6 and its absence in amyloid precursor protein (APP) knockout mice (APP‐KO), as well as in human liver spheroids with APP knockdown upregulates classical hallmarks of fibrosis, smooth muscle alpha‐actin, and collagen type I. Aβ absence in APP‐KO and deficiency in immunized mice lead to strong activation of transforming growth factor‐β (TGFβ), alpha secretases, NOTCH pathway, inflammation, decreased permeability of liver sinusoids, and epithelial‐mesenchymal transition. Inversely, increased systemic and intrahepatic levels of Aβ42 in transgenic AD mice and neprilysin inhibitor LBQ657‐treated wild‐type mice protect the liver against carbon tetrachloride (CCl4)‐induced injury. Transcriptomic analysis of CCl4‐treated transgenic AD mouse livers uncovers the regulatory effects of Aβ42 on mitochondrial function, lipid metabolism, and its onco‐suppressive effects accompanied by reduced synthesis of extracellular matrix proteins. Combined, these data reveal Aβ as an indispensable regulator of cell–cell interactions in healthy liver and a powerful protector against liver fibrosis.

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14

Halawany, Ali M. El, Nesrine S. EL Sayed, Hossam M. Abdallah, and Riham Salah El Dine. "Protective effects of gingerol on streptozotocin-induced sporadic Alzheimer’s disease: emphasis on inhibition of β-amyloid, COX-2, alpha-, beta - secretases and APH1a." Scientific Reports 7, no. 1 (June 6, 2017). http://dx.doi.org/10.1038/s41598-017-02961-0.

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15

El Halawany, Ali M., Nesrine S. EL Sayed, Hossam M. Abdallah, and Riham Salah El Dine. "Retraction Note: Protective effects of gingerol on streptozotocin-induced sporadic Alzheimer’s disease: emphasis on inhibition of β-amyloid, COX-2, alpha-, beta - secretases and APH1a." Scientific Reports 13, no. 1 (June 9, 2023). http://dx.doi.org/10.1038/s41598-023-36652-w.

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