The DOI matches its Crossref record.
Pharmacological Drug Treatment of Alzheimer Disease: The Cholinergic Hypothesis Revisited
Abstract
Christopher J. Ladner, PhD, John M. Lee, MD, PhD; Pharmacological Drug Treatment of Alzheimer Disease: The Cholinergic Hypothesis Revisited, Journal of Neu
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“reduced ACh, is associated with an insufficient synthetic action of choline O-acetyltransferase (ChAt) and a high catalytic action of acetylcholinesterase (AChE), finally, lead to the loss of cholinergic transmission at the pre-synaptic level [15].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [15]
In the citing paper
“The cholinergic hypothesis argues that the reduction of learning and mnemonic processes at the base of the disease are due to low levels of ACh in neurons”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [15]
Citations
Cited by
Sorted by citations
A review on cholinesterase inhibitors for Alzheimer’s disease
Anand, P., & Singh, B. (2013) · Archives of Pharmacal Research · doi:10.1007/s12272-013-0036-3 · Cited by 722
Scott, L. J., & Goa, K. L. (2000) · Drugs · doi:10.2165/00003495-200060050-00008 · Cited by 383
“[18-25] The cognitive deficits seen in patients with AD are thought to be primarily related to the degeneration of cholinergic neurons in the cortex and hippocampus (the cholinergic hypothesis of AD), resulting in deficits of cholinergic transmission and reduced levels of acetylcholine in these patients.[6,26-29] Howe…”
Interactions between β-amyloid and central cholinergic neurons: implications for Alzheimer’s disease
Kar, S., Slowikowski, S. P. M., Westaway, D. A., & Mount, H. T. J. (2004) · Journal of Psychiatry and Neuroscience · doi:10.1139/jpn.0442 · Cited by 366
“Cholinergic neurons in the brain stem and striatum are either spared or affected only in late stages of the disease.(45,47,48) Together with pharmacologic evidence of cholinergic involvement in the affected cognitive processes, these findings led to the development of a “cholinergic hypothesis” of AD.”
InfluentialBryant, J., Clegg, A. P., Nicholson, T., McIntyre, L., Broe, S. D., Gerard, K., & Waugh, N. R. (2001) · Health Technology Assessment · doi:10.3310/hta5010 · Cited by 246
Therapeutic Opportunities for Muscarinic Receptors in the Central Nervous System
Felder, C. C., Bymaster, F. P., Ward, J. S., & DeLapp, N. W. (2000) · Journal of Medicinal Chemistry · doi:10.1021/jm990607u · Cited by 235
Smoking, nicotine and neuropsychiatric disorders
Döme, P., Lazáry, J., Kalapos, M. P., & Rihmer, Z. (2009) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2009.07.013 · Cited by 227
Agis-Torres, A., Sollhuber, M., Fernandez, M., & Sanchez-Montero, J. M. (2014) · Current Neuropharmacology · doi:10.2174/1570159x113116660047 · Cited by 202
“It was also found that a reduction of the acetylcholine synthesizing enzyme (choline acetyltransferase, ChAT) correlates with the grade of dementia [55].”
BackgroundCorcoran, J. P. T., So, P. L., & Maden, M. (2004) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2004.03563.x · Cited by 195
“…markers choline acetyltransferase (chAT), which synthesizes acetylcholine, and acetylcholinesterase, which breaks down acetylcholine and, subsequently the loss of cholinergic neurons themselves (Coyle et al., 1983; Perry et al., 1992; Geula et al., 1998; Ladner & Lee, 1998; Talesa, 2001).”
BackgroundFamilial Alzheimer's disease: Site of mutation influences clinical phenotype
Lippa, C. F., Swearer, J. M., Kane, K., Nochlin, D., Bird, T. D., Ghetti, B. F., Nee, L. E., George‐Hyslop, P. S., Pollen, D. A., & Drachman, D. A. (2000) · Annals of Neurology · doi:10.1002/1531-8249(200009)48:3 · Cited by 67
Hawkes, C. A., & Kar, S. (2004) · Brain Research Reviews · doi:10.1016/j.brainresrev.2003.11.002 · Cited by 159
Cholinergic Changes in the APP23 Transgenic Mouse Model of Cerebral Amyloidosis
Boncristiano, S., Calhoun, M. E., Kelly, P. H., Pfeifer, M., Bondolfi, L., Stalder, M., Phinney, A. L., Abramowski, D., Sturchler-Pierrat, C., Enz, A., et al. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-08-03234.2002 · Cited by 160
“…signal transduction, and significant reductions in choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) enzyme activities have been reported (Coyle et al., 1983; Perry et al., 1992; Ransmayr et al., 1992; Bierer et al., 1995; Jope et al., 1997; Geula et al., 1998; Ladner and Lee, 1998).”
