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Nicotinamide Restores Cognition in Alzheimer's Disease Transgenic Mice via a Mechanism Involving Sirtuin Inhibition and Selective Reduction of Thr231-Phosphotau
Open accessAbstract
Memory loss is the signature feature of Alzheimer's disease, and therapies that prevent or delay its onset are urgently needed. Effective preventive strategies likely offer the greatest and most widespread benefits. Histone deacetylase (HDAC) inhibitors increase histone acetylation and enhance memory and synaptic plasticity. We evaluated the efficacy of nicotinamide, a competitive inhibitor of the sirtuins or class III NAD + -dependent HDACs in 3xTg-AD mice, and found that it restored cognitive deficits associated with pathology. Nicotinamide selectively reduces a specific phospho-species of tau (Thr231) that is associated with microtubule depolymerization, in a manner similar to inhibition of SirT1. Nicotinamide also dramatically increased acetylated α-tubulin, a primary substrate of SirT2, and MAP2c, both of which are linked to increased microtubule stability. Reduced phosphoThr231-tau was related to a reduction of monoubiquitin-conjugated tau, suggesting that this posttranslationally modified form of tau may be rapidly degraded. Overexpression of a Thr231-phospho-mimic tau in vitro increased clearance and decreased accumulation of tau compared with wild-type tau. These preclinical findings suggest that oral nicotinamide may represent a safe treatment for AD and other tauopathies, and that phosphorylation of tau at Thr231 may regulate tau stability.
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“Four months of NAM treatment increased the level of p25 2-fold, reduced p-TauThr231 levels, and improved cognitive function in 3xTgAD mice (Green et al., 2008).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Green et al., 2008
In the citing paper
“NAD+ augmentation inhibited Tau phosphorylation at different sites (Thr181, Ser202, Thr205, and Thr231) possibly through suppression of cyclin-dependent kinase 5 (Cdk5)-p25 complex activity (Fang et al., 2019; Green et al., 2008).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Green et al., 2008
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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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BackgroundTriple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
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BackgroundIncreased dosage of a sir-2 gene extends lifespan in Caenorhabditis elegans
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“The sirtuin family of deacetylases is implicated in cellular pathways that influence longevity in yeast, C. elegans, Drosophila, and mammals (Tissenbaum and Guarente, 2001; Anderson et al., 2003; Howitz et al., 2003; Wood et al., 2004; Baur et al., 2006).”
Background
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“SIRT1 was reported significantly reduced in AD affected brains, and this reduction paralleled the accumulation of tau [31,32], which raised the possibility that SIRT1 might regulate tau phosphorylation levels in vivo.”
BackgroundRole of Sirtuins in Physiology and Diseases of the Central Nervous System
Chojdak-Łukasiewicz, J., Bizoń, A., Waliszewska‐Prosół, M., Piwowar, A., Budrewicz, S. P., & Pokryszko‐Dragan, A. (2022) · Biomedicines · doi:10.3390/biomedicines10102434 · Cited by 33
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ResultShen, X., Li, H., Zhang, B., Li, Y., & Zhu, Z. (2025) · Cells · doi:10.3390/cells14191506 · Cited by 33
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“Consistently, another study with a 3xTg-AD mice model showed that nicotinamide administration was able to modulate SIRT1 activity and lysosomal proton gradient, thus promoting autolysosome acidification [358].”
BackgroundVibrational spectroscopic, molecular docking and quantum chemical studies on 6-aminonicotinamide
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“HDACi includes several subclasses, namely valproic acid (short chain fatty acids); vorinostat (hydroxamic acids); and suramin, nicotinamide/niacinamide (sirtuin inhibitors, class III HDACinhibitors)[6,13–15].”
Existing Evidence for the Repurposing of PARP-1 Inhibitors in Rare Demyelinating Diseases
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GTP energy dependence of endocytosis and autophagy in the aging brain and Alzheimer’s disease
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“Nicotinamide functions by lowering the levels of Thr231-Phosphotau, inhibiting sirtuin, and converting itself to NAD+ [315].”
