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Current and future treatments for Alzheimer's disease
Open accessAbstract
Alzheimer's dementia (AD) is increasingly being recognized as one of the most important medical and social problems in older people in industrialized and non-industrialized nations. To date, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance. Three cholinesterase inhibitors (CIs) are currently available and have been approved for the treatment of mild to moderate AD. A further therapeutic option available for moderate to severe AD is memantine, an N-methyl-D-aspartate receptor noncompetitive antagonist. Treatments capable of stopping or at least effectively modifying the course of AD, referred to as 'disease-modifying' drugs, are still under extensive research. To block the progression of the disease they have to interfere with the pathogenic steps responsible for the clinical symptoms, including the deposition of extracellular amyloid β plaques and intracellular neurofibrillary tangle formation, inflammation, oxidative damage, iron deregulation and cholesterol metabolism. In this review we discuss current symptomatic treatments and new potential disease-modifying therapies for AD that are currently being studied in phase I-III trials.
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In the citing paper
“After the sequential breakdown of the big precursor protein amyloid precursor protein (APP) by the β- and γ-e -secretase, Aβ peptides with A38, A40, and A42 being the most prevalent forms are generated (Yiannopoulou et al., 2013).”
From An update on the novel and approved drugs for Alzheimer disease (2022) · cites this paper as Yiannopoulou et al., 2013
In the citing paper
“Memantine is known to be a non-competitive NMDA receptor antagonist that counteracts the negative effects of high glutamate concentrations in the brain (Yiannopoulou et al., 2013).”
From An update on the novel and approved drugs for Alzheimer disease (2022) · cites this paper as Yiannopoulou et al., 2013
In the citing paper
“The most efficient and prospective class is passive Ab immunotherapy using mAbs. The chief disadvantages of this class of medicines are cerebral microhemorrhages and vasogenic edema (Yiannopoulou et al., 2013).”
From An update on the novel and approved drugs for Alzheimer disease (2022) · cites this paper as Yiannopoulou et al., 2013
In the citing paper
“Memantine is a noncompetitive low-affinity NMDA-receptor open-channel blocker and affects glutamatergic transmission.5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“AChEIs attempt at reducing the breakdown of acetylcholine levels in the brain of the patients with AD by inhibiting the responsible enzyme acetylcholinesterase in the synaptic cleft.5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“According to the “amyloid hypothesis” Aβ production in the brain initiates a cascade of events leading to the clinical syndrome of AD.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“The basic pathophysiology and neuropathology of AD that drives the current research suggests that the primary histopathologic lesions of AD are the extracellular amyloid plaques and the intracellular Tau neurofibrillary tangles (NFTs).5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“The elements of the cascade include local inflammation, oxidation, excitoxicity (excessive glutamate), and tau hyperphosphorylation.5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“The acetylocholinesterase inhibitors (AChEIs) which are approved for the treatment of AD are donepezil, galantamine, and rivastigmine.4,5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“It is the forming of amyloid oligomers to which neurotoxicity is mainly attributed and initiates the amyloid cascade.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Progressive neuronal destruction leads to shortage and imbalance between various neurotransmitters (eg, acetylcholine, dopamine, serotonin) and to the cognitive deficiencies seen in AD.5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“A further therapeutic agent approved for moderate to severe AD is the low-to-moderate affinity, noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist memantine.4,5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“The APP cleavage by α-secretase leads to nonamyloidogenic pathway, whereas APP cleavage by β-secretase (BACE1) leads to amyloidogenic pathway.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“The Aβ derives from a protein overexpressed in AD, APP through sequential proteolysis by β-secretase (BACE1) in the extracellular domain and γ-secretase in the transmembrane region.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Sequential cleavage of APP by BACE1 in the extracellular and γ-secretase in the transmembrane area results in the Aβ production.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“The crucial step in AD pathogenesis is the production of amyloid (Aβ), which forms SPs (insoluble and proteolysis-resistant fibrils).”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Aβ40 is somewhat aggregation-prone and it is mostly found in the cerebral vasculature as a main component of “cerebral amyloid angiopathy.””
