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Relevant bibliographies by topics / Cholinesterase; Alzheimer's disease

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Academic literature on the topic 'Cholinesterase; Alzheimer's disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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Journal articles on the topic "Cholinesterase; Alzheimer's disease"

1

Stahl, Stephen M. "Cholinesterase Inhibitors for Alzheimer's Disease." Hospital Practice 33, no. 11 (November 15, 1998): 131–36. http://dx.doi.org/10.3810/hp.1998.11.117.

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Finucane, Thomas E. "Cholinesterase inhibitors for Alzheimer's disease." Lancet 360, no. 9342 (October 2002): 1332. http://dx.doi.org/10.1016/s0140-6736(02)11328-6.

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Schneider, Lon S. "Cholinesterase inhibitors for Alzheimer's disease." Lancet 360, no. 9342 (October 2002): 1332–33. http://dx.doi.org/10.1016/s0140-6736(02)11329-8.

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Bullock, Roger. "Cholinesterase inhibitors in Alzheimer's disease." Human Psychopharmacology: Clinical and Experimental 16, no. 4 (2001): 360. http://dx.doi.org/10.1002/hup.281.

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Euba, Rafael. "Cholinesterase inhibitors and Alzheimer's disease." Psychiatric Bulletin 30, no. 2 (February 2006): 76. http://dx.doi.org/10.1192/pb.30.2.76-a.

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GIACOBINI, EZIO. "Cholinesterase Inhibitors Stabilize Alzheimer's Disease." Annals of the New York Academy of Sciences 920, no. 1 (January 25, 2006): 321–27. http://dx.doi.org/10.1111/j.1749-6632.2000.tb06942.x.

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Davis, Kenneth L. "Cholinesterase Inhibitors in Alzheimer's Disease." Neuropsychopharmacology 11, no. 4 (December 1994): 258. http://dx.doi.org/10.1038/sj.npp.1380115.

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Monacelli, Fiammetta, and Gianmarco Rosa. "Cholinesterase Inhibitors: Cardioprotection in Alzheimer's Disease." Journal of Alzheimer's Disease 42, no. 4 (October 10, 2014): 1071–77. http://dx.doi.org/10.3233/jad-141089.

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Hosoi, Misa, Koji Hori, Kimiko Konishi, Masayuki Tani, Hiroi Tomioka, Yuka Kitajima, Norihisa Akashi, et al. "Plasma Cholinesterase Activity in Alzheimer's Disease." Neurodegenerative Diseases 15, no. 3 (2015): 188–90. http://dx.doi.org/10.1159/000381532.

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Garcia, A., K. Thompson, K. Zanibbi, S. Geick, and R. Adams. "CHOLINESTERASE INHIBITORS AND ALZHEIMER'S DISEASE OUTCOMES." Journals of Gerontology Series A: Biological Sciences and Medical Sciences 62, no. 5 (May 1, 2007): 570. http://dx.doi.org/10.1093/gerona/62.5.570.

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Dissertations / Theses on the topic "Cholinesterase; Alzheimer's disease"

1

Giles, Kurt. "Post-translational modifications of acetylcholinesterase." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260127.

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Yau, Kenneth Kwok-Chi. "Assessing and predicting treatment responses to cholinesterase inhibitor pharmacotherapy in Alzheimer's disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0015/MQ54172.pdf.

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Connelly, Stephen. "Studies on pyroglutamyl carboxyl peptidase enzymes and cholinesterase inhibitors : implications for Alzheimer's disease." Thesis, University of Exeter, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430098.

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Spowart-Manning, Laura. "The evaluation of behavioural tasks and animal models of Alzheimer's disease for assessing putative cognition enhancers, using a cholinesterase inhibitor as reference compound." Thesis, University of Bristol, 2001. http://hdl.handle.net/1983/09e768fe-f64c-47c0-b4d4-d0a19b8ff23d.

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Foka, Germaine Boulenoue. "Synthesis and evaluation of novel coumarin-donepezil derivatives as dual acting monoamine oxidase B and cholinesterase in Alzheimer's disease." University of the Western Cape, 2016. http://hdl.handle.net/11394/5549.

