Relevant bibliographies by topics / BACE

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

Academic literature on the topic 'BACE'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "BACE"

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Casas, Silvia, Paola Casini, Sandra Piquer, Jordi Altirriba, Maud Soty, Lisa Cadavez, Ramon Gomis, and Anna Novials. "BACE2 plays a role in the insulin receptor trafficking in pancreatic β-cells." American Journal of Physiology-Endocrinology and Metabolism 299, no. 6 (December 2010): E1087—E1095. http://dx.doi.org/10.1152/ajpendo.00420.2010.

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BACE1 (β-site amyloidogenic cleavage of precursor protein-cleaving enzyme 1) is a β-secretase protein that plays a central role in the production of the β-amyloid peptide in the brain and is thought to be involved in the Alzheimer's pathogenesis. In type 2 diabetes, amyloid deposition within the pancreatic islets is a pathophysiological hallmark, making crucial the study in the pancreas of BACE1 and its homologous BACE2 to understand the pathological mechanisms of this disease. The objectives of the present study were to characterize the localization of BACE proteins in human pancreas and determine their function. High levels of BACE enzymatic activity were detected in human pancreas. In normal human pancreas, BACE1 was observed in endocrine as well as in exocrine pancreas, whereas BACE2 expression was restricted to β-cells. Intracellular analysis using immunofluorescence showed colocalization of BACE1 with insulin and BACE2 with clathrin-coated vesicles of the plasma membrane in MIN6 cells. When BACE1 and -2 were pharmacologically inhibited, BACE1 localization was not altered, whereas BACE2 content in clathrin-coated vesicles was increased. Insulin internalization rate was reduced, insulin receptor β-subunit (IRβ) expression was decreased at the plasma membrane and increased in the Golgi apparatus, and a significant reduction in insulin gene expression was detected. Similar results were obtained after specific BACE2 silencing in MIN6 cells. All these data point to a role for BACE2 in the IRβ trafficking and insulin signaling. In conclusion, BACE2 is hereby presented as an important enzyme in β-cell function.
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John, Varghese, James P. Beck, Michael J. Bienkowski, Sukanto Sinha, and Robert L. Heinrikson. "Human β-Secretase (BACE) and BACE Inhibitors." Journal of Medicinal Chemistry 46, no. 22 (October 2003): 4625–30. http://dx.doi.org/10.1021/jm030247h.

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John, Varghese. "Human β-secretase (BACE) and BACE Inhibitors: Progress Report." Current Topics in Medicinal Chemistry 6, no. 6 (March 1, 2006): 569–78. http://dx.doi.org/10.2174/156802606776743084.

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Rosse, Gerard. "Dihydrooxazines As Inhibitors of BACE-1 or BACE-2." ACS Medicinal Chemistry Letters 4, no. 5 (March 19, 2013): 433–34. http://dx.doi.org/10.1021/ml400104f.

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Bradley, Peter. "Back to BACE: one approach to fighting Alzheimer's." British Journal of Healthcare Assistants 11, no. 1 (January 2, 2017): 10–11. http://dx.doi.org/10.12968/bjha.2017.11.1.10.

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Luo, Gang, Hongxia Xu, Yinuo Huang, Dapeng Mo, Ligang Song, Baixue Jia, Bo Wang, Zhanqiang Jin, and Zhongrong Miao. "Deposition of BACE-1 Protein in the Brains of APP/PS1 Double Transgenic Mice." BioMed Research International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/8380618.

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The main causes of Alzheimer’s disease remain elusive. Previous data have implicated the BACE-1 protein as a central player in the pathogenesis of Alzheimer’s disease. However, many inhibitors of BACE-1 have failed during preclinical and clinical trials for AD treatment. Therefore, uncovering the exact role of BACE-1 in AD may have significant impact on the future development of therapeutic agents. Three- and six-month-old female APP/PS1 double transgenic mice were used to study abnormal accumulation of BACE-1 protein in brains of mice here. Immunofluorescence, immunohistochemistry, and western blot were performed to measure the distributing pattern and expression level of BACE-1. We found obvious BACE-1 protein accumulation in 3-month-old APP/PS1 mice, which had increased by the time of 6 months. Coimmunostaining results showed BACE-1 surrounded amyloid plaques in brain sections. The abnormal protein expression might not be attributable to the upregulation of BACE-1 protein, as no significant difference of protein expression was observed between wild-type and APP/PS1 mice. With antibodies against BACE-1 and CD31, we found a high immunoreactive density of BACE-1 protein on the outer layer of brain blood vessels. The aberrant distribution of BACE-1 in APP/PS1 mice suggests BACE-1 may be involved in the microvascular abnormality of AD.
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Osherovich, Lev. "Genentech plays BACE." Science-Business eXchange 4, no. 22 (June 2011): 619. http://dx.doi.org/10.1038/scibx.2011.619.

