Relevant bibliographies by topics / Beta-secretase

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Beta-secretase'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 July 2025

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Journal articles on the topic "Beta-secretase"

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Liao, Francesca-Fang, Ruishan Wang, and Edwards A. Park. "Repression of Alzheimer's beta-Secretase." Aging 5, no. 11 (2013): 789–90. http://dx.doi.org/10.18632/aging.100612.

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Kuentzel, S. L., S. M. Ali, R. A. Altman, B. D. Greenberg та T. J. Raub. "The Alzheimer β-amyloid protein precursor/protease nexin-II is cleaved by secretase in a trans-Golgi secretory compartment in human neuroglioma cells". Biochemical Journal 295, № 2 (1993): 367–78. http://dx.doi.org/10.1042/bj2950367.

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Alzheimer beta-amyloid protein precursor (beta APP) is expressed endogenously and abundantly by human neuroglioma (H4) cells. Its secretory processing has been shown to involve discrete proteolysis within the beta A4 region, thus preventing beta-amyloid formation, by an enzyme which has been referred to as ‘beta APP secretase’. This cleavage results in secretion of a soluble N-terminal 135 kDa protein and retention of an integral membrane C-terminal fragment within the cell. The membrane-associated C-terminal fragment is sorted to lysosomes where it undergoes limited degradation. We show here
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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 sec
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Made Galu Putra Ardiana and Ni Kadek Warditiani. "Potensi Ashwagandha (Withania somnifera (L.) Dunal) sebagai Pengobatan Alzheimer." Prosiding Workshop dan Seminar Nasional Farmasi 3 (June 8, 2025): 56–63. https://doi.org/10.24843/wsnf.2024.v03.p06.

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Ashwagandha (Withania somnifera (L.) Dunal) adalah tanaman herbal yang telah lama digunakan dalam pengobatan tradisional Ayurveda. Penelitian ilmiah terbaru mengungkap potensi neuroprotektif Ashwagandha dalam konteks penyakit neurodegeneratif seperti Alzheimer. Senyawa utama dalam Ashwagandha adalah Withaferin A dan Withanolides. Withanolides meningkatkan aktivitas α-secretase yang mempromosikan pemotongan APP menjadi produk nonamyloidogenic, sedangkan Withaferin A menghambat aktivitas β-secretase, mencegah pembentukan fragmen amyloid-beta yang beracun. Selain itu, withanolides juga menghambat
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Chang, Wan‐Pin, Deborah Downs, Xiang‐Ping Huang, Huining Da, Kar‐Ming Fung, and Jordan Tang. "Amyloid‐beta reduction by memapsin 2 (beta‐secretase) immunization." FASEB Journal 21, no. 12 (2007): 3184–96. http://dx.doi.org/10.1096/fj.06-7993com.

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Venugopal, Chitra, Christina Demos, K. Jagannatha Rao, Miguel Pappolla, and Kumar Sambamurti. "Beta-Secretase: Structure, Function, and Evolution." CNS & Neurological Disorders - Drug Targets 7, no. 3 (2008): 278–94. http://dx.doi.org/10.2174/187152708784936626.

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Vassar, Robert. "PL-04-01: Targeting beta-secretase." Alzheimer's & Dementia 9 (July 2013): P677. http://dx.doi.org/10.1016/j.jalz.2013.04.332.

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Nawrot, Barbara. "Targeting BACE with small inhibitory nucleic acids - a future for Alzheimer's disease therapy?" Acta Biochimica Polonica 51, no. 2 (2004): 431–44. http://dx.doi.org/10.18388/abp.2004_3582.

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beta-Secretase, a beta-site amyloid precursor protein (APP) cleaving enzyme (BACE), participates in the secretion of beta-amyloid peptides (Abeta), the major components of the toxic amyloid plaques found in the brains of patients with Alzheimer's disease (AD). According to the amyloid hypothesis, accumulation of Abeta is the primary influence driving AD pathogenesis. Lowering of Abeta secretion can be achieved by decreasing BACE activity rather than by down-regulation of the APP substrate protein. Therefore, beta-secretase is a primary target for anti-amyloid therapeutic drug design. Several a
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Naushad, Mehjabeen, Siva Sundara Kumar Durairajan, Amal Kanti Bera, Sanjib Senapati та Min Li. "Natural Compounds with Anti-BACE1 Activity as Promising Therapeutic Drugs for Treating Alzheimerʼs Disease". Planta Medica 85, № 17 (2019): 1316–25. http://dx.doi.org/10.1055/a-1019-9819.

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AbstractAlzheimerʼs disease is a neurodegenerative disease that leads to irreversible neuronal damage. Senile plaques, composed of amyloid beta peptide, is the principal abnormal characteristic of the disease. Among the factors involved, the secretase enzymes, namely, α secretase, beta-site amyloid precursor protein-cleaving enzyme, β secretase, and γ secretase, hold consequential importance. Beta-site amyloid precursor protein-cleaving enzyme 1 is considered to be the rate-limiting factor in the production of amyloid beta peptide. Research supporting the concept of inhibition of beta-site amy
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Farah, MohamedH, and Carolyn Tallon. "Beta secretase activity in peripheral nerve regeneration." Neural Regeneration Research 12, no. 10 (2017): 1565. http://dx.doi.org/10.4103/1673-5374.217319.

