Relevant bibliographies by topics / Alpha-secretases

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Alpha-secretases'

Author: Grafiati
Published: 25 May 2024
Last updated: 31 July 2025

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Journal articles on the topic "Alpha-secretases"

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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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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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Mezyk, Renata, Monika Bzowska, and Joanna Bereta. "Structure and functions of tumor necrosis factor-alpha converting enzyme." Acta Biochimica Polonica 50, no. 3 (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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Saha, Nayanendu, Eric Chan, Rachelle P. Mendoza, Yevgeniy Romin, Murray J. Tipping, and Dimitar B. Nikolov. "Antibodies targeting ADAM17 reverse neurite outgrowth inhibition by myelin-associated inhibitors." Life Science Alliance 8, no. 6 (2025): e202403126. https://doi.org/10.26508/lsa.202403126.

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Upon spinal cord injury, axons attempting to regenerate need to overcome the repulsive actions of myelin-associated inhibitors, including the myelin-associated glycoprotein, Nogo-A, and the oligodendrocyte myelin glycoprotein. These inhibitors bind and signal through a neuronal receptor/co-receptor/transducer complex composed of NgR1, Lingo-1, and p75. Consequently, p75 is cleaved by alpha secretase followed by gamma-secretase, triggering downstream signaling that inhibits axonal regrowth. ADAM10 and ADAM17 are both known to function as alpha secretases in neurons. Here we show that ADAM17, an
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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 (2017): 833–38. http://dx.doi.org/10.1016/j.bbrc.2017.01.184.

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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 (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
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Manav, Kumar 1. Alok Kumar1 Kajal Kumari1 Priyanka Kumari1 Shweta Kumari1 Divya Roshni Panna1 Suman Kumari1 Bina Kumari1 Sapna Kumari1 Anuradha Kumari1 Asfaque Ali1 Najibullah Mujahid 1. Laxman Kumar Mahto1 Maheshwar Kumar1 Saurav Kumar1 Ved Prakash Singh1 Soyab Akhtar1 Arnab Roy2*. "A Detailed Analysis Of Alzheimer's Disease Pathophysiology: The Influence Of Oxidative Stress On Amyloid Precursor Protein Metabolism And Secretase Activity." International Journal in Pharmaceutical Sciences 2, no. 9 (2024): 439–57. https://doi.org/10.5281/zenodo.13732112.

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Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by cognitive decline, memory impairment, and distinct neuropathological features such as amyloid-beta (Aβ) plaques and neurofibrillary tangles. Despite extensive research, the molecular mechanisms underlying AD remain incompletely understood, posing challenges for therapeutic intervention. This review delves into the intricate processes of amyloid precursor protein (APP) processing, focusing on the roles of α-, β-, and γ-secretases in the generation of neurotoxic Aβ peptides. We explore th
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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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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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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 (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 ortho
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Dissertations / Theses on the topic "Alpha-secretases"

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Cochet, Maud. "Implication du complexe récepteur 5-HT4/APP/ADAM10 dans la voie non-amyloïdogénique de la maladie d’Alzheimer." Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON1T005.

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En plus d'être clivée par les β- et les γ-sécrétases lors du processus amyloïdogénique de la maladie d'Alzheimer, l'APP (Amyloid Precursor Protein) peut également subir un clivage grâce à l'α-sécrétase qui conduit à la libération des fragments d'APP soluble α (sAPPα)(voie non-amyloïdogénique) prévenant ainsi l'accumulation des peptides β-amyloïdes pathogènes. Les études sur le clivage de l'APP par l'α-sécrétase ont montré que l'activité de cette enzyme était constitutive mais aussi régulée. Lors de mon travail de thèse, nous avons montré que l'expression du récepteur de la sérotonine de type 4
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Padilla, Ferrer Aïda. "ADAM10 in myelination of the central nervous system : study of ADAM10 localization and development of an inducible oligodendroglial ADAM10 knock out (KOOLA10) mouse strain." Electronic Thesis or Diss., Université Paris Cité, 2022. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=4270&f=41801.

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Dans le système nerveux central (SNC), les oligodendrocytes (OL) enveloppent les axones de leurs prolongements membranaires formant ainsi les gaines de myéline. La mort des OL et la perte de myéline (démyélinisation) surviennent dans les maladies démyélinisantes telles que la sclérose en plaques, pour lesquelles il n'existe pas de traitement efficace. Notre objectif est de stimuler des processus de réparation endogène via la voie ADAM10/sAPPa. Le fragment soluble sAPPa est un peptide neuroprotecteur issu du clivage de la protéine précurseur de l'amyloïde (APP) par les a-secrétases de la famill
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Woodard-Grice, Alencia V. "Hyposialylation regulates [alpha]4[beta]1 integrin binding to VCAM-1." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/woodard.pdf.

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Book chapters on the topic "Alpha-secretases"

1

Anand, Abhinav, Neha Sharma, Monica Gulati, and Navneet Khurana. "Amyloid Beta." In Research Anthology on Diagnosing and Treating Neurocognitive Disorders. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-3441-0.ch001.

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Alzheimer's disease (AD), exhibiting accumulation of amyloid beta (Aβ) peptide as a foremost protagonist, is one of the top five causes of deaths. It is a neurodegenerative disorder (ND) that causes a progressive decline in memory and cognitive abilities. It is characterized by deposition of Aβ plaques and neurofibrillary tangles (NFTs) in the neurons, which in turn causes a decline in the brain acetylcholine levels. Aβ hypothesis is the most accepted hypothesis pertaining to the pathogenesis of AD. Amyloid Precursor Protein (APP) is constitutively present in brain and it is cleaved by three p
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Anand, Abhinav, Neha Sharma, Monica Gulati, and Navneet Khurana. "Amyloid Beta." In Advances in Medical Diagnosis, Treatment, and Care. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-5282-6.ch011.

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Alzheimer's disease (AD), exhibiting accumulation of amyloid beta (Aβ) peptide as a foremost protagonist, is one of the top five causes of deaths. It is a neurodegenerative disorder (ND) that causes a progressive decline in memory and cognitive abilities. It is characterized by deposition of Aβ plaques and neurofibrillary tangles (NFTs) in the neurons, which in turn causes a decline in the brain acetylcholine levels. Aβ hypothesis is the most accepted hypothesis pertaining to the pathogenesis of AD. Amyloid Precursor Protein (APP) is constitutively present in brain and it is cleaved by three p
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