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Wong, Philip. "[AM-10]: BACE." Alzheimer's & Dementia 1 (July 2005): S3. http://dx.doi.org/10.1016/j.jalz.2005.06.037.

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Joseph, Ogunleye Adewale, Kikiowo Babatomiwa, Adelakun Niyi, Omotuyi Olaposi, and Inyang Olumide. "Molecular Docking and 3D Qsar Studies of C000000956 as a Potent Inhibitor of Bace-1." Drug Research 69, no. 08 (February 19, 2019): 451–57. http://dx.doi.org/10.1055/a-0849-9377.

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Abstract Background BACE-1 is an aspartate protease that is responsible for the proteolysis of amyloid precursor proteins (APP) into beta-amyloid (Aβ), a neurotoxic peptide in patients with Alzheimer’s disease (AD). As such, BACE-1 is a prime pharmacological target in the control of Aβ in the brain and its inhibition will be a sound approach in AD therapy. Methods The computational pipeline which comprised molecular docking (MD), Quantitative Structure Activity Relationship (QSAR) modelling and Absorption, Distribution, Metabolism, Excretion and Toxicity (ADMET) studies enabled the prediction of molecular interaction and relative inhibitory potentials of the hit compound. Results and Discussion The current study reports a naturally sourced small molecule inhibitor of BACE1 (C000000956) which was obtained through a computational pipeline. Also, pharmacological constraints such as pH dependent activity of the enzyme and blood brain barrier permeation which have been associated with the efficacy of previous BACE-1 inhibitors were well catered for. Our results suggest that orally delivered C000000956 is a potential small molecule inhibitor of BACE-1 which may find usefulness in AD-therapy.
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Saric, Arman, Lars zur Brügge, Dirk Müller-Pompalla, Thomas Rysiok, Solenne Ousson, Bruno Permanne, Anna Quattropani, Michael Busch, Dirk Beher, and Ishrut Hussain. "Development and Characterization of a Novel Membrane Assay for Full-Length BACE-1 at pH 6.0." Journal of Biomolecular Screening 18, no. 3 (September 27, 2012): 277–85. http://dx.doi.org/10.1177/1087057112462237.

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β-Site amyloid precursor protein cleaving enzyme–1 (BACE-1) is a transmembrane aspartic protease that mediates the initial cleavage of the amyloid precursor protein (APP), leading to the generation of amyloid-β (Aβ) peptides that are thought to be causative of Alzheimer’s disease (AD). Consequently, inhibition of BACE-1 is an attractive therapeutic approach for the treatment of AD. In general, in vitro biochemical assays to monitor BACE-1 activity have used the extracellular domain of the protein that contains the catalytic active site. This form of BACE-1 is catalytically active at acidic pH and cleaves APP-based peptide substrates at the β-site. However, this form of BACE-1 does not mimic the natural physiology of BACE-1 and shows minimal activity at pH 6.0, which is more representative of the pH within the intracellular compartments where BACE-1 resides. Moreover, high-throughput screens with recombinant BACE-1 at pH 4.5 have failed to identify tractable leads for drug discovery, and hence, BACE-1 inhibitor development has adopted a rational drug design approach. Here we describe the development and validation of a novel membrane assay comprising full-length BACE-1 with measurable activity at pH 6.0, which could be used for the identification of novel inhibitors of BACE-1.
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Dissertations / Theses on the topic "BACE"

1

Fluhrer, Regina. "Zwei neuartige Aspartylproteasen BACE-1 und BACE-2." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-14423.

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Wilson, D. M. "Platelet BACE Activity and its relationship to genetic variation at the BACE locus, in patients with different types of dementia." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517654.

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Strauss, Markus. "Funktionelle Analyse der humanen [beta]-Sekretase [Beta-Sekretase] (BACE)." [S.l.] : [s.n.], 2005. http://www.diss.fu-berlin.de/2005/45/index.html.

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Fuzaro, Junior Gilson [UNESP]. "Nível de atividade física, estado nutricional e níveis de BACE 1 e BACE 2 em idosos neurologicamente saudáveis e com doença de Alzheimer." Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/138561.