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Oligomers can form Aβ-fibrils that will eventually form amyloid plaques.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Major sites of γ-secretase cleavage usually occur in positions 40 and 42 of Aβ, thus Aβ40 and Aβ42 oligomers are the main products of the sequential APP cleavage, as the amyloidogenic pathway is favored in neurons because of the greater plentifulness of BACE1.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Aβ40 usually constitutes more than 50% of total detected Aβ.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Unluckily, concerning γ-secretase, in addition to APP, this particular enzyme acts on many other substances and cleaves different transmembrane proteins. Notch receptor 1, which is essential for control of normal cell differentiation and communication, is among them.5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Aβ42 is the most aggregation-prone form and has the tendency to cluster into oligomers.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Aβ38 is soluble, present in the vasculature of patients with sporadic and familial AD.”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“On the contrary, the nonamyloidogenic processing is more favored in other cells without BACE1 predominance.5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Cerebral microhemorrhages and vasogenic edema are the main drawbacks in this group of agents.5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
In the citing paper
“Abnormal accumulation or dyshomeostasis of metal ions such as iron, copper, and zinc has been associated with the pathophysiology of AD.5”
From Current and Future Treatments in Alzheimer Disease: An Update (2020) · cites this paper as [5]
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Citations
Cites
Sperling, R. A., Aisen, P. S., Beckett, L. A., Bennett, D. A., Craft, S., Fagan, A. M., Iwatsubo, T., Jack, C. R., Kaye, J., Montine, T. J., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.003 · Cited by 7,155
The cholinergic hypothesis of geriatric memory dysfunction
Bartus, R. T., Dean, R. L., Beer, B., & Lippa, A. S. (1982) · Science · doi:10.1126/science.7046051 · Cited by 5,545
Global prevalence of dementia: a Delphi consensus study
Ferri, C. P., Prince, M. J., Brayne, C., Brodaty, H., Fratiglioni, L., Ganguli, M., Hall, K. S., Hasegawa, K., Hendrie, H. C., Huang, Y., et al. (2005) · The Lancet · doi:10.1016/s0140-6736(05)67889-0 · Cited by 5,336
Cholinesterase inhibitors for Alzheimer's disease
Birks, J. S. (2006) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd005593 · Cited by 1,906
Revising the definition of Alzheimer's disease: a new lexicon
Dubois, B., Feldman, H. H., Jacova, C., Cummings, J. L., DeKosky, S. T., Barberger-Gateau, P., Delacourte, A., Frisoni, G., Fox, N. C., Galasko, D., et al. (2010) · The Lancet Neurology · doi:10.1016/s1474-4422(10)70223-4 · Cited by 1,869
Statins and the risk of dementia
Jick, H., Zornberg, G. L., Jick, S. S., Seshadri, S. S., & Drachman, D. (2000) · The Lancet · doi:10.1016/s0140-6736(00)03155-x · Cited by 1,764
Tariot, P. N., Farlow, M. R., Grossberg, G. T., Graham, S. M., McDonald, S., Gergel, I., & for the Memantine Study Group (2004) · JAMA · doi:10.1001/jama.291.3.317 · Cited by 1,403
Clinical effects of Aβ immunization (AN1792) in patients with AD in an interrupted trial
Gilman, S., Koller, M., Black, R. S., Jenkins, L., Griffith, S. G., Fox, N. C., Eisner, L., Kirby, L., Rovira, M. B., Forette, F., et al. (2005) · Neurology · doi:10.1212/01.wnl.0000159740.16984.3c · Cited by 1,329
