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Dissertations / Theses on the topic 'Amyloid beta-protein precursor'

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Published: 4 June 2021

Last updated: 26 July 2024

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1

Dooley, Nora P. "Analysis of beta-amyloid precursor protein in Alzheimer's fibroblasts." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56982.

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One of the hallmarks of Alzheimer's disease is the accumulation of beta-amyloid protein in the core of neuritic plaques. This 38-40 amino acid polypeptide is derived from a larger precursor known as beta-amyloid precursor protein (BAPP). In this thesis the expression of this precursor in cultured human fibroblasts obtained from Alzheimer's patients and age-matched controls is examined at the mRNA and protein level. Using the technique of reverse transcriptase-polymerase chain reaction, human fibroblasts were found to express BAPP transcripts encoding 770, 751, 714, and 695 amino acids. In immu

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2

Stephens, David John. "Intracellular processing of the Alzheimer's #beta#-amyloid precursor protein." Thesis, St George's, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362427.

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3

Jung, Sonia Sun-Yung. "Expression and processing of the Alzheimer's beta-amyloid precursor protein." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0031/NQ64584.pdf.

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4

Jung, Sonia Sun-Yung 1968. "Expression and processing of the Alzheimer's beta-amyloid precursor protein." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36618.

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Alzheimer's disease (AD) is the most common neurodegenerative disease affecting the elderly. One of the main pathological hallmarks of AD is abundant senile plaques found in brain parenchyma and in the meningovasculature. The core of these senile plaques is predominantly composed of the 40--43 amino acid beta-amyloid (Abeta) peptide which arises from proteolytic cleavage of the beta-amyloid precursor protein (betaAPP), a glycoprotein with a predicted structure of a transmembrane protein. Most studies of betaAPP expression and processing have focused on cultured cell systems. Previously, our la

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5

Kim, Joung-Hun. "Electrophysiological and biochemical studies of #beta#-amyloid precursor protein fragments." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394383.

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6

Sultana, Joynab. "Behavioral Effects of Amyloid Precursor Protein beta Mutation in zebrafish." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-421155.

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Amyloid precursor protein beta (βAPP) plays an important role in the pathogenesis of Alzheimer’s disease. An appb mutant strain of zebrafish has been previously generated and has shown increased boldness. Here we tested boldness by Novel Tank Diving Test and compared the results between the wildtype AB strain controls (WT) (N=16) and appb mutant strain (N=28), as well as between two Swedish testing institutions that use different protocols. Fish were tracked by automated video tracking in Ethovision. Compared with the wild type fish, using both the Uppsala and Gothenburg protocols, the mutant

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7

Selivanova, Alexandra. "Intracellular dynamics of Alzheimer disease-related proteins /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-234-7/.

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8

Heuvel, Corinna van den. "Studies on upregulation of amyloid precursor protein in response to traumatic brain injury /." Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phv22723.pdf.

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9

Ly, Philip T. T. "Glycogen synthase kinase-3 signaling in Alzheimer's disease : regulation of beta-amyloid precursor protein processing and amyloid beta protein production." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42848.

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Glycogen synthase kinase 3 (GSK3) is a serine/threonine kinase that plays a part in a number of physiological processes ranging from glycogen metabolism to gene transcription. Recent studies indicated that GSK3 also involved in the formation of Alzheimer’s disease (AD) pathologies: neurofibrillary tangles and amyloid plaques. Neurofibrillary tangles develop when abnormal tau proteins accumulate inside neurons and form insoluble filaments, and amyloid plaques develop when the amyloid β protein (Aβ) accumulates in increasingly insoluble forms. The Aβ peptide is generated through sequential cleav

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10

Leutz, Steffen. "Neuronaler Zelltod bei der Alzheimer-Demenz : Einfluss von b-Amyloid [Beta-Amyloid] und Amyloid-precursor-Protein /." Aachen : Shaker, 2002. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=009735379&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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11

Nilsson, Tatjana. "Amyloid precursor protein: cellular studies and animal models /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-832-0/.

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12

Golde, Todd Eliot. "Analysis of the beta amyloid precursor protein mRNAs in Alzheimer's disease." Case Western Reserve University School of Graduate Studies / OhioLINK, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=case1056572599.

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13

Flood, Fiona. "Alzheimer's disease-related amyloid precursor protein and presenilin genes : normal function and pathophysiology /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-050-8/.