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Made available in DSpace on 2016-05-17T16:51:55Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-12-07. Added 1 bitstream(s) on 2016-05-17T16:55:51Z : No. of bitstreams: 1 000863012.pdf: 1359589 bytes, checksum: a5d767aad97ebd041c16c340e5476d28 (MD5)
A Doença de Alzheimer (DA) é neurodegenerativa, progressiva e causa comprometimento cognitivo em idosos. Além da terapia medicamentosa, alternativas não farmacológicas, como atividade física e orientação nutricional, podem auxiliar no tratamento da doença. A influência desses fatores em alguns biomarcadores, como as β-secretases, tem sido relacionada a alterações em alguns quadros da doença. Assim, o objetivo do presente estudo foi analisar o nível de atividade física, estado nutricional e níveis plaquetários de BACE 1 e BACE 2 em idosos com doença de Alzheimer nos estágios leve e moderado e em idosos cognitivamente preservados. Ainda, comparar grupos e a correlacionar estas variáveis. Para tanto, participaram do estudo 32 idosos com DA e 32 idosos hígidos. Para verificar o nível de atividade física os idosos utilizaram um acelerômetro e responderam ao questionário Baecke modificado para idosos. A avaliação do estado nutricional consistiu na coleta das medidas antropométricas: peso (kg), estatura (m), circunferências e pregas cutâneas. Também foi aplicada a Mini Avaliação Nutricional. Por meio de coleta sanguínea, foram analisados os níveis plaquetários de BACE 1 e BACE 2 dos grupos. Além disso, foram aplicados testes de rastreamento da função cognitiva, estagiamento da DA e sintomas depressivos dos participantes. Para análise dos dados, foi verificada a normalidade da amostra por meio do teste de Shapiro Wilk. Para dados paramétricos, foi utilizado o teste t de Student e correlação de Pearson, para dados não paramétricos, foi utilizado o teste U de Mann-Whitney e correlação de Spearman. Foi admitido um nível de significância de p<0,05. Os resultados indicam que houve diferença significativa nas médias de nível de atividade física, nas concentrações de BACE 1 e 2 e para a variável Mini Avaliação Nutricional entre os grupos, sendo que o grupo DA apresentou menor nível de atividade física...
Alzheimer's disease (AD) is a neurodegenerative, progressive and causes cognitive impairment in the elderly. Besides drug therapy, nonpharmacological alternatives such as physical activity and nutritional counseling, can help in treating the disease. The influence of these factors in some biomarkers such as β-secretase, has been related to changes in certain tables of the disease. The objective of this study was to analyze the level of physical activity, nutritional status and platelet levels of BACE BACE 1 and 2 in elderly patients with Alzheimer's disease in mild and moderate stages and cognitively preserved elderly. Also compare groups and to correlate these variables. To do so, participated in the study 32 elderly with AD and 32 healthy elderly. To check the level of physical activity the elderly used an accelerometer and the questionnaire Baecke modified for the elderly. The assessment of nutritional status consisted of the collection of anthropometric measurements: weight (kg), height (m), circumference and skinfold thickness. It has also been applied to Mini Nutritional Assessment. Through blood collection, platelet levels of BACE and BACE 1 of 2 groups were analyzed. Furthermore, screening tests were applied cognitive function, depressive symptoms and the staging of the attendees. For data analysis, the normality of the sample using the Shapiro-Wilk test was verified. For parametric data, we used the Student t test and Pearson's correlation to non-parametric data, the Mann-Whitney U test and Spearman correlation. It was admitted a significance level of p <0.05. The results indicate a significant difference in the average level of physical activity at concentrations of BACE 1 and 2 and the variable Mini Nutritional Assessment between the groups, with the DA group had lower levels of physical activity, higher concentrations of BACE and worse nutritional status. In addition, the Spearman test showed negative correlation between the...
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Fuzaro, Junior Gilson. "Nível de atividade física, estado nutricional e níveis de BACE 1 e BACE 2 em idosos neurologicamente saudáveis e com doença de Alzheimer /." Rio Claro, 2015. http://hdl.handle.net/11449/138561.