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Magister Pharmaceuticae - MPharm
Alzheimer's disease is a progressive neurodegenerative disease characterised by low acetylcholine (ACh) levels in the hippocampus and cortex of the brain, causing symptoms like progressive memory loss, decline in language skills and other cognitive impairments to occur. The hallmarks of AD include the presence of extracellular insoluble amyloid beta plaques, intracellular neurofibrillary tangles, and the decrease in ACh concentration. The pathophysiology of AD is not well understood, however, acetylcholinesterase (AChE), butyrylcholinesterase (BuChE) and monoamine oxidases (MAO) are conspicuous role players in AD pathogenesis. Based on the cholinergic hypothesis, the AChE inhibitor donepezil was developed and has been used effectively clinically in the management of AD, with minimal side effects. Studies regarding the binding interactions of donepezil with AChE has shown that the benzyl-piperidine moiety of this compound shows substantial binding interactions at the CAS site of AChE where it blocks AChE activity. Coumarin is a compound of natural source that has shown some MAO inhibitory activity. Further studies done to clarify the potential of coumarin as a drug against AD has shown that coumarin has the capacity to bind at the PAS site of AChE, thus giving it the potential to prevent AChE induced amyloid plaque formation. Due to the multifactorial nature of AD, the drugs in the market show limited therapeutic benefits and are mainly for symptomatic relief. In order to address this limitation in AD treatment, researchers are exploring the possibility of designing a multi-target-directed-ligand (MTDL). The aim of this study was to synthesise a series of compounds out of pharmacophoric groups of donepezil and coumarin that will be able to inhibit both cholinesterases and MAO B. Four series of 5 compounds per series were synthesised. The first series of compounds consisted of the coumarin moiety to which a 1,4-dibromo benzene moiety was attached. The second series represented the coumarin moiety to which a piperidine (donepezil moiety shown to confer cholinesterase inhibitory property) was attached. The third series represented the coumarin moiety to which bromobenzyl-piperazine was attached and in the last series were compounds similar in structure to series 1 with an unsubstituted benzyl moiety as opposed to the dibromobenzyl moiety. Prior to the synthesis, molecular modelling was conducted in order to have an idea of the binding capacity of the compounds to MAO A and B and cholinesterases. In vitro biological evaluation of the compounds was done and used to determine the IC₅₀ values of the compounds. Nineteen compounds were synthesised and purified successfully as shown by their NMR, MS and IR spectra. The compounds to which dual inhibitory activity was conferred were those in series 2 and 3, of which series 2 showed the best overall inhibitory activity with IC₅₀ values within the low μM range. The compound with the best overall activity was Cp 9. Molecular modelling of Cp 9 showed that the coumarin core was located in the PAS region of AChE while the benzyl-piperidine moiety was situated in the CAS region of the enzyme. This compound orientation demonstrates the potential of Cp 9 to inhibit AChE induced amyloid beta plaque formation. Cp 9 showed no inhibitory activity towards MAO A, but showed good inhibitory activity towards MAO B with an IC₅₀ value of 0.30 μM. Its inhibitory activity towards cholinesterases also fell within the low μM range (AChE IC50 = 9.1 μM and BuChE IC₅₀ = 5.9 μM). From the results, it can be concluded that Cp 9 was able to inhibit both cholinesterase and MAO B catalytic activities at low μM concentrations. This thus means that our novel compound will not only increase ACh levels in the brain thus improving cognitive activity, but it will also have neuroprotective effect from its MAO B inhibitory property and also potentially slow down amyloid plaque formation due to AChE activity.
National Research Foundation (NRF)

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Svensson, Anne-Lie. "Cholinesterase inhibitors in Alzheimer's disease : an experimental study on mechanisms of interaction with muscarinic and nicotinic receptors and neuroprotection /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2733-2.

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Anderholm, Louise. "Behandling av beteendemässiga ochpsykiska symtom med fokus påagitation hos äldre med Alzheimerssjukdom. : En jämförelse mellan neuroleptika ochacetylkolinesterashämmare." Thesis, Umeå universitet, Farmakologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-119733.