McShane, R., Areosa Sastre, A., & Minakaran, N. (2006) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd003154.pub5 · Cited by 1,155
Clinical trial of indomethacin in Alzheimer's disease
Rogers, J., Kirby, L., Hempelman, S. R., Berry, D. A., McGeer, P. L., Kaszniak, A. W., Zalinski, J., Cofield, M., Mansukhani, L., Willson, P., et al. (1993) · Neurology · doi:10.1212/wnl.43.8.1609 · Cited by 991
Donepezil and memantine for moderate-to-severe Alzheimer's disease
Howard, R., McShane, R., Lindesay, J., Ritchie, C., Baldwin, A., Barber, R., Burns, A., Dening, T., Findlay, D., Holmes, C., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1106668 · Cited by 782
Wong, G. T., Manfra, D. J., Poulet, F. M., Zhang, Q., Josien, H. B., Bara, T. A., Engstrom, L., Pinzon-Ortiz, M. C., Fine, J. S., Lee, H.-J. J., et al. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m311652200 · Cited by 723
Berendsen, A. A. M., Kang, J. H., van de Rest, O., Jankovic, N., Kampman, E., Jong, J. C. K., Franco, O. H., Ikram, M. A., Pikhart, H., Nilsson, L. M., et al. (2017) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000464269 · Cited by 566
Banerjee, S., Hellier, J., Dewey, M., Romeo, R., Ballard, C., Baldwin, R., Bentham, P., Fox, C., Holmes, C., Katona, C., et al. (2011) · The Lancet · doi:10.1016/s0140-6736(11)60830-1 · Cited by 532
Hansen, R. A., Webb, A. P., Moore, C. G., Gartlehner, G., Jonas, D. E., & Morgan, L. C. (2020) · PubMed Central · doi:10.17615/ae8c-2p76 · Cited by 523
Randomized controlled trial of atorvastatin in mild to moderate Alzheimer disease: LEADe
Feldman, H. H., Doody, R. S., Kivipelto, M., Sparks, D. L., Waters, D. D., Jones, R. W., Schwam, E., Schindler, R., Hey-Hadavi, J., DeMicco, D. A., et al. (2010) · Neurology · doi:10.1212/wnl.0b013e3181d6476a · Cited by 438
Forlenza, O. V., Diniz, B. S., Radanovic, M., Santos, F. S., Talib, L. L., & Gattaz, W. F. (2011) · The British Journal of Psychiatry · doi:10.1192/bjp.bp.110.080044 · Cited by 411
PBT2 Rapidly Improves Cognition in Alzheimer's Disease: Additional Phase II Analyses
Faux, N. G., Ritchie, C. W., Gunn, A. P., Rembach, A., Tsatsanis, A., Bedő, J., Harrison, J., Lannfelt, L., Blennow, K., Zetterberg, H., et al. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-1390 · Cited by 406
BACE1: The β-Secretase Enzyme in Alzheimer's Disease
Vassar, R. J. (2004) · Journal of Molecular Neuroscience · doi:10.1385/jmn:23:1-2:105 · Cited by 383
Qaseem, A., Snow, V. T., Cross, J. T., Forciea, M. A., HOPKINS, R. H., Shekelle, P., Adelman, A., Mehr, D. R., Schellhase, K. G., Campos-Outcalt, D. E., et al. (2008) · Annals of Internal Medicine · doi:10.7326/0003-4819-148-5-200803040-00008 · Cited by 353
Inflammation and neurodegenerative diseases
Griffin, W. S. T. (2006) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/83.2.470s · Cited by 351
A randomized, double-blind, placebo-controlled trial of simvastatin to treat Alzheimer disease
Sano, M., Bell, K. L., Galasko, D., Galvin, J. E., Thomas, R. G., van Dyck, C. H., & Aisen, P. S. S. (2011) · Neurology · doi:10.1212/wnl.0b013e318228bf11 · Cited by 347
Salomone, S., Caraci, F., Leggio, G. M., Fedotova, J., & Drago, F. (2011) · British Journal of Clinical Pharmacology · doi:10.1111/j.1365-2125.2011.04134.x · Cited by 335
Farlow, M., Anand, R., Messina Jr, J., Hartman, R., & Veach, J. (2000) · European Neurology · doi:10.1159/000008243 · Cited by 332 · cited 1×
“A 52-week study of the efficacy of rivastigmine in patients with mild to moderately severe AD reported that patients with AD who started the CI 6 months later achieved lower cognitive performance than those who started the drug immediately after the diagnosis [Farlow et al. 2000].”