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Orientador: José Luiz Riani Costa
Banca: Thays Martins Vital
Banca: Alexandre Gabarra de Oliveira
Resumo: A Doença de Alzheimer (DA) é neurodegenerativa, progressiva e causa comprometimento cognitivo em idosos. Além da terapia medicamentosa, alternativas não farmacológicas, como atividade física e orientação nutricional, podem auxiliar no tratamento da doença. A influência desses fatores em alguns biomarcadores, como as β-secretases, tem sido relacionada a alterações em alguns quadros da doença. Assim, o objetivo do presente estudo foi analisar o nível de atividade física, estado nutricional e níveis plaquetários de BACE 1 e BACE 2 em idosos com doença de Alzheimer nos estágios leve e moderado e em idosos cognitivamente preservados. Ainda, comparar grupos e a correlacionar estas variáveis. Para tanto, participaram do estudo 32 idosos com DA e 32 idosos hígidos. Para verificar o nível de atividade física os idosos utilizaram um acelerômetro e responderam ao questionário Baecke modificado para idosos. A avaliação do estado nutricional consistiu na coleta das medidas antropométricas: peso (kg), estatura (m), circunferências e pregas cutâneas. Também foi aplicada a Mini Avaliação Nutricional. Por meio de coleta sanguínea, foram analisados os níveis plaquetários de BACE 1 e BACE 2 dos grupos. Além disso, foram aplicados testes de rastreamento da função cognitiva, estagiamento da DA e sintomas depressivos dos participantes. Para análise dos dados, foi verificada a normalidade da amostra por meio do teste de Shapiro Wilk. Para dados paramétricos, foi utilizado o teste t de Student e correlação de Pearson, para dados não paramétricos, foi utilizado o teste U de Mann-Whitney e correlação de Spearman. Foi admitido um nível de significância de p<0,05. Os resultados indicam que houve diferença significativa nas médias de nível de atividade física, nas concentrações de BACE 1 e 2 e para a variável Mini Avaliação Nutricional entre os grupos, sendo que o grupo DA apresentou menor nível de atividade física...
Abstract: Alzheimer's disease (AD) is a neurodegenerative, progressive and causes cognitive impairment in the elderly. Besides drug therapy, nonpharmacological alternatives such as physical activity and nutritional counseling, can help in treating the disease. The influence of these factors in some biomarkers such as β-secretase, has been related to changes in certain tables of the disease. The objective of this study was to analyze the level of physical activity, nutritional status and platelet levels of BACE BACE 1 and 2 in elderly patients with Alzheimer's disease in mild and moderate stages and cognitively preserved elderly. Also compare groups and to correlate these variables. To do so, participated in the study 32 elderly with AD and 32 healthy elderly. To check the level of physical activity the elderly used an accelerometer and the questionnaire Baecke modified for the elderly. The assessment of nutritional status consisted of the collection of anthropometric measurements: weight (kg), height (m), circumference and skinfold thickness. It has also been applied to Mini Nutritional Assessment. Through blood collection, platelet levels of BACE and BACE 1 of 2 groups were analyzed. Furthermore, screening tests were applied cognitive function, depressive symptoms and the staging of the attendees. For data analysis, the normality of the sample using the Shapiro-Wilk test was verified. For parametric data, we used the Student t test and Pearson's correlation to non-parametric data, the Mann-Whitney U test and Spearman correlation. It was admitted a significance level of p <0.05. The results indicate a significant difference in the average level of physical activity at concentrations of BACE 1 and 2 and the variable Mini Nutritional Assessment between the groups, with the DA group had lower levels of physical activity, higher concentrations of BACE and worse nutritional status. In addition, the Spearman test showed negative correlation between the...
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Kobayashi, Dione T. "Behavioral and histochemical characterization of a novel BACE Knockout x PDAPP mouse model of Alzheimer's Disease : examination of potential effects of BACE inhibition on Alzheimer's Disease and the role of APP, Aβ and BACE in normal and pathological memory function." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29204.