BackgroundFisher, A. (2008) · Neurotherapeutics · doi:10.1016/j.nurt.2008.05.002 · Cited by 151
M1 muscarinic acetylcholine receptor in Alzheimer’s disease
Jiang, S., Li, Y., Zhang, C., Zhao, Y., Bu, G., Xu, H., & Zhang, Y. (2014) · Neuroscience Bulletin · doi:10.1007/s12264-013-1406-z · Cited by 147
Aspirin and non-steroidal anti-inflammatory drugs inhibit amyloid-β aggregation
Thomas, T., Nadackal, T. G., & Thomas, K. (2001) · Neuroreport · doi:10.1097/00001756-200110290-00024 · Cited by 128
A review of rivastigmine: A reversible cholinesterase inhibitor
Williams, B. R., Nazarians, A., & Gill, M. A. (2003) · Clinical Therapeutics · doi:10.1016/s0149-2918(03)80160-1 · Cited by 122
Sharifi-Rad, J., Rapposelli, S., Sestito, S., Herrera-Bravo, J., Arancibia-Diaz, A., Salazar, L. A., Yeskaliyeva, B., Beyatli, A., Leyva-Gómez, G., González-Contreras, C., et al. (2022) · Journal of Personalized Medicine · doi:10.3390/jpm12091515 · Cited by 125
“The cholinergic hypothesis argues that the reduction of learning and mnemonic processes at the base of the disease are due to low levels of ACh in neurons; reduced ACh, is associated with an insufficient synthetic action of choline O-acetyltransferase (ChAt) and a high catalytic action of acetylcholinesterase (AChE),…”
BackgroundKabir, M. T., Uddin, M. S., Begum, M. M., Thangapandiyan, S., Rahman, M. S., Aleya, L., Mathew, B., Ahmed, M., Barreto, G. E., & Ashraf, G. M. (2019) · Current Pharmaceutical Design · doi:10.2174/1381612825666191008103141 · Cited by 119
Protein kinase C isoforms as therapeutic targets in nervous system disease states
Battaini, F. (2001) · Pharmacological Research · doi:10.1006/phrs.2001.0893 · Cited by 115
Atanasova, M., Stavrakov, G., Philipova, I., Zheleva, D., Yordanov, N., & Doytchinova, I. A. (2015) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2015.07.058 · Cited by 95
Hu, L., Wong, T. P., Côté, S. L., Bell, K. F. S., & Cuello, A. C. (2003) · Neuroscience · doi:10.1016/s0306-4522(03)00394-4 · Cited by 90
M1 muscarinic receptor signaling in mouse hippocampus and cortex
Porter, A. C., Bymaster, F. P., DeLapp, N. W., Yamada, M., Wess, J., Hamilton, S. E., Nathanson, N. M., & Felder, C. C. (2002) · Brain Research · doi:10.1016/s0006-8993(02)02721-x · Cited by 90
Protein kinase C anchoring deficit in postmortem brains of Alzheimer's disease patients.
Battaini, F., Pascale, A., Lucchi, L., Pasinetti, G., & Govoni, S. (1999) · Experimental Neurology · doi:10.1006/exnr.1999.7151 · Cited by 82
Neurophysiological support of consciousness during waking and sleep
Gottesmann, C. (1999) · Progress in Neurobiology · doi:10.1016/s0301-0082(99)00014-3 · Cited by 85
Hiremathad, A., Keri, R. S., Esteves, A. R., Cardoso, S. M., Chaves, S., & Santos, M. A. (2018) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2018.02.023 · Cited by 82
Kukolja, J., Thiel, C. M., & Fink, G. R. (2009) · Journal of Neuroscience · doi:10.1523/jneurosci.0203-09.2009 · Cited by 86
“Whereas an abundance of research studies has concentrated on elucidating neuropharmacological alterations in AD (Ladner and Lee, 1998; Selkoe, 2002; Cummings et al., 2007; Bentley et al., 2008), there is comparatively little information about the development of neurotransmitter systems in healthy human aging.”