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14

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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15

Andrew, Robert. "Differential proteolysis of the amyloid precursor protein isoforms : the role of cellular location and protein-protein interactions." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/differential-proteolysis-of-the-amyloid-precursor-protein-isoforms-the-role-of-cellular-location-and-proteinprotein-interactions(5390e8fa-fc5e-4357-8109-cb2bb1c49212).html.

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Dementia, the most common cause of which is Alzheimer's disease (AD), currently affects 850,000 people in the UK, a figure set to rise to over 1 million by 2025. There is currently no disease modifying therapy available to slow or halt this progressive disease. Current understanding of AD implicates the neurotoxic amyloid-β (Aβ) peptide as the primary initiator in a cascade of events leading to the neuronal cell death and brain atrophy associated with the disease. Therefore, inhibiting the production or enhancing the clearance of Aβ within the brain has become a major target for the production

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16

Wilcock, Donna Marie. "Mechanisms of [beta]-amyloid clearance by anti-a[beta] antibody therapy." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0001169.

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17

Palmert, Mark Raney. "The beta amyloid protein precursor of Alzheimer's disease: Analysis of mRNAs and protein products." Case Western Reserve University School of Graduate Studies / OhioLINK, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=case1054920188.

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18

Lu, Daniel C. "Intracytoplasmic caspase cleavage of [beta]-amyloid precursor protein : implications for Alzheimer's disease /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3022210.

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19

Kirouac, Lisa. "The Concerted Regulation of Intracellular Signaling by Amyloid Precursor Protein and Aβ Peptide". Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6278.

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It is widely accepted that A-beta (Aβ) generated from amyloid precursor protein (APP) oligomerizes and fibrillizes to form neuritic plaques in the Alzheimer’s disease (AD) brain, yet little is known about the contribution of APP preceding AD pathogenesis. Our data presented here suggest that APP has a functional role in cell cycle regulation and proliferation. First, we demonstrat that APP is pathologically phosphorylated at Thr668 and that P-APP localizes to the centrosomes. Furthermore, P-APP is proteolytically processed in a cell cycle -dependent manner to generate its pathogenic metabolite

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20

Ostrowski, Stephen M. "Pleiotropic mechanisms of statin action in Alzheimer's Disease." Cleveland, Ohio : Case Western Reserve University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1190669698.

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21

Taylor, Chanel Jayne, and n/a. "Secreted amyloid precursor protein-alpha modulates hippocampal long-term potentiation, in vivo." University of Otago. Department of Psychology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20081217.144344.

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Alzheimer�s disease (AD) is a neurodegenerative disorder, charaeterised by progressive loss of memory. It is important to understand what factors initiate the onset of AD so that effective therapeutic treatments can be developed to target the precise mechanisms that initiate this disease. Currently, synaptic dysfunction is widely believed to be the first significant alteration preceding the onset of AD, and is thought to be initiated by an intracellular accumulation of amyloid-β (Aβ), or a free radical-induced increase of oxidative stress. As Aβ levels rise during the onset of AD, a concomitan

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22

Ting, Jonathan T. "Molecular mechanisms of synapse dysfunction : modeling neurological disease by viral-mediated protein overexpression in mammalian CNS neurons /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/10671.

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23

Pasternack, Jennifer Martine. "The Alzheimer's disease beta amyloid protein precursor: Analysis of the carboxyl terminus of its soluble derivatives." Case Western Reserve University School of Graduate Studies / OhioLINK, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=case1060094123.

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24

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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25

Rijal, Upadhaya Ajeet [Verfasser]. "Analysis of Amyloid beta (Aβ) protein in Amyloid precursor protein (APP) transgenic mouse models of Alzheimer’s disease (AD) and in human brains / Ajeet Rijal Upadhaya". Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1025715012/34.

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26

Li, Xiaoman. "Study on memapsin 2 cleavage properties and its interacting proteins." Oklahoma City : [s.n.], 2010.

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27

Herber, Donna Lorraine. "Neuroinflammation in Alzheimers disease : characterization and modification of the response of transgenic mice to intrahippocampal lipopolysaccharide administration /." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0001075.

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28

Lebson, Lori Ann. "Monocytes as gene therapy vectors for the treatment of Alzheimer's disease." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002793.

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29

Zhang, Shuting. "The effect of FAD-associated mutations in amyloid-beta precursor protein and presenilin-1 genes on Alzheimer’s disease pathogenesis." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44983.