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Dissertations / Theses on the topic "Beta-secretase"

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Mok, Ngai Yi. "Design, synthesis and biological evaluation of new beta-secretase inhibitors." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496529.

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Roberts, Hazel. "Alpha-synuclein expression influences the processing of the amyloid precursor protein." Thesis, University of Bath, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.707587.

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In certain neurodegenerative diseases such Dementia with Lewy Bodies (DLB), it is hypothesised that misfolded α-synuclein (α-syn) and β-amyloid both contribute to pathology. α-Syn and β-amyloid have been suggested to synergistically promote one another’s accumulation and aggregation, but the mechanisms are unknown. β-Amyloid is generated from β-/γ-secretase-mediated processing of the amyloid precursor protein (APP). This study investigated how α-syn overexpression in cells affects β-amyloid production from APP, using multiplex assays, luciferase reporter assays, and western blotting. Wildtype
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Liu, Wei Wei. "An investigation of beta-secretase activity and regulation in Alzheimer's disease." Thesis, Queen's University Belfast, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486241.

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Alzheimer's disease (AD) is the most common cause of dementia, characterized by the • presence of extracellular amyloid plaques and intracellular tangles in the brain. The principal component of amyloid plaques is the amyloid 13 (A13) peptide, cleaved from amyloid precursor protein (APP) by 13-secretase and y-secretase. Two proteases with 13-secretase activity have been identified: 13-site APP-cleaving enzymes 1 and 2 (BACE1 and BACE2). Previous post. mortem studies have revealed an increase of 13-secretase activity in brain tissue of individuals with sporadic AD. This study aimed to invest
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Semighini, Evandro Pizeta. "Planejamento racional de inibidores da beta-secretase em mal de Alzheimer." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/60/60136/tde-06092013-102421/.

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O Mal de Alzheimer é o maior causador de demência em idosos: acomete 10% da população mundial com idade em torno dos 65 anos e atinge cerca de 50% dos indivíduos com mais de 85 anos. A progressão dos sintomas da doença está associada a modificações estruturais nas sinapses colinérgicas em determinadas regiões cerebrais. A maior característica fisiopatológica do AD é a deposição de placas neuríticas extracelulares em áreas cerebrais relacionadas à memória, placas constituídas pelo peptídeo ?-amiloide 40/42, que é formado pela clivagem da Proteína Precursora Amiloide, durante seu metabolismo pel
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Cordy, Joanna Margaret. "The involvement of lipid rafts in the regulation of beta-secretase activity." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411357.

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Chiocco, Matthew J. "Beta-Secretase Trangenic Mice: Effects of BACE1 and BACE2 on Alzheimer's Disease Pathogenesis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=case1111597750.

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Chiocco, Matthew J. "Beta-secretase transgenic mice effects of BACE1 and BACE2 on Alzheimer's disease pathogenesis /." Connect to text online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1111597750.

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Wiley, Jesse Carey. "Familial Alzheimer's disease mutations decrease gamma-secretase processing of beta amyloid precurson [sic] protein /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/4985.

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MuÑoz, Gimenez Noeli. "Identification et Caractérisation d'une Enzyme de type beta-Secretase Impliquée dans la Maturation Protéolytique du Précurseur du Peptide beta-Amyloide." Paris 6, 1999. http://www.theses.fr/1999PA066688.

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Matera, Riccardo <1977&gt. "Design and synthesis of novel non peptidomimtic beta-secretase inhibitors in the treatment of Alzheimer's disease." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2009. http://amsdottorato.unibo.it/1711/1/Matera_Riccardo_tesi.pdf.

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The aspartic protease BACE1 (β-amyloid precursor protein cleaving enzyme, β-secretase) is recognized as one of the most promising targets in the treatment of Alzheimer's disease (AD). The accumulation of β-amyloid peptide (Aβ) in the brain is a major factor in the pathogenesis of AD. Aβ is formed by initial cleavage of β-amyloid precursor protein (APP) by β-secretase, therefore BACE1 inhibition represents one of the therapeutic approaches to control progression of AD, by preventing the abnormal generation of Aβ. For this reason, in the last decade, many research efforts have focused at
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Books on the topic "Beta-secretase"

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Hemming, Matthew L. Identification of [beta]-secretase (BACE1) substrates using quantitative proteomics. 2012.

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Book chapters on the topic "Beta-secretase"

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Schejbal, Jan, Roman Řemínek, and Zdeněk Glatz. "Screening of Beta-Secretase Inhibitors by Capillary Electrophoresis-Mass Spectrometry." In Methods in Molecular Biology. Springer US, 2019. http://dx.doi.org/10.1007/978-1-0716-0163-1_9.

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Okochi, M., A. Fukumori, Y. Satoh, et al. "Alzheimer�s γ-Secretase Mechanism Produces Amyloid-β-Protein Like Peptides Simultaneously with Release of Intracellular Signaling Fragments." In Molecular Neurobiology of Alzheimer Disease and Related Disorders. KARGER, 2004. http://dx.doi.org/10.1159/000078524.