BackgroundZhao, C., Zhang, C., Zheng, X., Ahmad, Z., Li, J., & Chang, M. (2018) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2018.10.076 · Cited by 80
Therapeutic Strategies in Alzheimer’s Disease: Ml Muscarinic Agonists
Fisher, A. (2000) · The Japanese Journal of Pharmacology · doi:10.1254/jjp.84.101 · Cited by 80
Fisher, A., Brandeis, R., Bar-Ner, R. H. N., Kliger-Spatz, M., Natan, N., Sonego, H., Marcovitch, I., & Pittel, Z. (2002) · Journal of Molecular Neuroscience · doi:10.1007/s12031-002-0025-3 · Cited by 80
Formaldehyde toxicity in age-related neurological dementia
Kou, Y., Zhao, H., Cui, D., Han, H., & Tong, Z. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101512 · Cited by 82
“reduction of acetylcholine (Ach) levels in the brains lead to AD onset (Ladner and Lee, 1998; Wevers et al., 2000).”
Scheiderer, C. L., McCutchen, E., Thacker, E. E., Kolasa, K., Ward, M. K., Parsons, D. S., Harrell, L. E., Dobrunz, L. E., & McMahon, L. L. (2006) · Journal of Neuroscience · doi:10.1523/jneurosci.5507-05.2006 · Cited by 78
“…PI turnover is compromised in humans with AD and in animal models after loss of cholinergic innervation (Pearce and Potter, 1991; Ferrari-DiLeo and Flynn, 1993; Ferrari-DiLeo et al., 1995; Ladner et al., 1995; Ladner and Lee, 1998; Potter et al., 1999, 2002; Muma et al., 2003; Kelly et al., 2005).”
BackgroundRecent Progress in Repositioning Alzheimer'S Disease Drugs Based on a Multitarget Strategy
Santos, M. A., Chand, K., & Chaves, S. (2016) · Future Medicinal Chemistry · doi:10.4155/fmc-2016-0103 · Cited by 79
Hellström‐Lindahl, E. (2000) · European Journal of Pharmacology · doi:10.1016/s0014-2999(00)00028-5 · Cited by 76
Dysfunction of the Blood-Brain Barrier—A Key Step in Neurodegeneration and Dementia
Noe, C. R., Noe-Letschnig, M., Handschuh, P. A., Noe, C. A., & Lanzenberger, R. R. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00185 · Cited by 76
“Therefore, the therapy of AD includes the administration of acetylcholinesterase inhibitors (Ladner and Lee, 1998), substances that are meant to prevent the breakdown of acetylcholine.”
BackgroundWu, W., Dai, Y.-C., Li, N., Dong, Z., Gu, T., Shi, Z., Xue, X., Tang, Y., & Duan, J. (2017) · Journal of Enzyme Inhibition and Medicinal Chemistry · doi:10.1080/14756366.2016.1210139 · Cited by 75
Potier, B., Jouvenceau, A., Epelbaum, J., & Dutar, P. (2006) · Neuroscience · doi:10.1016/j.neuroscience.2006.06.040 · Cited by 72
The Cholinergic Deficiency Syndrome and Its Therapeutic Implications
Lemstra, A. W., Eikelenboom, P., & van Gool, W. A. (2002) · Gerontology · doi:10.1159/000066508 · Cited by 66
Wang, Y., MacDonald, R. G., Thinakaran, G., & Kar, S. (2016) · Molecular Neurobiology · doi:10.1007/s12035-016-9849-7 · Cited by 68
Zhao, T., Su, G., Wang, S., Zhang, Q., Zhang, J., Zheng, L. P., Sun, B., & Zhao, M. (2017) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.7b03945 · Cited by 65
Hu, M., Schurdak, M. E., Puttfarcken, P. S., Kouhen, R. E., Gopalakrishnan, M., & Li, J. (2007) · Brain Research · doi:10.1016/j.brainres.2007.03.051 · Cited by 60
G Protein–Coupled Receptors, Cholinergic Dysfunction, and Aβ Toxicity in Alzheimer’s Disease
Thathiah, A., & Strooper, B. D. (2009) · Science Signaling · doi:10.1126/scisignal.293re8 · Cited by 59
Scarpa, M., Hesse, S., & Bradley, S. J. (2020) · Advances in pharmacology · doi:10.1016/bs.apha.2019.12.003 · Cited by 55
Jakubík, J., El‐Fakahany, E. E., & Doležal, V. (2006) · Molecular Pharmacology · doi:10.1124/mol.106.023762 · Cited by 54
“This decrease in cholinergic input is not accompanied by changes in the density of postsynaptic M1 receptors (Ladner and Lee, 1998).”