BackgroundMetals and Alzheimer's disease
Adlard, P. A., & Bush, A. I. (2006) · Journal of Alzheimer's Disease · doi:10.3233/jad-2006-102-303 · Cited by 324
Syncope and Its Consequences in Patients With Dementia Receiving Cholinesterase Inhibitors
Gill, S. S., Anderson, G., Fischer, H. D., Bell, C. M., Li, P., Normand, S. T., & Rochon, P. A. (2009) · Archives of Internal Medicine · doi:10.1001/archinternmed.2009.43 · Cited by 306
Hampel, H. J., Ewers, M., Bürger, K., Annas, P., Mörtberg, A., Bogstedt, A., Frölich, L., Schröder, J., Schönknecht, P., Riepe, M. W., et al. (2009) · PubMed · Cited by 305
Lithium Trial in Alzheimer's Disease
Hampel, H. J., Ewers, M., Bürger, K., Annas, P., Mörtberg, A., Bogstedt, A., Frölich, L., Schröder, J., Schönknecht, P., Riepe, M. W., et al. (2009) · The Journal of Clinical Psychiatry · doi:10.4088/jcp.08m04606 · Cited by 297
Oxidative Stress in Diabetes and Alzheimer's Disease
Reddy, V. P., Zhu, X., Perry, G. L., & Smith, M. A. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1013 · Cited by 286
Developing β‐secretase inhibitors for treatment of Alzheimer’s disease
Ghosh, A. K., Brindisi, M., & Tang, J. (2011) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2011.07476.x · Cited by 282
The Cholinergic Hypothesis of Neuropsychiatric Symptoms in Alzheimer's Disease
Cummings, J. L., & Back, C. (1998) · American Journal of Geriatric Psychiatry · doi:10.1097/00019442-199821001-00009 · Cited by 276
A phase 2 randomized trial of ELND005, scyllo-inositol, in mild to moderate Alzheimer disease
Salloway, S., Sperling, R., Keren, R., Porsteinsson, A. P., van Dyck, C. H., Tariot, P. N., Gilman, S., Arnold, D., Abushakra, S., Hernandez, C., et al. (2011) · Neurology · doi:10.1212/wnl.0b013e3182309fa5 · Cited by 258 · cited 1×
“The safety and cerebrospinal fluid (CSF) biomarker results will guide selection of the optimal dose for future studies, which will target earlier stages of AD [Salloway et al. 2011].”
BackgroundActive and passive immunotherapy for neurodegenerative disorders
Brody, D. L., & Holtzman, D. M. (2008) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.31.060407.125529 · Cited by 250
Current and Emerging Drug Treatment Options for Alzheimerʼs Disease
Herrmann, N., Chau, S. A., Kircanski, I., & Lanctôt, K. L. (2011) · Drugs · doi:10.2165/11595870-000000000-00000 · Cited by 245
Statins for the treatment of dementia
McGuinness, B., Craig, D., Bullock, R. A., Malouf, R. S., & Passmore, P. (2014) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd007514.pub3 · Cited by 236
Siemers, E., Skinner, M., Dean, R. A., Gonzales, C., Satterwhite, J. H., Farlow, M. R., NESS, D. K., & May, P. C. (2005) · Clinical Neuropharmacology · doi:10.1097/01.wnf.0000167360.27670.29 · Cited by 215
A Phase II study targeting amyloid-β with 3APS in mild-to-moderate Alzheimer disease
Aisen, P. S. S., Saumier, D., Briand, R., Laurin, J., Gervais, F., Tremblay, P., & Garceau, D. (2006) · Neurology · doi:10.1212/01.wnl.0000244346.08950.64 · Cited by 198
Imbimbo, B. P., & Giardina, G. A. M. (2011) · Current Topics in Medicinal Chemistry · doi:10.2174/156802611795860942 · Cited by 196
Randomized pilot study of nimesulide treatment in Alzheimer’s disease
Aisen, P. S. S., Schmeidler, J., & Pasinetti, G. M. (2002) · Neurology · doi:10.1212/wnl.58.7.1050 · Cited by 179
Amyloid-β immunisation for Alzheimer's disease
Wisniewski, T., & Konietzko, U. (2008) · The Lancet Neurology · doi:10.1016/s1474-4422(08)70170-4 · Cited by 155
Disease-modifying trials in Alzheimer's disease: a European task force consensus.