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Inledning: År 2030 uppskattas det vara ungefär 230 000 stycken människor i Sverige somhar drabbats av någon typ av demenssjukdom. Sjukdomens stadier delas in i begynnande,mild, måttlig och svår demens. Där första symtomen i den begynnande fasen brukar vara attden drabbade inte kommer ihåg vart den lagt sina saker. I den svåra fasen av sjukdomen ärpatienten förmodligen beroende av dygnet runt vård, patienten brukar även ha svårt attprata, enstaka ord eller meningar brukar upprepas. Beteendemässiga och psykiska symtom(BPSD) hos demenssjuka är symtom som kan orsaka lidande hos patienten och dessanhöriga. Symtomen delas in i fyra undergrupper affektiva, psykossymtom, hyperaktivitetoch apati. Riskfaktorn med högst evidens är Apolipoprotein E (ApoE), ApoEε4-allelen.Riskfaktorer med lägre evidensgrad är t.ex. låg utbildning och släktskap. Sjukdomen orsakas av att nervcellerna i hjärnan dör, framförallt i delen av hjärnan därminnet sitter. En röntgen av hjärnan visar onormala proteininlagringar, amyloida plack.Amyloidhypotesen påstår att det blir en överproduktion av amyloid-beta proteinet vilken trosvara den patologiska händelsen vid Alzheimers sjukdom. Tauproteinet hyperfosfyleras till enisoform som är tre gånger större än i en frisk hjärna, om överproduktion av tau på specifikaställen eller hela hjärnan orsakar sjukdomen har forskarna inte kommit fram till ännu. Mildtill måttlig Alzheimers sjukdom behandlas med acetylkolinesterashämmarna donepezil,rivastagmin och galantamin. Svår Alzheimers sjukdom behandlas med en NMDAreceptoragonist,memantin. Syfte: Att undersöka om acetylkolinesterashämmare eller neuroleptika fungerar bäst vidsymtom som uppkommer vid BPSD, samt undersöka vilka biverkningar som är vanligast. Metod: PubMed har använts för att hitta studier som stämmer in på inklusionskriterierna.Studier som exkluderas är de som undersökt fel substans, fel indikation eller fel preparat t.ex.omega-3. Resultat: De vanligaste biverkningarna som rapporterats hos acetylkolinesterashämmarnaär bland annat illamående och kräkningar. Av neuroleptika preparaten verkar det varasömnighet som är den mest rapporterade biverkningen. Studierna som undersökteneuroleptika kom fram till ungefär samma sak, att preparaten kan förbättra symtomen. Av destudier som undersökte acetylkolinesterashämmarna var det tre studier som drog slutsatsenatt de kan ha effekt. En studie säger att det inte sågs någon skillnad mellan donepezil ochplacebo vid dessa typer av symtom. Diskussion: Då de olika studierna som använts i arbetet har undersökt olika effektmått hardet varit svårt att göra en rättvis bedömning om läkemedlen fungerar eller ej. Då i de flestafall bara gått och jämföra ett effektmått från studierna. Hade jag bestämt vilka effektmåttsom fick finnas i varje studie redan från början och sedan gjort en exkludering utifrån det,hade det varit enklare att jämföra studierna och därefter kommit fram till en bra slutsats. Viden jämförelse mellan de olika substanserna ur neuroleptikagruppen, är sömnighet denvanligaste biverkningen i tre av fyra grupper. Viktökning är också en av de vanligastebiverkningarna i två av grupperna där ungefär 32% drabbades av just denna biverkning.Varför patienterna ökat i vikt framgår inte i studierna. Slutsats: Acetylkolinesterashämmare och neuroleptika kan ha effekt vid symtom somuppkommer vid BPSD. Acetylkolinesterashämmarna bör provas i första hand om intebehandlingen redan är insatt.

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Forsström, Karin. "Longitudinal Changes in Astroglial and Inflammatory Markers in Patients with MCI and AD." Thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-192975.