BackgroundJalili‐Baleh, L., Nadri, H., Forootanfar, H., Samzadeh‐Kermani, A., Küçükkılınç, T. T., Ayazgök, B., Rahimifard, M., Baeeri, M., Doostmohammadi, M., Firoozpour, L., et al. (2018) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2018.04.030 · Cited by 53
Maudsley, S. R., Martin, B., & Luttrell, L. M. (2007) · Current Alzheimer Research · doi:10.2174/156720507779939850 · Cited by 50
New Acetylcholinesterase‐Inhibitory Pregnane Glycosides of Cynanchum atratum Roots
Lee, K. Y., Sung, S. H., & Kim, Y. C. (2003) · Helvetica Chimica Acta · doi:10.1002/hlca.200390047 · Cited by 49
Shanmuganathan, B., Suryanarayanan, V., Sathya, S., Narenkumar, M., Singh, S. K., Kandasamy, R., & Devi, K. P. (2017) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2017.10.017 · Cited by 50
Interaction of anandamide with the M1 and M4 muscarinic acetylcholine receptors
Christopoulos, A., & Wilson, K. (2001) · Brain Research · doi:10.1016/s0006-8993(01)02825-6 · Cited by 48
Härtig, W., Bauer, A., Brauer, K., Grosche, J., Hortobágyi, T., Penke, B., Schliebs, R., & Harkany, T. (2002) · Reviews in the Neurosciences · doi:10.1515/revneuro.2002.13.2.95 · Cited by 49
Sathya, S., Shanmuganathan, B., & Devi, K. P. (2020) · Colloids and Surfaces B Biointerfaces · doi:10.1016/j.colsurfb.2020.110948 · Cited by 47
Synthesis and Pharmacological Evaluation of Dimeric Muscarinic Acetylcholine Receptor Agonists
Christopoulos, A., Grant, M. K. O., Ayoubzadeh, N., et al. (2001) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(24)29501-x · Cited by 47
Sun, K., Bai, Y., Zhao, R., Guo, Z., Su, X., Li, P., & Yang, P. (2018) · Metabolic Brain Disease · doi:10.1007/s11011-018-0335-y · Cited by 46
Muma, N. A., Mariyappa, R., Williams, K., & Lee, J. M. (2002) · Synapse · doi:10.1002/syn.10153 · Cited by 42
Self-citationRoßner, S., Beck, M., Stahl, T., Mendla, K. D., Schliebs, R., & Bigl, V. (2000) · European Journal of Neuroscience · doi:10.1046/j.1460-9568.2000.00211.x · Cited by 41
dos Santos, L. C., Mendiola, J. A., Sánchez‐Camargo, A. D. P., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126248 · Cited by 39
“On the one hand, AChE is an important enzyme in the cholinergic system, responsible for the hydrolysis of acetylcholine, a neurotransmitter distributed all over the central nervous system [18].”
BackgroundGRK5 Deficiency Accelerates β-Amyloid Accumulation in Tg2576 Mice via Impaired Cholinergic Activity
Cheng, S., Li, L., He, S., Liu, J., Sun, Y., He, M., Grasing, K., Premont, R. T., & Suo, W. Z. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.170894 · Cited by 41
Zha, G., Zhang, C., Qin, H., Jantan, I., Sher, M., Amjad, M. W., Hussain, M. A., Hussain, Z., & Bukhari, S. N. A. (2016) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2016.04.015 · Cited by 39
Persistent Binding and Functional Antagonism by Xanomeline at the Muscarinic M5 Receptor
Grant, M. K. O., & El‐Fakahany, E. E. (2005) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.105.090134 · Cited by 38
“Although the disease is accompanied by a marked loss of presynaptic cholinergic neurons, postsynaptic M1 muscarinic receptors, which are involved in learning and memory, remain largely intact (Ladner and Lee, 1998).”