Vellas, B., Andrieu, S., Sampaio, C., & Wilcock, G. (2007) · Lancet Neurology · doi:10.1016/s1474-4422(06)70677-9 · Cited by 154
Management of Neuropsychiatric Symptoms in People with Dementia
Ballard, C., & Corbett, A. (2010) · CNS Drugs · doi:10.2165/11319240-000000000-00000 · Cited by 147
Gauthier, S. G., Aisen, P. S. S., Ferris, S. H., Saumier, D., Duong, A., Haine, D., Garceau, D., Suhy, J., Oh, J., Lau, W. C., et al. (2009) · The journal of nutrition health & aging · doi:10.1007/s12603-009-0106-x · Cited by 136
Cholesterol in Alzheimers Disease: Unresolved Questions
Stefani, M., & Liguri, G. (2009) · Current Alzheimer Research · doi:10.2174/156720509787313899 · Cited by 136
EHT0202 in Alzheimers Disease: A 3-Month, Randomized, Placebo- Controlled, Double-Blind Study
Vellas, B., Sol, O., J. Snyder, P., Ousset, P.-J., Haddad, R., Maurin, M., Lemarie, J.-C., Desire, L., & P. Pando, M. (2011) · Current Alzheimer Research · doi:10.2174/156720511795256053 · Cited by 133 · cited 1×
“At present, the focus in AD drug development is shifting from treatment to prevention [Salomone et al. 2011; Vellas et al. 2011].”
BackgroundDisease-modifying treatments for Alzheimer’s disease
Galimberti, D., & Scarpini, E. A. (2011) · Therapeutic Advances in Neurological Disorders · doi:10.1177/1756285611404470 · Cited by 128
GSK-3 Inhibitors: A Ray of Hope for the Treatment of Alzheimer's Disease?
Martı́nez, A., & Pérez, D. I. (2008) · Journal of Alzheimer s Disease · doi:10.3233/jad-2008-15204 · Cited by 124
Therapeutic Strategies for Alzheimer’s Disease
Barten, D. M., & Albright, C. F. (2008) · Molecular Neurobiology · doi:10.1007/s12035-008-8031-2 · Cited by 124
Hope in Alzheimer's fight emerges from unexpected places
Gura, T. (2008) · Nature Medicine · doi:10.1038/nm0908-894 · Cited by 123
Maidment, I., Fox, C., Boustani, M. A., Menés, J. R., Brown, R. C., & Katona, C. (2007) · Annals of Pharmacotherapy · doi:10.1345/aph.1k372 · Cited by 121
Silvestri, R. (2008) · Medicinal Research Reviews · doi:10.1002/med.20132 · Cited by 118
Bilikiewicz, A., & Gaus, W. (2004) · Journal of Alzheimer s Disease · doi:10.3233/jad-2004-6103 · Cited by 117
Ballard, C. G., Corbett, A., Chitramohan, R., & Aarsland, D. (2009) · Current Opinion in Psychiatry · doi:10.1097/yco.0b013e32833111f9 · Cited by 116
Fatty acids, lipid metabolism and Alzheimer pathology
Hooijmans, C. R., & Kiliaan, A. J. (2008) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2007.11.081 · Cited by 115
Intravenous Immunoglobulins as a Treatment for Alzheimerʼs Disease
Dodel, R. C., Neff, F., Noelker, C., Pul, R., Du, Y., Bacher, M., & Oertel, W. H. (2010) · Drugs · doi:10.2165/11533070-000000000-00000 · Cited by 113
A Clinical Overview of Cholinesterase Inhibitors in Alzheimer’s Disease
Farlow, M. R. (2002) · International Psychogeriatrics · doi:10.1017/s1041610203008688 · Cited by 100
Golde, T. E. (2006) · Brain Pathology · doi:10.1111/j.1750-3639.2005.tb00104.x · Cited by 99
Wilcock, D. M., Jantzen, P. T., Li, Q., Morgan, D., & Gordon, M. N. (2006) · Neuroscience · doi:10.1016/j.neuroscience.2006.10.020 · Cited by 95
Statins for the treatment of dementia
McGuinness, B., O’Hare, J., Craig, D., Bullock, R. A., Malouf, R. S., & Passmore, P. (2010) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd007514.pub2 · Cited by 93
Disease-Modifying Approach to the Treatment of Alzheimerʼs Disease