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This dissertation describes the phenotypic characterisation of a BACE knockout (KO) x PDAPP transgenic mouse line, utilising behavioural, histochemical, and pharmagologic methods. Several transgenic mouse models have been created that overexpress human mutant Amyloid Precursor Protein (hAPP) that reproduced many of the cognitive and histopathological features of AD. Recently, the β-site cleaving enzyme (BACE) responsible for the first proteolytic cleavage of APP has been characterised, and subsequent research has led to the propagation of BACE inhibition as a prime experimental strategy for AD therapy. Examining the behavioural and histological phenotypes of BACE KO animals on normal and hAPP overexpressing backgrounds is an effective way to assess whether the inhibition of BACE is a reasonable strategy for the treatment of AD. Behavioural studies were conducted using homozygous and hemizygous BACE KO mice, PDAPP mice, and BACE KO: PDAPP lines together with relevant controls. The results form the characterisation of the BACE KO x PDAPP mouse line indicate that the absolute loss of BACE and Aβ caused profound spatial memory deficits, sometimes greater even than that of hAPP mice alone. BACE KO was associated with spontaneous seizures as well as greater seizure activity in drug-induced seizure experiments. However, the partial hemizygous deletion of the BACE gene on a hAPP background appeared to improve spatial memory performance on certain measures and protect against drug-induced seizure responses relative to hAPP mice. The research described in this dissertation is consistent with the notion that, under certain circumstances, therapeutic inhibition of BACE may prove to be a valuable strategy for treatment of AD. These studies also support an important role for the APP processing pathway in “normal” learning and memory processes, possibly by regulating neuronal activity levels.
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Capell, Anja. "Funktionelle Charakterisierung von BACE, einer für die Alzheimer Krankheit relevanten Protease." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976576228.

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Griffiths, Heledd Hâf. "Mechanisms of cellular prion protein regulation of the β-secretase, BACE." Thesis, University of Leeds, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.515339.

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Capell, Anja. "Funktionelle Charakterisierung von BACE, einer für die Alzheimer Krankheit relevanten Protease." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2005. http://dx.doi.org/10.18452/15321.

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Die Alzheimer Krankheit ist die häufigste Altersdemenz. Ein spezifisches pathologisches Merkmal der Alzheimer Krankheit ist die Amyloid-Ablagerung im Gehirn. Die Hauptkomponente der so genannten Amyloid-Plaques ist das Amyloid beta-Peptid (A-beta). A-beta entsteht durch sequenzielle proteolytische Spaltung aus einem membrangebundenen Vorläuferprotein, dem beta-APP (betaamyloid precursor protein). Die kürzlich identifizierte beta-Sekretase (BACE, beta-site APPcleaving enzyme) generiert den Schnitt am N-Terminus von A-beta. Es entsteht ein C-terminales, membrangebundenes beta-APP-Fragment, das beta-APP-CTF. Beta-APP-CTF ist das direkte Substrat für die gamma-Sekretase, die innerhalb der Membrandomäne schneidet, wodurch A-beta freigesetzt wird. In der vorliegenden Arbeit kann erstmalig gezeigt werden, dass BACE auf dem sekretorischen Transportweg aus dem Endoplasmatischen Retikulum (ER), über den Golgi-Apparat zur Zelloberfläche transportiert wird. Auf dem Transport wird BACE durch N-Glycosylierung und Propeptidabspaltung posttranslational modifiziert. BACE wird im ER N-glycosyliert und die mannosereichen Zucker werden auf dem Transport durch den Golgi-Apparat in Endoglycosidase H resistente Zucker des komplexen Typs modifiziert. Die Propeptidabspaltung, durch Furin oder furinähnliche Propeptidkonvertasen, findet unmittelbar vor dem Aufbau der komplexen Zucker statt. Ferner konnte gezeigt werden, dass der Transport von BACE die A-beta-Entstehung limitieren kann. In polarisierten Madin-Darby canine kidney (MDCK) Zellen wird BACE überwiegend zur apikalen Plasmamembran transportiert und damit entgegengesetzt zu seinem Substrat beta-APP. Der gegensätzliche Transport von BACE und beta-APP begrenzt die A-beta Entstehung. Wird der apikale Transport von beta-APP durch Deletion seines basolateralen Sortierungssignals erhöht, entsteht vermehrt A-beta. Der differenzielle Transport von BACE und beta-APP könnte ein Hinweis darauf sein, dass beta-APP nicht das physiologische Substrat von BACE ist.
Alzheimer`s disease is the most common cause of progressive cognitive decline in the aged population. Pathologically Alzheimer`s disease is characterized by the invariant accumulation of senile plaques. Senile plaques are predominantly composed of the amyloid beta-peptide (A-beta), which is derived from the membrane bound beta-amyloid precursor protein (beta-APP) by sequential proteolytic cleavage. The recently identified beta-secretase (BACE) is responsible for the cleavage at the N-terminus of the A-beta domain. This cleavage generates membrane-bound beta-APP-Cterminal fragments (beta-APP-CTF) which are the immediate precursor for gamma-secretase cleavage and therefore for liberation of A-beta. The present work shows that BACE moves along the secretory pathway, while it undergoes post-translational modifications, which can be monitored by a significant increase in the molecular mass and cleavage of its pro-peptide. BACE becomes N-glycosylated within the ER and the increase in molecular mass is caused by complex N-glycosylation. The mature form of BACE is resistant to endoglycosidase H treatment; this indicates that BACE traffics through the Golgi. Furthermore the mature form of BACE does not contain the pro-peptide anymore. Pro-BACE is predominantly located within the endoplasmic reticulum. Pro-peptide cleavage occurs immediately before full maturation by furin or a furin-like proprotein convertase. Moreover traffic of BACE can limit A-beta generation. In the well established model system of polarized Madin-Darby canine kidney (MDCK) cells, the majority of BACE is sorted to the apical domain. Interestingly it has been shown previously that the substrate of BACE, beta-APP is transported to the basolateral surface of MCDK cells. Therefore, substantial amounts of BACE are targeted away from beta-APP to a non-amyloidogenic compartment, a cellular mechanism that limits A-beta generation. Upon deletion of the basolateral sorting signal of beta-APP, apically missorted beta-APP is processed by BACE. The differential targeting of BACE and its substrate beta-APP suggest that beta-APP might not be the major physiological substrate of BACE.
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Magnatti, Giorgia. "Discovery of BACE-1 inhibitors using an integrated computational and experimental approach." Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/8344/.