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Pathogenic mutations in amyloid-β precursor protein (APP) and presenilins (PS) genes cause familial Alzheimer’s disease (FAD). FAD is an uncommon form of Alzheimer’s disease (AD) with early onset (before age 65) and a rapid progression but its neuropathology is indistinguishable from the sporadic AD. Amyloid plaque is the unique hallmark of AD, which consists primarily of 40- and 42-residue amyloid β protein (Aβ40 and Aβ42) with the more hydrophobic Aβ42 as its major component. Aβ is derived from APP through sequential cleavages by β-secretase and γ-secretase. According to the “Amyloid

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30

Vrotsos, Emmanuel George. "MCP-1 and APP involvement in glial differentiation and migration of neuroprogenitor cells." Orlando, Fla. : University of Central Florida, 2009. http://purl.fcla.edu/fcla/etd/CFE0002517.

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31

Wu, Jinfang. "Alzheimer's disease (AD) like pathology following developmental lead exposure in primates and the role of aging in AD-related genes regulation in rodents and primates /." View online ; access limited to URI, 2008. http://0-digitalcommons.uri.edu.helin.uri.edu/dissertations/AAI3314462.

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32

Xu, Guilian. "Some studies on the cholinergic and somatostatinergic systems in the brain of mouse alzheimer models with transgenes for amyloid precursor protein (APP) and presenilin." Hong Kong : University of HOng Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23540400.

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33

Ouellet, Stéphane. "Études des mécanismes de régulation de la transcription des gènes humains P21CIP1/WAF1, GPC3 (GLYPICAN 3) et A-beta-PP (AMYLOID beta-PRECURSOR PROTEIN)." Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27537/27537.pdf.

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La connaissance des mécanismes qui contrôlent la transcription des gènes, comme l’interaction de facteurs protéiques au niveau des promoteurs, est essentielle pour comprendre plusieurs fonctions biologiques et espérer traiter certaines pathologies. Nous nous sommes attardés à mieux comprendre les mécanismes qui régulent trois gènes humains dont les patrons d’expression sont différents et qui sont impliqués dans diverses pathologies en tentant de mettre en parallèle les différences structurales et fonctionnelles entre ceux-ci. Les gènes AβPP et p21 sont exprimés chez l’adulte alors que GPC3 est

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34

THERIN, SEBASTIEN. "USE OF A CELL PERMEABLE PEPTIDE TO MODULATE ADAM10 SYNAPTIC LOCALIZATION AND ACTIVITY IN A MOUSE MODEL OF ALZHEIMER'S DISEASE." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/649095.

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Alzheimer’s disease (AD) is characterized by the aggregation of amyloid beta peptide (Aβ). Aβ derives from the amyloid precursor protein (APP), which can undergo two mutually exclusive pathways. The amyloidogenic pathway involves BACE and γ-secretase activities and leads to Aβ formation. While, the non-amyloidogenic pathway involves ADAM10, a disintegrin and metalloproteinase 10, which cleaves APP within the domain corresponding to Aβ, thus precluding Aβ production. Recently, we identified a new ADAM10 binding partner, named AP2, which is responsible for ADAM10 internalization, therefore affec

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35

Kyriazis, George A. "The endocytic protein Numb regulates APP metabolism and Notch signaling implications for Alzheimer's disease /." Orlando, Fla. : University of Central Florida, 2008. http://purl.fcla.edu/fcla/etd/CFE0002233.

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36

Nilsberth, Camilla. "Distribution and pathophysiological role of amyloid precursor protein and presenilin 1 : characterization in rats and in vitro studies on the pathogenic arctic mutation /." Stockholm : Karolinska Univ. Press, 2002. http://diss.kib.ki.se/2002/91-7349-329-5/.

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37

Jefferson, Tamara [Verfasser]. "Molecular interaction of the human metalloprotease meprin beta with the amyloid precursor protein, ADAM10, and ADAM17 based on proteomics / Tamara Jefferson." Mainz : Universitätsbibliothek Mainz, 2011. http://d-nb.info/1018183647/34.

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38

Fisher, Linda. "Inflammatory cytokines and NFkB in Alzheimer's disease /." Stockholm : Department of Neurochemistry, Stockholm University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-990.

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39

Smotherman, Jesse M. "The Impact of Causative Genes on Neuropsychological Functioning in Familial Early-Onset Alzheimer's Disease: A Meta-Analysis." Thesis, University of North Texas, 2017. https://digital.library.unt.edu/ark:/67531/metadc984161/.