Firdaus, Z., & Li, X. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252111658 · Cited by 26
“Furthermore, SIRT1, a NAD-dependent HDAC implicated in the neurodegeneration associated with AD and HD, has piqued the curiosity of many researchers [222,223].”
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Self-citationNAD augmentation as a disease-modifying strategy for neurodegeneration
Dölle, C., & Tzoulis, C. (2025) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2025.03.013 · Cited by 25
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“, oral administration of NA cannot modulate the activity of GSK3β and cdk5, but can enhance learning and memory via the upregulation of structural and synaptic proteins (Green et al. 2008).”
BackgroundResultInfluentialPan-HDAC Inhibitors Promote Tau Aggregation by Increasing the Level of Acetylated Tau
Jeong, H., Shin, S., Lee, J., Lee, S. H., Baik, J., Lim, S., & Kim, Y. K. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20174283 · Cited by 21
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“It has been reported that treatment with nicotinamide rescues both short- and long-term memory impairment in 3xTg-AD mice, the triple-transgenic mice which harbor a knock-in mutation of PSEN1M146V, the Swedish double mutation of APPKM670/671NL, and a frontotemporal dementia mutation in tau (tauP301L) on a 129/C57BL/6…”
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“In recent years, NA has attracted scientists’ attention for delaying the progression of Alzheimer’s disease in preclinical studies.(16) Acquiring the high encapsulated system of this freely soluble compound not only benefits the controlled delivery of NA itself, but can also enunciate the possibility of delivering oth…”
BackgroundChromatin Alterations in Neurological Disorders and Strategies of (Epi)Genome Rescue
Janowski, M., Milewska, M., Zare, P., & Pękowska, A. (2021) · Pharmaceuticals · doi:10.3390/ph14080765 · Cited by 21
Multifaced role of protein deacetylase sirtuins in neurodegenerative disease
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Nicotinamide, a vitamin B3 ameliorates depressive behaviors independent of SIRT1 activity in mice
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“Nicotinamide restored cognitive deficits in vivo using the 3x-Tg AD mice model by selectively reducing Thr231 in a Tau protein associated with microtubule depolymerization and increasing the acetylated α-tubulin [31].”
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Nicotinamide reduces dopamine in postnatal hypothalamus and causes dopamine-deficient phenotype
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Nutraceutical Strategies for Targeting Mitochondrial Dysfunction in Neurodegenerative Diseases
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“The proposed mechanism of action for nicotinamide involves its conversion to NAD + , which then inhibits sirtuin and reduces levels of Thr231-Phosphotau [229].”
Nicotinamide breaks effector CD8 T cell responses by targeting mTOR signaling
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“NAM was shown to be a SIRT1 inhibitor, facilitating the expansion of hematopoietic progenitors, restoring cognition in Alzheimer’s diseases, and ameliorating mouse health span (Green et al., 2008; Mitchell et al., 2018; Peled et al., 2012).”
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Virtual Screening in the Identification of Sirtuins’ Activity Modulators
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“However, the increased expression of SIRT-2 with age suggests that the preferential target of nicotinamide in AD is SIRT-2 [214,215].”
BackgroundBioinorganic Chemistry of Micronutrients Related to Alzheimer’s and Parkinson’s Diseases
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Novel 7‐secretase inhibitors uncover a common nucleotide‐binding site in JAK3, SIRT2, and PS1
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“and possibly mammals (17), are considered potential”
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Recent Nanoscale Carriers for Therapy of Alzheimer's Disease: Current Strategies and Perspectives
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“In this regard, the present study adds IVIG to a very small list of other FDA-approved drugs, including lithium [35], pioglitazone [36], and nicotinamide [37], which are capable of reducing NFT pathology in preclinical mouse models.”