Panza, F., Solfrizzi, V., Frisardi, V., Capurso, C. A., D’Introno, A., Colacicco, A. M., Vendemiale, G., Capurso, A., & Imbimbo, B. P. (2009) · Drugs & Aging · doi:10.2165/11315770-000000000-00000 · Cited by 87
Santa‐María, I., Hernández, F., Rio, J. D., Moreno, F. J., & Ávila, J. (2007) · Molecular Neurodegeneration · doi:10.1186/1750-1326-2-17 · Cited by 86
John, S., Thangapandian, S., Sakkiah, S., & Lee, K. W. (2011) · BMC Bioinformatics · doi:10.1186/1471-2105-12-s1-s28 · Cited by 80
Prevention trials in Alzheimer's disease: An EU-US task force report
Vellas, B. J., Aisen, P. S. S., Sampaio, C., Carrillo, M. C., Scheltens, P., Scherrer, B., Frisoni, G. B., Weiner, M. W., Schneider, L. S. S., Gauthier, S. G., et al. (2011) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2011.08.014 · Cited by 78
Caregiver preference for rivastigmine patches versus capsules for the treatment of Alzheimer disease
Blesa, R., Ballard, C. G., Orgogozo, J., Lane, R. M., & Thomas, S. K. (2007) · Neurology · doi:10.1212/01.wnl.0000281848.25142.11 · Cited by 75
Feldman, H., Schmitt, F. A., & Olin, J. T. (2006) · Alzheimer Disease & Associated Disorders · doi:10.1097/01.wad.0000213859.35355.59 · Cited by 73
Perispinal etanercept: Potential as an Alzheimer therapeutic
Griffin, W. S. T. (2008) · Journal of Neuroinflammation · doi:10.1186/1742-2094-5-3 · Cited by 66
Tong, G., Wang, J.-S., Sverdlov, O., Huang, S., Slemmon, R., Croop, R. S., Castaneda, L., Gu, H., Wong, O. T., Li, H., et al. (2012) · Clinical Therapeutics · doi:10.1016/j.clinthera.2012.01.022 · Cited by 65
Farlow, M. R., Alva, G., Meng, X., & Olin, J. T. (2009) · Current Medical Research and Opinion · doi:10.1185/03007990903434914 · Cited by 60
Zec, R. F., & Burkett, N. R. (2008) · Neurorehabilitation · doi:10.3233/nre-2008-23506 · Cited by 58
Almkvist, O., Darreh‐Shori, T., Stefanova, E. D., Spiegel, R., & Nordberg, A. K. (2004) · European Journal of Neurology · doi:10.1046/j.1468-1331.2003.00757.x · Cited by 57
Relative tolerability of Alzheimer's disease treatments.
Alva, G., & Cummings, J. L. (2008) · Europe PMC (PubMed Central) · Cited by 53
Pharmacologists and Alzheimer disease therapy: to boldly go where no scientist has gone before
Mancuso, C., Siciliano, R., Barone, E., Butterfield, D. A., & Preziosi, P. (2011) · Expert Opinion on Investigational Drugs · doi:10.1517/13543784.2011.601740 · Cited by 53
Rakover, I. S., Arbel, M., & Solomon, B. (2007) · Neurodegenerative Diseases · doi:10.1159/000103250 · Cited by 45
Tacrine-induced liver damage: an analysis of 19 candidate genes
Alfirevic, A., Mills, T., Carr, D. F., Barratt, B. J., Jawaid, A., Sherwood, J. L., Smith, J. C., Tugwood, J. D., Hartkoorn, R. C., Owen, A., et al. (2007) · Pharmacogenetics and Genomics · doi:10.1097/fpc.0b013e3282f1f12b · Cited by 43
P3‐391: Statins for the treatment of dementia
McGuinness, B., O’Hare, J., Bullock, R. A., Malouf, R. S., Craig, D., & Passmore, P. (2010) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2010.05.1933 · Cited by 40
Effect of Donepezil on Cognition in Severe Alzheimer's Disease: A Pooled Data Analysis
Cummings, J. L., Jones, R. W., Wilkinson, D. G., López, O. L., Gauthier, S. G., Waldemar, G., Zhang, R. H., Xu, Y., Sun, Y., Richardson, S., et al. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-100078 · Cited by 36
Progress in the Development of β-secretase Inhibitors for Alzheimer's Disease
Albert, J. S. (2009) · Progress in medicinal chemistry · doi:10.1016/s0079-6468(09)04804-8 · Cited by 34