BackgroundPharmacological models in Alzheimer's disease research
Gilles, C., & Ertle, S. (2000) · Dialogues in Clinical Neuroscience · doi:10.31887/dcns.2000.2.3/cgilles · Cited by 38
Bono, G. F., Simão-Silva, D. P., Batistela, M. S., Josviak, N. D., Dias, P. F. R., do Nascimento, G. A., de Souza, R. L. R., Piovezan, M. R., de Souza, R. K. M., & Alle, L. F. (2015) · Neurochemistry International · doi:10.1016/j.neuint.2014.12.009 · Cited by 37
Kar, S., & Quirion, R. (2004) · Progress in brain research · doi:10.1016/s0079-6123(03)45018-8 · Cited by 37
Thompson, T. P., Lunsford, L. D., & Kondziolka, D. S. (1999) · Neurosurgery · doi:10.1097/00006123-199910000-00001 · Cited by 36
Haroon, M., Khalid, M., Shahzadi, K., et al. (2021) · Journal of Molecular Structure · doi:10.1016/j.molstruc.2021.131063 · Cited by 36
Dysfunction of G Protein-Coupled Receptor Kinases in Alzheimer's Disease
Suo, W. Z., & Li, L. (2010) · The Scientific World JOURNAL · doi:10.1100/tsw.2010.154 · Cited by 37
“Although the detailed descriptions may evolve over time with increasing insights into the disease pathogenesis, the principal concepts of these hypotheses appear to stand solidly up to now[6,71,73,74,75,76,77,78].”
BackgroundShiri, F., Pirhadi, S., & Ghasemi, J. B. (2018) · Journal of Biomolecular Structure and Dynamics · doi:10.1080/07391102.2018.1468281 · Cited by 35
“The most obvious clinical finding in AD represents that levels of acetylcholine (ACh), as a neurotransmitter responsible for the conduction of electrical impulses from one nerve cell to another, are decreased (Ladner & Lee, 1998; Mehta, Adem, & Sabbagh, 2011).”
BackgroundZhang, H.-Y., Watson, M. L., Gallagher, M., & Nicolle, M. M. (2006) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.02.016 · Cited by 34
Chand, K., Rajeshwari, K., Candeias, E., Cardoso, S. M., Chaves, S., & Santos, M. A. (2018) · Metallomics · doi:10.1039/c8mt00143j · Cited by 33
Park, H., & Kim, J. (2022) · Journal of Pineal Research · doi:10.1111/jpi.12787 · Cited by 33
“Instead, AD patients are currently treated with compounds that merely decelerate AD progression.(62,63) Several studies have reported that melatonin secretion is greatly inhibited in aged and AD patients.”
BackgroundOrhan, İ. E. (2020) · Current Neuropharmacology · doi:10.2174/1570159x18666201119153807 · Cited by 34
Ladner, C. J., & Lee, J. M. (1999) · Experimental Neurology · doi:10.1006/exnr.1999.7116 · Cited by 31
Self-citationHan, G., Zhen, W., Dai, Y., Yu, H., Li, D., & Ma, T. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.873929 · Cited by 30
Takadoi, M., Katoh, T., Ishiwata, A., et al. (2002) · Tetrahedron · doi:10.1016/s0040-4020(02)01358-3 · Cited by 30
Flavanone glycosides as acetylcholinesterase inhibitors: computational and experimental evidence.
Remya, C., Dileep, K. V., Tintu, I., Variyar, E. J., & Sadasivan, C. (2014) · PubMed Central · Cited by 27
Differential regulation of muscarinic M1 receptors by orthosteric and allosteric ligands
Davis, C. N., Bradley, S. R., Schiffer, H. H., et al. (2009) · BMC Pharmacology · doi:10.1186/1471-2210-9-14 · Cited by 28
“Xanomeline, N-desmethylclozapine (NDMC), AC260584 (4-[3-(4-butylpiperidin-1-yl)propyl]-7-fluoro2H-benzo[b][1,4]oxazin-3-one)), AC-42 (4-(4-butylpiperdin-1-yl)-1-(2-methylphenyl)butan-1-one), AC260515 (4-[3-(4-butyl-piperidin-1-yl)-propyl]-7-chloro2H-benzo[b][1,4]oxazin-3-one), AC-262469 (4-[3-(4cyclopropylmethyloxypip…”
BackgroundAksu, K., Akıncıoğlu, H., Akıncıoğlu, A., et al. (2018) · Archiv der Pharmazie · doi:10.1002/ardp.201800150 · Cited by 26
Docking-based Design of Galantamine Derivatives with Dual-site Binding to Acetylcholinesterase
Stavrakov, G., Philipova, I., Zheleva‐Dimitrova, D., Atanasova, M., Konstantinov, S., & Doytchinova, I. A. (2016) · Molecular Informatics · doi:10.1002/minf.201600041 · Cited by 28
Shanmuganathan, B., & Devi, K. P. (2016) · European Journal of Phycology · doi:10.1080/09670262.2016.1218938 · Cited by 25
“Notable cholinergic changes are observed in patients with AD (Terry & Buccafusco, 2003) such as decreased ACh levels in the synaptic cleft due to its rapid hydrolysis by the enzyme acetylcholinesterase (AChE) (Lasner & Lee, 1998).”