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Singh, Varinder, Amit Kumar, Parul Sood, et al. "Exploring Beta Secretase Inhibitors as the Evergreen Drug Target for Alzheimer's Disease: Calling Herbal Therapies to the Rescue." In Neuro-Nutraceuticals and Drug Discovery and Delivery in Alzheimer’s Disease. Apple Academic Press, 2025. https://doi.org/10.1201/9781003570585-3.

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Sambamurti, Kumar. "Beta Secretase." In xPharm: The Comprehensive Pharmacology Reference. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.60570-7.

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Rodrigues, Alda dos Santos, Rafael Rezende, Divan Henrique Fernandes Barcelos, Flávia de Paula, Estevão Carlos Silva Barcelos, and Flávia Imbroisi Valle Errera. "VIAS EMERGENTES NA NEURODEGENERAÇÃO: O PAPEL DE NOTCH1 E GAMA-SECRETASE COMO ALVOS TERAPÊUTICOS." In Medicina Personalizada: Genética e Inovações no Tratamento de Doenças. Editora Científica Digital, 2025. https://doi.org/10.37885/250519435.

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Introdução: A via de sinalização Notch1 é fundamental para o desenvolvimento neural, a neuroplasticidade e a homeostase do sistema nervoso central. Sua ativação, mediada por ligantes como JAG1 e JAG2, regula processos como diferenciação celular e resposta ao estresse. No cérebro, NOTCH1 é expresso em regiões como o hipocampo e o córtex, estando associado à memória e à adaptação ao estresse. Disfunções nessa via têm sido relacionadas a doenças neurológicas, como a depressão e a Doença de Alzheimer (DA). Métodos: O capítulo consiste numa revisão narrativa da literatura científica, reunindo estud
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Villamil-Ortiz, J., B. J. L. Eggen, and G. P. Cardona-Gómez. "Lipids, beta-secretase 1, and Alzheimer disease." In Factors Affecting Neurological Aging. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-817990-1.00026-3.

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Korabecny, Jan, Katarina Spilovska, Ondrej Soukup, Rafael Dolezal, and Kamil Kuca. "Amyloid Beta Hypothesis: Attention to β- and γ-Secretase Modulators." In Alzheimer's Disease - The 21st Century Challenge. InTech, 2018. http://dx.doi.org/10.5772/intechopen.75629.

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Read, Justin, and Cenk Suphioglu. "Dropping the BACE: Beta Secretase (BACE1) as an Alzheimer’s Disease Intervention Target." In Neurodegenerative Diseases. InTech, 2013. http://dx.doi.org/10.5772/53603.

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Reinhardt, Sven, and Kristina Endres. "Implications of alpha- and beta-secretase expression and function in Alzheimer's disease." In Genetics, Neurology, Behavior, and Diet in Dementia. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-815868-5.00016-5.

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"γ-Secretase and Presenilin." In A-Beta Metabolism and Alzheimer's Disease. CRC Press, 2003. http://dx.doi.org/10.1201/9781498713641-10.

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Conference papers on the topic "Beta-secretase"

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Junkes, Giovanna Braz, Diego Akyo Hoshina dos Santos, Julia Petry, and Meria Eduarda Mendes Hibarino. "A ATROFIA NEURONAL E SUA RELAÇÃO COM A DOENÇA DE ALZHEIMER." In I Congresso Brasileiro de Estudos Patológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbesp/81.

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Introdução: O Alzheimer é uma patologia neurodegenerativa que afeta o Sistema Nervoso Central por causar atrofia neuronal derivada do acúmulo do peptídeo Beta Amilóide e da proteína Tau. A doença é comumente associada à idade e caracteriza-se pela demência, apresentando sintomas como disfunções na cognição e distúrbios comportamentais e na memória. Objetivo: O objetivo desse trabalho é informar sobre aspectos fisiopatológicos da doença de Alzheimer e esclarecer minimamente como ocorre o seu desenvolvimento. Material e métodos: Trata-se de uma revisão bibliográfica baseada em artigos, escritos
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Prado Prado, Francisco, Jan-carlo Díaz-González, Francisco Aguirre-Crespo, and Xerardo García-Mera. "New theoretical model for the study of new β-secretase inhibitors." In MOL2NET, International Conference on Multidisciplinary Sciences. MDPI, 2015. http://dx.doi.org/10.3390/mol2net-1-e011.

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von Arnim, Christine, Michael Wagner, Petra Weber, and Herbert Schneckenburger. "TIRET microscopy: monitoring protein (amyloid precursor protein and beta-secretase) interaction on the surface of living cells." In Biomedical Optics (BiOS) 2007, edited by Daniel L. Farkas, Robert C. Leif, and Dan V. Nicolau. SPIE, 2007. http://dx.doi.org/10.1117/12.699856.

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Gwin, M., S. B. Voth, C. M. Francis, R. Balczon, and T. Stevens. "Gamma Secretase Activating Protein is Necessary for Endothelial Dysfunction and Production of Cytotoxic Beta Amyloid During Bacterial Infection." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1975.

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