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Since neuroinflammation is present in patients with mild cognitive impairment (MCI) andAlzheimer's disease (AD) and since cholinesterase inhibitors increases the level ofacetylcholine, the aim was to investigate whether inflammatory markers of cholinoceptive cellsare affected in these patients. Near a biological hallmark of AD, amyloid plaque, activatedastrocytes and microglia can be found and higher levels of proinflammatory cytokines, i.e. IL-1β. To study the inflammatory response, proteins GFAP and S100B are used as CSF glialmarkers. IL-1β can bind to the membrane-bound IL-1 receptor or soluble sIL-1β-RII. When IL-1β binds to the soluble receptor instead of the membrane-bound receptor, no intracellular signalpropagation occur, thereby sIL-1βRII exerts an antagonistic effect and diminishedinflammatory responses. Thus a reduction in ratio of IL-1β to sIL-1RII levels may be indicativeof anti-inflammatory response. Available data on CSF GFAP, S100B, IL-1β and sIL-1β-RIIlevels in AD patients and MCI patients was used. MCI group were longitudinally followedafter start of treatment with a cholinesterase inhibitor (ChEI). AD group had data from baselineand after short-term treatment with a ChEI. The statistics application StatView was used toanalyse data. The activity of the cholinesterase enzymes, BuChE and AChE showed significantinhibition in the CSF of the MCI patients compared to baseline CSF GFAP level wassignificantly lower in MCI than AD patients at baseline. The levels of both GFAP and S100Bwere increased with time in MCI patients to comparable levels in the AD patients, indicative ofastroglial activation in MCI patients. However, the ratio of IL-1β to sIL-1RII showed alongitudinal reduction in the MCI patients after the treatment with the ChEIso that this ratiowas significantly higher in AD than in MCI patients. Thus despite the activation of astroglialcells in the treated MCI patients the proinflammatory effect of IL-1β was prevented byinduction of sIL-1βRII levels indicative of an anti-inflammatory outcome of treatment. Thisstudy suggests that proper activation of astroglial cells may have beneficial effect on ADpathogenesis, and conversion of MCI to AD. It also suggests that cholinesterase inhibitors may have an anti-inflammatory effect.

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Navaratnam, Dasakumar Selveraj. "Cholinesterases in Alzheimer's disease." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306734.

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Blanco, Silvente Lídia. "La relación beneficio-riesgo del tratamiento farmacológico para la enfermedad de Alzheimer." Doctoral thesis, Universitat de Girona, 2019. http://hdl.handle.net/10803/667938.

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The evidence available in the medical literature is conclusive that the risk-benefit relationship of the current medications for Alzheimer's disease is not favourable. This risk-benefit relationship is not significantly modified by any factor related to the design of the clinical trials, neither with the intervention nor with patient’s characteristics. It is also important to highlight that redundant studies that do not provide new evidence have been identified, so the realization of new clinical trials to evaluate the efficacy and safety of current medications for Alzheimer's disease would be questionable. The findings of this thesis show the need to take positions by the responsible regarding the use of cholinesterase inhibitors and memantine in patients with Alzheimer's disease.
Les evidències disponibles en la literatura mèdica són concloents que la relació benefici-risc dels medicaments actualment indicats per la malaltia d'Alzheimer no és favorable. Aquesta relació benefici-risc no es troba modificada de manera rellevant per cap factor relacionat ni amb el disseny dels assaigs clínics, ni amb la intervenció ni amb les característiques dels pacients. És important destacar també que s’ha identificat estudis redundants que no aporten noves evidències, de tal manera que la realització de nous assajos clínics per avaluar la eficàcia i la seguretat dels actuals medicaments per la malaltia d'Alzheimer seria qüestionable. Les troballes d’aquesta tesi posen de manifest la necessitat de prendre posició per part dels organismes responsables en quant a l’ús dels inhibidors de la colinesterasa i de la memantina en pacients amb malaltia d'Alzheimer.

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Books on the topic "Cholinesterase; Alzheimer's disease"

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Yau, Kenneth Kwok Chi. Assessing and predicting treatment responses to cholinesterase inhibitor pharmacotherapy in Alzheimer's disease. Ottawa: National Library of Canada, 2000.