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There are numerous complementary approaches to facilitate the identification of novel inhibitors for biological targets, including high throughput screening and fragment-based drug discovery. Computational tools are often employed to predict binding pose and affinity of the new inhibitors. In this thesis an integrated computational and experimental approach to identify novel inhibitors is described. The approach involves the design of a virtual library of likely synthetically accessible lead-like molecules, followed by virtual high throughput screening (vHTS) against target protein. To exemplify the approach, BACE-1 was selected as an example target protein. BACE-1 is responsible for the formation of amyloidal plaque in brains affected by Alzheimer’s disease and therefore is a potential target for the treatment of the disease. A virtual library of lead-like molecules was generated based on diversity-oriented synthesis methods established in our laboratory. The library underwent virtual high throughput screening (vHTS) against BACE-1 by using eHiTS and two families of putative inhibitors were identified with high predicted ligand efficiency (cLE). The in silico approach employed to identify novel putative BACE-1 inhibitors is schematically represented as follows. [Unable to display image from abstract] A focused library based on the selected putative inhibitors was designed and synthesised, and biological activity was assessed via a fluorimetric assay. Structure-activity relationship (SAR) studies were conducted to rationalise the activity of the inhibitors and to confirm the validity of the integrated approach in identifying new inhibitors for biological targets. A novel series of BACE-1 inhibitors was identified and is herein described.
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Books on the topic "BACE"

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John, Varghese, ed. BACE. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470594087.

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Fagge, Sa'adatu Baba Ahmad. Kishiya ba laifi bace. Nigeria: s.n., 2001.

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Jo bace ḥain̲ sang--. Lāhaur: Sang-i Mīl Pablīkeshanz, 2007.

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Fagge, Sa'adatu Baba Ahmad. Kishiya ba laifi bace. [Nigeria: s.n., 2001.

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Fagge, Sa'adatu Baba Ahmad. Kishiya ba laifi bace: Littafi na daya. [Nigeria: s.n.], 2001.

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Jo bace hain̲ sang sameṭ lo: Nāvliṭ. Naʼī Dihlī: Nāvilistān, 1990.

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Mahdī, Ṣug̲h̲rā. Jo bace hain̲ sang sameṭ lo: Nāvliṭ. Naʾī Dihlī: Nāvilistān, 1990.

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Tanejā, Komala. Bace vyañjanoṃ se bane nae vyañjana =: Makeover for leftover. Naī Dillī: Fusion Books, 2008.

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Doppelhofer, Gernot. Determinants of long-term growth: A Bayesian averaging of classical estimates (BACE) approach. Cambridge, MA: National Bureau of Economic Research, 2000.

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Wo ai Bahe: Bahe gang qin tan zou dao du = I love Bach. Shanghai: Shanghai yin yue chu ban she, 2004.

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Book chapters on the topic "BACE"

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Wyss, Daniel F., Jared N. Cumming, Corey O. Strickland, and Andrew W. Stamford. "BACE Inhibitors." In Fragment-based Drug Discovery Lessons and Outlook, 327–54. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2016. http://dx.doi.org/10.1002/9783527683604.ch14.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, N. Melnichenko-Koblyuk, et al. "BaCe[CO3]2F." In Structure Types. Part 5: Space Groups (173) P63 - (166) R-3m, 757. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46933-9_624.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, N. Melnichenko-Koblyuk, et al. "BaCe[CO3]2F." In Landolt-Börnstein - Group III Condensed Matter, 771. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-44752-8_654.