BackgroundLanzafame, A. A., Guida, E., & Christopoulos, A. (2004) · Biochemical Pharmacology · doi:10.1016/j.bcp.2004.08.005 · Cited by 24
Anand, P., & Singh, B. (2012) · Medicinal Chemistry Research · doi:10.1007/s00044-012-0162-3 · Cited by 23
“The most potent test compound (5f0) was evaluated in vivo for memory restorative actions in scopolamine (0.4 mg/kg)- induced amnesia in mice by Morris water maze test.”
BackgroundInfluentialChristopoulos, A., Parsons, A. M., & El‐Fakahany, E. E. (1999) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(24)38262-x · Cited by 23
Alzheimer's disease: Its diagnosis and pathogenesis
Kril, J. J., & Halliday, G. M. (2001) · International review of neurobiology · doi:10.1016/s0074-7742(01)48016-0 · Cited by 22
Okadaic Acid and Hypoxia Induced Dementia Model of Alzheimer’s Type in Rats
Kaushal, A., Wani, W. Y., Bal, A., Gill, K. D., & Kaur, J. (2019) · Neurotoxicity Research · doi:10.1007/s12640-019-0005-9 · Cited by 21
Acetylcholinergic neurotransmission and the β-amyloid cascade: implications for Alzheimer’s disease
Verhoeff, N. P. L. G. (2005) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.5.2.277 · Cited by 21
Synthesis of a hybrid analog of the acetylcholinesterase inhibitors huperzine A and huperzine B
Rajendran, V., Rong, S.-B., Saxena, A., et al. (2001) · Tetrahedron Letters · doi:10.1016/s0040-4039(01)01008-5 · Cited by 21
Impact of muscarinic agonists for successful therapy of Alzheimer’s disease
Fisher, A., Brandeis, R., Haring, R., Bar-Ner, N., Kliger-Spatz, M., Natan, N., Sonego, H., Marcovitch, I., & Pittel, Z. (2002) · Journal of neural transmission. Supplementum · doi:10.1007/978-3-7091-6139-5_18 · Cited by 19
QT interval prolongation and Torsades de Pointes with donepezil, rivastigmine and galantamine
Malone, K., & Hancox, J. C. (2020) · Therapeutic Advances in Drug Safety · doi:10.1177/2042098620942416 · Cited by 18
Chen, M. (1999) · Frontiers in bioscience · doi:10.2741/a400 · Cited by 18
“It is also supported by a rapidly growing body of evidence emerging from various research areas ( 13-15 ).”
BackgroundAntiamnesic Effects of Walnuts Consumption on Scopolamine-Induced Memory Impairments in Rats.
Harandi, S., Golchin, L., Ansari, M., et al. (2015) · PubMed · Cited by 17
Billard, W., Binch, H., Bratzler, K., et al. (2000) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/s0960-894x(00)00437-6 · Cited by 17
Wienrich, M., Ceci, A., Ensinger, H. A., Gaida, W., Mendla, K. D., Osugi, T., Raschig, A., & Weiser, T. W. (2002) · Drug Development Research · doi:10.1002/ddr.10085 · Cited by 17
Zhu, Z., Zhang, L., Cui, Y., et al. (2020) · Neuroscience · doi:10.1016/j.neuroscience.2020.05.016 · Cited by 16
Effects of muscarinic and adrenergic agonism on auditory P300 in the macaque
O’Neill, J., Halgren, E., Marinković, K., Siembieda, D. W., Refai, D., Fitten, L. J., Perryman, K. M., & Fisher, A. (2000) · Physiology & Behavior · doi:10.1016/s0031-9384(00)00258-4 · Cited by 16
“For example, P3 amplitude decline and latency retardation exceeding those observed in normal aging are long established in Alzheimer’s disease [42], but it is not known how these electrophysiological symptoms relate to the histochemically determined central cholinergic [23,25] and adrenergic [5,9,36,44] deficiencies o…”
BackgroundErythrocyte membrane fluidity in mild cognitive impairment and Alzheimer's disease patients
Vignini, A., Alia, S., Pugnaloni, S., Giulietti, A., Bacchetti, T., Mazzanti, L., Luzzi, S., & Fiorini, R. (2019) · Experimental Gerontology · doi:10.1016/j.exger.2019.110754 · Cited by 15
Amadoruge, P. C., & Barnham, K. J. (2011) · International Journal of Alzheimer s Disease · doi:10.4061/2011/542043 · Cited by 14
“Reductions in ChAT activity are the greatest [71, 72] and correlate with disease severity [68, 73].”