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National Institute for Clinical Excellence (Great Britain). Guidance on the use of donepezil, rivastigmine and galantamine for the treatment of Alzheimer's disease. London: National Institute for Clinical Excellence, 2001.

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Parker, James N., and Philip M. Parker. Donepezil: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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Cholinesterase Inhibitors in Alzheimer's Disease. Lippincott Williams & Wilkins, 1999.

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Giacobini, Ezio. Cholinesterase Inhibitors: Their Role in the Therapeutic Management of Alzheimer's Disease Pocketbook (Medical Pocketbooks). MARTIN DUNITZ, 2001.

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Ezio, Giacobini, and Becker Robert E, eds. Current research in Alzheimer therapy: Cholinesterase inhibitors. New York: Taylor & Francis, 1988.

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Alzheimer Disease: From Molecular Biology to Therapy (Advances in Alzheimer Disease Therapy). Birkhäuser Boston, 1996.

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Cholinesterase inhibitors for Alzheimer's disease: A systematic review of randomized controlled trials. Ottawa: Canadian Coordinating Office for Health Technology Assessment, 2005.

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E, Becker Robert, and Giacobini Ezio, eds. Alzheimer disease: From molecular biology to therapy. Cambridge, MA, U.S.A: Birkhäuser, 1997.

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Behl, Pearl. Differential long-term cognitive, functional, and behavioral effects of cholinesterase inhibitors in Alzheimer's disease. 2006.

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Book chapters on the topic "Cholinesterase; Alzheimer's disease"

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Wilcock, Gordon Keith. "The Pharmacological Treatment of Alzheimer's Disease with Cholinesterase Inhibitors and Memantine." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 36–49. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_3.

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Sakya, Subas, and Kapil Karki. "Donepezil, Rivastigmine and Galantamine: Cholinesterase Inhibitors for Alzheimer's Disease." In Modern Drug Synthesis, 249–74. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470768594.ch17.

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Giacobini, Ezio. "Cholinesterase Inhibitors Do More than Inhibit Cholinesterase." In Alzheimer Disease, 187–204. Boston, MA: Birkhäuser Boston, 1997. http://dx.doi.org/10.1007/978-1-4612-4116-4_29.

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Mesulam, M. Marsel. "Cholinesterases in Alzheimer’s Disease." In Enzymes of the Cholinesterase Family, 451–54. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1051-6_96.

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Becker, Robert E., Pamela Moriearty, Rita Surbeck, Latha Unni, Andrew Varney, and Sandra K. Vicari. "Second and Third Generation Cholinesterase Inhibitors: Clinical Aspects." In Alzheimer Disease, 172–78. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4615-8149-9_29.

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Kumar, Vinod. "Introduction to Cholinesterase Inhibitors Used in Alzheimer’s Disease Therapy." In Alzheimer Disease, 99–102. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4615-8149-9_17.

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Enz, Albert, and Philipp Floersheim. "Cholinesterase Inhibitors: An Overview of their Mechanisms of Action." In Alzheimer Disease, 211–15. Boston, MA: Birkhäuser Boston, 1997. http://dx.doi.org/10.1007/978-1-4612-4116-4_31.

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Soreq, Hermona, Rachel Beeri, Shlomo Seidman, Rina Timberg, Yael Loewenstein, Meira Sternfeld, Christian Andres, and Moshe Shani. "Modulating Cholinergic Neurotransmission Through Transgenic Overexpression of Human Cholinesterases." In Alzheimer Disease, 84–87. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4615-8149-9_14.

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Enz, Albert, Dieter Meier, and René Spiegel. "Effects of Novel Cholinesterase Inhibitors Based on the Mechanism of Enzyme Inhibition." In Alzheimer Disease, 125–30. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4615-8149-9_22.

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Giacobini, Ezio, and Gabriel Cuadra. "Second and Third Generation Cholinesterase Inhibitors: From Preclinical Studies to Clinical Efficacy." In Alzheimer Disease, 155–71. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4615-8149-9_28.

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