MethodThe Therapeutic Potential of Epigenetic Modifications in Alzheimer’s Disease
Bufill, E., Nogué, R. R., & Blesa, R. (2020) · Exon Publications eBooks · doi:10.36255/exonpublications.alzheimersdisease.2020.ch9 · Cited by 15
“This compound can delay aging in mouse oocytes and delay cognitive impairment in a mouse model of AD (60).”
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“In a mouse model, nicotinamide lowers phosphorylated tau and protects microtubule stability 141 .”
Passos, C. D. S., Klein‐Júnior, L. C., Andrade, J. M. D. M., Matté, C., & Henriques, A. T. (2015) · Revista Brasileira de Farmacognosia · doi:10.1016/j.bjp.2015.07.002 · Cited by 15
“The nonselective inhibition of SIRT1 and SIRT2 enzymes by nicotinamide has shown to promote the restoration of cognitive deficits in a mice model of Alzheimer’s disease (Green et al., 2008).”
BackgroundTranscriptional signatures mediated by acetylation overlap with early-stage Alzheimer’s disease
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Qader, M. A., Hosseini, L., Abolhasanpour, N., Oghbaei, F., Maghsoumi‐Norouzabad, L., Salehi‐Pourmehr, H., Fattahi, F., & Sadeh, R. N. (2025) · BMC Neuroscience · doi:10.1186/s12868-025-00937-9 · Cited by 16
“…evaluated NOR test [6, 12, 21, 27–29, 39, 40], 4 studies evaluated the Y maze [12, 14, 18, 19], 4 studies evaluated passive avoidance test[25, 27, 31, 41], 3 studies evaluated Barnes [6, 39, 40] and fear conditioning test[12, 20, 28], 2 studies evaluated open field [24, 28] and EPM test [21,…”
InfluentialMitochondrial Dysfunction in Aging: Future Therapies and Precision Medicine Approaches
Jia, L., Wei, Z., Luoqian, J., Wang, X., & Huang, C. (2025) · MedComm – Future Medicine · doi:10.1002/mef2.70026 · Cited by 14
Geroprotective interventions in the 3xTg mouse model of Alzheimer’s disease
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“Administration of nicotinamide for 4 months to 4-month-old 3xTg mice improved both short- and long-term spatial learning in the MWM and improved contextual learning in the fear-conditioning assay [290].”
BackgroundMartens, N., Zhan, N., Yam, S. C., Leijten, F. P. J., Palumbo, M., Caspers, M. P. M., Tiane, A., Friedrichs, S., Li, Y., der Zee, L. V. V., et al. (2024) · Nutrients · doi:10.3390/nu16111614 · Cited by 15
“In addition, several studies reported preservation of cognitive decline despite the presence of A β plaques [19,24,53], suggesting that insoluble A β plaques may not directly cause clinical symptoms and that decreasing these A β plaques is not crucial for ameliorating AD symptoms.”