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Roßner, S., and S. F. Lichtenthaler. "Alzheimer's Disease BACE Proteases." In Handbook of Neurochemistry and Molecular Neurobiology, 261–84. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-32671-9_11.

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Paz, Odailson Santos, Thamires Quadros Froes, Franco Henrique Leite, and Marcelo Santos Castilho. "Modeling of BACE-1 Inhibitors as Anti-Alzheimer’s Agents." In Neuromethods, 177–206. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7404-7_7.

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Sinha, Sukanto. "BACE: A (Almost) Perfect Target for Staving off Alzheimer's Disease." In Aspartic Acid Proteases as Therapeutic Targets, 391–412. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527630943.ch14.

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Bhattacharjee, Atanu, Raja Chakraborty, and Saikat Sen. "Plant-Based β-Secretase (BACE-1) Inhibitors: A Mechanistic Approach to Encounter Alzheimer’s Disorder." In Evidence Based Validation of Traditional Medicines, 163–75. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-8127-4_8.

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Bowman, Gregory R. "A Tutorial on Building Markov State Models with MSMBuilder and Coarse-Graining Them with BACE." In Protein Dynamics, 141–58. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-658-0_8.

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Fretheim, B. Solveig. "Back to Bach." In Narratives and Reflections in Music Education, 237–54. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-28707-8_18.

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Wyss, Daniel F., Yu-Sen Wang, Hugh L. Eaton, Corey Strickland, Johannes H. Voigt, Zhaoning Zhu, and Andrew W. Stamford. "Combining NMR and X-ray Crystallography in Fragment-Based Drug Discovery: Discovery of Highly Potent and Selective BACE-1 Inhibitors." In Topics in Current Chemistry, 83–114. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/128_2011_183.

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Conference papers on the topic "BACE"

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LU, JINLING, JIE YANG, SHAOQUN ZENG, and ZHIHONG ZHANG. "DETECTION OF BACE CLEAVAGE IN THE SECRETARY PATHWAY." In Proceedings of the 6th International Conference on Photonics and Imaging in Biology and Medicine (PIBM 2007). WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812832344_0037.

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Vannucchi, S., F. Pasquali, P. Bianchi-ni, and M. Ruggiero. "BINDING AND METABOLISM OF HEPARIN BY ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644187.

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In this study we show that bovineadrenal capillary endothelial cells(BACE) contain heparin (HP); this HP has been found associated with the cell surface (i.e; trypsin-removable^and intracellularly. How-ever, experiments with [ sjsodium sulfate labelling, demonstrate that BACE cells donot synthesize HP de novo, but they uptake it from serum. We have studied binding, uptake, and metabolism odifferent molecular weight-HPs: 13 Kd-HP from bovine source, 14 Kd-HP from porcine source, 4.5 Kd, and 2.5-HP fragments. Comparison among different HPs, was carried out by calculating the IC from competition curves for [3HJ- HP. Binding of labelled-HP to BACE cells was specificand saturable. Dextran sulfate and glycosaminoglycans did not compete for binding; only heparan sulfate showed some competition. Binding of different HPs was strictly dependent on their molecular weight; 2.5 Kd- HP was unable to bind to cells, although sulfation degree of this fragment and of unfractionated HP was almost identical. Therefore, we assume that a specific oligosaccharide sequence could be responsible for HP binding to BACE cells; this hypothetical "binding sequence" could then be lost in very low molecular weight-HP fragments. BACE cells are also able to internalize HP, and they release its low molecular weight degradation products into culture medium. Thus we suggest that endothelial cells might represent a site for the metabolism of endogenous and exogenous HP in vivo.
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Kumar, Akhil, Gaurava Srivastava, and Ashok Sharma. "In silico interaction studies of first dual inhibitor against BACE-1/GSK-3β." In 2016 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2016. http://dx.doi.org/10.1109/bsb.2016.7552161.

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Shao, Zhiwei. "Investment Trend and Influential Factors Research in Xiran Real Estate Development - Based on BACE." In 2018 6th International Conference on Machinery, Materials and Computing Technology (ICMMCT 2018). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/icmmct-18.2018.69.