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Mutations of three genes encoding amyloid precursor protein (APP), presenilin-1 (PSEN1), and presenilin-2 (PSEN2) have been shown to reliably result in familial early-onset Alzheimer's disease (FAD); a rare, but catastrophic, subtype of Alzheimer's disease (AD) marked by symptom emergence before age 65 as well as accelerated cognitive deterioration. The current study represents the first known meta-analysis on the association of APP, PSEN1 or PSEN2 on neurocognitive variables. A total of 278 FAD mutation-carriers (FAD-MC) and 284 cognitively healthy non-mutation-carriers (NC) across 10 indepen

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40

Linning, Philipp, Ute Haussmann, Isaak Beyer, Sebastian Weidlich, Heinke Schieb, Jens Wiltfang, Hans-Wolfgang Klafki, and Hans-Joachim Knölker. "Optimisation of BACE1 inhibition of tripartite structures by modification of membrane anchors, spacers and pharmacophores – development of potential agents for the treatment of Alzheimer's disease." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-138993.

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Systematic variation of membrane anchor, spacer and pharmacophore building blocks leads to an optimisation of the inhibitory effect of tripartite structures towards BACE1-induced cleavage of the amyloid precursor protein (APP)<br>Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich

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41

Itkin, Anna. "Multidisniplinary study of Alzheimer's disease-related peptides : from amyloid precursor protein (APP) to amyloid β-oligomers and γ-secretase modulators". Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAF051/document.

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Une des caractéristiques histopathologiques de la maladie d'Alzheimer (AD) est la présence de plaques amyloïdes formées par les peptides amyloïdes β (Aβ) de 40 et 42 résidus, qui sont les produits de clivage par des protéases de l'APP. Afin de comprendre le rôle des variations structurelles du TM dans le traitement de l'APP, les peptides APP_TM4K ont été étudiés dans la bicouche lipidique en utilisant l’ATR-FTIR et ssNMR. Tandis que la structure secondaire globale du peptide APP_TM4K est hélicoidale, hétérogénéité de conformation et d'orientation a été observée pour le site de clivage γ et ,

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42

Linning, Philipp, Ute Haussmann, Isaak Beyer, Sebastian Weidlich, Heinke Schieb, Jens Wiltfang, Hans-Wolfgang Klafki, and Hans-Joachim Knölker. "Optimisation of BACE1 inhibition of tripartite structures by modification of membrane anchors, spacers and pharmacophores – development of potential agents for the treatment of Alzheimer's disease." Royal Society of Chemistry, 2012. https://tud.qucosa.de/id/qucosa%3A27800.

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Systematic variation of membrane anchor, spacer and pharmacophore building blocks leads to an optimisation of the inhibitory effect of tripartite structures towards BACE1-induced cleavage of the amyloid precursor protein (APP).<br>Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

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43

許瑰蓮 and Guilian Xu. "Some studies on the cholinergic and somatostatinergic systems in the brain of mouse alzheimer models with transgenes for amyloid precursorprotein (APP) and presenilin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31242534.

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44

Ill-Raga, Gerard. "Study of the pathophysiological role of nitric oxide and nitrative stress in brain: translational effects on the cleavage of the amyloid precursor protein in Alzheimer's disease and post-translational effects on fibrinogen in brain ischemia." Doctoral thesis, Universitat Pompeu Fabra, 2010. http://hdl.handle.net/10803/31907.

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Nitric oxide (NO) is a neurotransmitter involved in memory processes. Currently, the only recognized physiological signalling pathway controlled by NO is the activation of guanylyl cyclase. In this thesis, we propose an alternative NO-signalling pathway that involves the Heme-regulated eukaryotic initiation factor-2a kinase (HRI) and eIF2a phosphorylation. We have found that the enzyme BACE1, a key protein in Alzheimer’s disease (AD), is controlled by this novel pathway. This pathway would be involved in the physiology of memory formation and learning processes. We have also studied how

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45

MAROLDA, ROBERTA. "Effetto antiamiloidogenico della Sostanza P in un modello apoptotico di granuli cerebellari: possibili implicazioni nella patologia di Alzheimer." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/209099.