BackgroundKar, S. (2002) · Drug Development Research · doi:10.1002/ddr.10080 · Cited by 14
“…enzyme choline acetyltransferase (ChAT) in the neocortex of AD brains, which correlates positively with the clinical severity of dementia [Davies and Maloney, 1976; Whitehouse et al., 1982; Quirion, 1993; Geula and Mesulam, 1994; Kasa et al., 1997; Ladner and Lee, 1998; Blusztajn and Berse, 2000].”
InfluentialJearjaroen, P., Pakdeepak, K., Tocharus, C., Chaichompoo, W., Suksamrarn, A., & Tocharus, J. (2020) · Neurotoxicity Research · doi:10.1007/s12640-020-00269-y · Cited by 13
Rispoli, V., Marra, R., Costa, N., Scipione, L., Rotiroti, D., Vita, D. D., Liberatore, F., & Carelli, V. (2006) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2006.06.009 · Cited by 13
Activation of muscarinic receptors inhibits glutamate-induced GSK-3β overactivation in PC12 cells
Ma, K., Yang, L., Chen, H., et al. (2013) · Acta Pharmacologica Sinica · doi:10.1038/aps.2013.42 · Cited by 13
Barik, J., Dajas‐Bailador, F., & Wonnacott, S. (2005) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0706278 · Cited by 13
“AD, which accounts for 70% of dementia cases in most industrialised countries, is characterised by cell atrophy and extensive neurone loss, with a marked reduction in cholinergic transmission in the cortex and hippocampus (Coyle et al., 1983; Ladner & Lee, 1998).”
BackgroundTurégano, L., Martínez-Rodríguez, R., Álvarez, M., Gragera, R., Segura, A., de Miguel, E., & Tolédano, A. (2001) · Journal of Neuroscience Research · doi:10.1002/jnr.1116 · Cited by 12
“…(Kasa et al., 1997; Ladner and Lee, 1998; Lawrence and Sahakian, 1998; Bartus, 2000); but, up to now, “cholinergic therapies” have not obtained the expected success (Ladner and Lee, 1998; Lawrence and Sahakian, 1998; Samuels and Davis, 1998; Lemiere et al., 1999; Richards and Hendrie, 1999).”
BackgroundTakadoi, M., Yamaguchi, K., & Terashima, S. (2003) · Bioorganic & Medicinal Chemistry · doi:10.1016/s0968-0896(02)00665-x · Cited by 12
Metadata
- Authors
- Ladner, C. J., & Lee, J. M.
- Affiliations
- Loyola University Medical Center (US)
- Corresponding author
- Lee, John M.
- ORCID
- Lee, John M.
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 1998-08
- Volume
- 57
- Issue
- 8
- Pages
- 719-731
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W2061570982
- Cited by
- 142
- References
- 0
- Citations by year
- 2025: 2 · 2023: 3 · 2022: 8 · 2021: 4 · 2020: 7 · 2019: 3 · 2018: 8 · 2017: 3 · 2016: 7 · 2015: 4 · 2014: 4 · 2013: 5 · 2012: 1
- FWCI
- 7.08
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Cholinesterase and Neurodegenerative Diseases
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, cholinergic hypothesis, cholinesterase inhibitors, acetylcholinesterase, pharmacotherapy, cholinergic system
- MeSH terms
- Acetylcholine, Alzheimer Disease, Central Nervous System, Humans, Receptors, Muscarinic, Receptors, Nicotinic
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review