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Zambello Palumbo, Lissa, WANDA PEREIRA ALMEIDA, and Renata Parruca Sakata. "Síntese, caracterização e avaliação de 2’-aminochalconas como inibidores da β-secretase (BACE-1)." In XXV Congresso de Iniciação Cientifica da Unicamp. Campinas - SP, Brazil: Galoa, 2017. http://dx.doi.org/10.19146/pibic-2017-78531.

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Smith, Emily F., Mary C. Lonsdale, Lyle L. Nelson, Anne-sofie Ahm, Eben B. Hodgin, Lucy C. Webb, Uyanga Bold, et al. "ALL ABOUT THAT BACE: INTERPRETING THE CARBON ISOTOPE RECORD OF THE EDIACARAN–CAMBRIAN TRANSITION." In GSA 2020 Connects Online. Geological Society of America, 2020. http://dx.doi.org/10.1130/abs/2020am-356511.

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Vermeersch, Kristina, Maria Gabrovska, Joseph Aumann, Ingel K. Demedts, Jean-Louis Corhay, Eric Marchand, Hans Slabbynck, et al. "Late Breaking Abstract - Azithromycin for acute COPD exacerbations requiring hospitalization – the BACE trial results." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa1654.

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Suthaharan, Sivanujan. "3-APS against BACE-1 target in Alzheimer’s disease; DFT calculations and molecular docking." In 7th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11444.

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Garrocho, Charles Tim Batista, Karine Nogueira Oliveira, David Jose Sena, Carlos Frederico Marcelo da Cunha Cavalcanti, and Ricardo Augusto Rabelo Oliveira. "BACE: Blockchain-based Access Control at the Edge for Industrial Control Devices of Industry 4.0." In 2021 XI Brazilian Symposium on Computing Systems Engineering (SBESC). IEEE, 2021. http://dx.doi.org/10.1109/sbesc53686.2021.9628291.

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Gosoi, Dipshikha, Ratul Saikia, Jatin Kalita, Rasana Paul, Devo Kanta Pegu, Subrata Sinha, and Surabhi Johari. "Combining Virtual Screening, Molecular Docking and Simulation studies towards the discovery of β-secretase (BACE) inhibitors." In 2018 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2018. http://dx.doi.org/10.1109/bsb.2018.8770645.

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Reports on the topic "BACE"

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Doppelhofer, Gernot, Ronald Miller, and Xavier Sala-i-Martin. Determinants of Long-Term Growth: A Bayesian Averaging of Classical Estimates (BACE) Approach. Cambridge, MA: National Bureau of Economic Research, June 2000. http://dx.doi.org/10.3386/w7750.

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GEORGIA INST OF TECH ATLANTA. Next Generation Bare Base Waste Processing System (Phase 1). Fort Belvoir, VA: Defense Technical Information Center, August 1997. http://dx.doi.org/10.21236/ada583029.

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Bergantz, Joseph L. Getting the U.S. Defense Technology Base Back on Track. Fort Belvoir, VA: Defense Technical Information Center, March 1992. http://dx.doi.org/10.21236/ada249828.

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Wager, Vic, and III. Bare Base Equipment and Support of the Expeditionary Air Force. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada424751.

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SECRETARY OF THE AIR FORCE WASHINGTON DC. Guide To Bare Base Development - Air Force Handbook 10-222, Volume 1. Fort Belvoir, VA: Defense Technical Information Center, July 1996. http://dx.doi.org/10.21236/ada423947.

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SECRETARY OF THE AIR FORCE WASHINGTON DC. Guide To Bare Base Assets - Air Force Handbook 10-222, Volume 2. Fort Belvoir, VA: Defense Technical Information Center, December 1996. http://dx.doi.org/10.21236/ada423969.

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Trautmann, Jr, and William D. Designing Bare Base Systems for Logistics Efficiency in the Joint Operational Environment. Fort Belvoir, VA: Defense Technical Information Center, December 2007. http://dx.doi.org/10.21236/ada476277.

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Maglin, Mark P. Back to the Future: Staying Power and Operational Protection of the Sea Base. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada426042.

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SECRETARY OF THE AIR FORCE WASHINGTON DC. Guide To Bare Base Facility Erection - Air Force Handbook 10-222, Volume 6. Fort Belvoir, VA: Defense Technical Information Center, April 1999. http://dx.doi.org/10.21236/ada423974.

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SECRETARY OF THE AIR FORCE WASHINGTON DC. Guide To Bare Base Power Plant Installation - Air Force Handbook 10-222, Volume 5. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/ada423972.

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