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La Sostanza P (SP) è un neuropeptide di 11 aminoacidi, membro della famiglia delle tachichinine, ampiamente distribuita nel sistema nervoso centrale ed ha un ruolo funzionale sia in condizioni fisiologiche che patologiche, tra le quali le malattie neurodegenerative (Raffa, 1998; Severini et al., 2002). Alterati livelli di SP sono stati riscontrati nelle regioni corticali di tessuti cerebrali di pazienti malati di Alzheimer (AD) (Quigley and Kowall, 1991; Waters and Davis, 1997). Recentemente, è anche stata riportata una riduzione della SP nella corteccia cerebrale, nell’ippocampo, nei gangli b

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46

Arano, Rodriguez Ivan. "Rab Proteins and Alzheimer's: A Current Review of Their Involvement in Amyloid Beta Generation with Focus on Rab10 Expression in N2A-695 Cells." BYU ScholarsArchive, 2015. https://scholarsarchive.byu.edu/etd/5648.

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This thesis work describes the role of Rab proteins in amyloid processing and clearance in different cell pathways. It also describes an experimental approach used to analyze the expression effects of Rab10 in amyloid beta production. Since the main theory behind neurodegeneration in Alzheimer's disease claims that high levels of amyloid beta 42 (Aβ42) molecules trigger widespread neuronal death, control of Aβ42 has been a main target in Alzheimer's disease research. In addition, several studies show increased levels of particular Rab proteins in Alzheimer's pathogenesis. However, no review co

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47

Mora, García Natalia. "Analisis de la expresión y la función del gen beta-amyloid protein precursor like en relación a la vía de RasI en el disco imaginal de ojo de Drosophila melanogaster." Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/104149.

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Drosophila es un modelo versátil para entender las bases genéticas de la señalización celular. En particular, el ojo compuesto de Drosophila proporciona un tejido ideal para estudiar los mecanismos de integración de señales que dirigen la formación de la red de neuronas fotorreceptoras. La vía de Ras/MAPK está involucrada en la determinación de todos los fotorreceptores, pero es particularmente necesaria para la especificación del fotorreceptor R7, ya que su ausencia determina la transformación del R7 en una célula no neural. De manera que durante el desarrollo del ojo, Ras media la decisión

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48

Pavoni, Serena. "Mise au point d’un nouveau modèle d’organoïde cérébral humain pour l’étude des mécanismes d’interaction de la protéine prion et de l’amyloïde β". Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS427.

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Les mécanismes de type prion sont désormais reconnus comme sous-tendant la plupart des maladies neurodégénératives humaines, avec en premier lieu la maladie d’Alzheimer (MA) au niveau de ses 2 marqueurs spécifiques, l’amyloïde β (Aβ à l’origine de l’hypothèse étiopathogénique de la cascade amyloïde) et la protéine Tau phosphorylée. Par ailleurs la protéine du prion (PrPC) est décrite comme interagissant à de multiples niveaux avec le métabolisme de l’Aβ sans que les mécanismes physiopathologiques sous-jacents n’aient pu être expliqués. Pour sortir de l’impasse actuelle concernant le développem

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49

Fiorelli, Tina N. "Proteolytic Processing of the Amyloid Precursor Protein During Apoptosis and Cell Cycle: Implications for Alzheimer's Disease." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4486.

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Alzheimer's disease is characterized by the presence of amyloid plaques, made up primarily of Aϐ peptides, and neurofibrillary tangles, containing hyperphosphorylated tau. Aϐ is generated by sequential proteolysis of the amyloid precursor protein (APP) by beta and gamma secretases. The leading hypothesis of Alzheimer's disease pathogenesis is the amyloid cascade hypothesis, which suggests that amyloid is central to the disease process. However, tau pathology correlates more closely with cognitive dysfunction and follows a predictable anatomical course through the brain. We hypothesize that if

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50

Guix, Ràfols Francesc Xavier. "Study of the pathophysiological role of nitric oxide on the amyloid-induced toxicity attending to the biochemical modifications and cellular damages." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7162.

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Aquesta tesi demostra que el peroxinitrit produït com a conseqüència del pèptid beta-amiloide (A) contribueix l'augment de la relació A42/A40 que ocorre a la malaltia d'Alzheimer. L'A42 contribueix a l'aparició de la malaltia degut a la seva major toxicitat (quan es compara amb l'A40) que resulta d'una gran estabilitat i capacitat agregativa. A més el peroxinitrit incrementa la toxicitat d'aquest degut a què potencia la seva agregació en forma d'oligomers altament tòxics. De fet els oligomers formats de nitro-A42 presenten una major toxicitat que

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