Qu, B. X., Lambracht‐Washington, D., Fu, M., Eagar, T. N., Stüve, O., & Rosenberg, R. N. (2010) · Vaccine · doi:10.1016/j.vaccine.2010.05.054 · Cited by 34
Optimizing phase II of drug development for disease‐modifying compounds
Cummings, J. L. (2008) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2007.10.002 · Cited by 31
Clinical Observations with AN-1792 Using TAPIR Analyses
Höck, C., & Nitsch, R. M. (2005) · Neurodegenerative Diseases · doi:10.1159/000090368 · Cited by 23
Hara, H., Mouri, A., Yonemitsu, Y., Nabeshima, T., & Tabira, T. (2011) · Vaccine · doi:10.1016/j.vaccine.2011.07.057 · Cited by 13
Aisen, P. S., Schafer, K. A., Grundman, M., Pfeiffer, E., Sano, M., Davis, K. L., Farlow, M. R., Jin, S., Thomas, R. G., Thal, L. J., et al. (2003) · JAMA · doi:10.1001/jama.289.21.2819 · Cited by 5
Research works printed but not linked: 6
- Alva G., 2008, Psychiatry (Edgmont), 5, 27
- Ballard C., 2010, CNS Drugs, 24, 729
- Cummings J., 2008, Primary Psychiatry, 15, 66
- Hansen R., 2008, Clin Interv Aging, 3, 211
- Hey J., Koelsch G., Bilcer G., Jacobs A., Tolar M., Tang J. (2008) Single dose administration of the b-secretase inhibitor CTS21166 (ASP1720) reduces plasma Aβ40 in human subjects. Presented by Dr Koelsch in the International Conference on Alzheimer’s Disease (ICAD), Chicago, IL, USA, 26–31 July 2008. Available at: http://www.alzforum.org/new/detail.asp?id=1790
- Yiannopoulou K., 2009, Primary Psychiatry, 16, 29
Cited by
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The multiplex model of the genetics of Alzheimer's disease
Sims, R., Hill, M., & Williams, J. (2020) · Nature Neuroscience · doi:10.1038/s41593-020-0599-5 · Cited by 466
The Pivotal Role of NF-kB in the Pathogenesis and Therapeutics of Alzheimer’s Disease
Sun, E., Motolani, A., Campos, L., & Lu, T. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23168972 · Cited by 381
Gadhave, D. G., Sugandhi, V. V., Jha, S. K., Nangare, S., Gupta, G., Singh, S. K., Dua, K., Cho, H., Hansbro, P. M., & Paudel, K. R. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102357 · Cited by 420
Zhang, X., Tian, Y., Zeng, L., Tian, X., Sun, H., Liu, H., Moore, A. V., & Ran, C. (2013) · Journal of the American Chemical Society · doi:10.1021/ja405239v · Cited by 354
Metadata
- Authors
- Yiannopoulou, K. G., & Papageorgiou, S. G.
- Affiliations
- Laiko General Hospital of Athens (GR)
- National and Kapodistrian University of Athens (GR)
- Venue
- Therapeutic Advances in Neurological Disorders
- Publisher
- SAGE Publications
- Published
- 2012-10-15
- Volume
- 6
- Issue
- 1
- Pages
- 19-33
- ISSN
- 1756-2856 (ISSN-L)
- 1756-2864
- PMC
- PMC3526946
- OpenAlex
- W1987204546
- Cited by
- 677
- References
- 83
- Citations by year
- 2026: 35 · 2025: 55 · 2024: 66 · 2023: 70 · 2022: 84 · 2021: 81 · 2020: 83 · 2019: 61 · 2018: 45 · 2017: 37 · 2016: 27 · 2015: 9 · 2014: 9 · 2013: 14
- FWCI
- 6.86
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Therapeutic Advances in Neurological Disorders (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- 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
- Health Sciences › Medicine › Pharmacology (medical) › Cholinesterase and Neurodegenerative Diseases
- Keywords
- Alzheimer's disease, cholinesterase inhibitors, memantine, disease-modifying therapy, symptomatic treatment, amyloid plaques, neurofibrillary tangles, oxidative stress, neuroinflammation, cholesterol metabolism, NMDA receptor antagonists, clinical trials
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