BackgroundAlkaloids from Psychotria Target Sirtuins: In Silico and In Vitro Interaction Studies
Sacconnay, L., Ryckewaert, L., Passos, C. D. S., Guerra, M., Kato, L., de Oliveira, C. A., Henriques, A. T., Carrupt, P., Simões‐Pires, C. A., & Nurisso, A. (2014) · Planta Medica · doi:10.1055/s-0034-1383261 · Cited by 14
Ji, F., Luan, H., Huang, Y., Cai, Z., & Li, M. (2017) · Journal of Analysis and Testing · doi:10.1007/s41664-017-0026-4 · Cited by 14
“To name a few notable downstream metabolites of tryptophan pathway, quinolinic acid is known as an excitotoxin in the central nervous system, 3-hydroxykynurenine is a potential endogenous neurotoxin whose increased levels have been described in several neurodegenerative disorders [27], kynurenic acid is an neuroprotec…”
BackgroundEpigenetic Drug Discovery for Alzheimer’s Disease
Cacabelos, R., & Teijido, Ó. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-811060-7.00022-x · Cited by 14
Mitophagy in Alzheimer's disease and its potential as a therapeutic target
Wei, J., Xiao, T., Lyu, J., Zhao, Y., Zhang, Y., Du, X., He, Y., Zhao, M., Yang, X., Yao, Y., et al. (2025) · Neurobiology of Disease · doi:10.1016/j.nbd.2025.107162 · Cited by 13
Apicidin attenuates memory deficits by reducing the Aβ load in APP / PS1 mice
Luo, B., Chen, J., Zhou, G., Xie, X., Tang, J., Wen, Q., Li, S., Xie, S., Long, Y., Chen, G., et al. (2023) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14102 · Cited by 12
Matysek, A., Sun, L., Kimmantudawage, S. P., Feng, L., & Maier, A. B. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.102029 · Cited by 15
“Nicotinamide derivatives paradoxically inhibit SIRT1 activity, via the reduction of tau species Thr231 leading to decreased microtubule depolymerization (Green et al., 2008), with downstream effects including reduction in tau protein via increased degradation, and decreased accumulation.”
Turek, M., Różycka‐Sokołowska, E., Owsianik, K., & Bałczewski, P. (2023) · Molecular Pharmaceutics · doi:10.1021/acs.molpharmaceut.3c00959 · Cited by 13
Ziman, B., Karabinis, P., Barghouth, P. G., & Oviedo, N. J. (2020) · Journal of Cell Science · doi:10.1242/jcs.239467 · Cited by 14
“Conversely, the specific effects achieved with RNAi could also be induced with NAM treatment, which is commonly used to inhibit sirtuin function in other experimental models (Avalos et al., 2005; Bitterman et al., 2002; Green et al., 2008; Sauve and Schramm, 2003).”
BackgroundThe use of Nicotinamide and Nicotinamide riboside as an adjunct therapy in the treatment of glaucoma
Silva, S. G. N. E., Occhiutto, M. L., & Costa, V. P. (2023) · European Journal of Ophthalmology · doi:10.1177/11206721231161101 · Cited by 14
Importance of NAD+ Anabolism in Metabolic, Cardiovascular and Neurodegenerative Disorders
Helman, T. J., & Braidy, N. (2022) · Drugs & Aging · doi:10.1007/s40266-022-00989-0 · Cited by 13
“NAM supplementation improved mitochondrial integrity, lowered the distribution of plaque and hyperphosphorylated tau pathologies, maintained microtubule stability [175] and attenuated cognitive deficits in a murine model [176].”
BackgroundNanotechnology Therapy for Alzheimer′s Disease Memory Impairment Attenuation
Ribarič, S. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22031102 · Cited by 13
“Previous research reported that nicotinamide restores cognition in AD model animals by sirtuin inhibition, and selective reduction of phosphorylated tau [85].”
BackgroundGoyal, S., Tiwari, S., Seth, B., Phoolmala, Tandon, A., & Chaturvedi, R. K. (2022) · Molecular Neurobiology · doi:10.1007/s12035-022-02862-y · Cited by 11
“The neuroprotective mechanism of nicotinamide is well reported against cognitive deterioration in several neurodegenerative diseases such as AD-specific rodent models [44, 45].”
BackgroundAfsheen, N., Rafique, S., Rafeeq, H., Irshad, K., Hussain, A., Huma, Z., Kumar, V., Bilal, M., Aleya, L., & Iqbal, H. M. N. (2022) · Environmental Science and Pollution Research · doi:10.1007/s11356-022-22779-2 · Cited by 11
Metabolism and Receptor Mechanisms of Niacin Action
Boronovskiy, S. E., Сергеевна, К. В., & Nartsissov, Y. R. (2024) · Cell and Tissue Biology · doi:10.1134/s1990519x23700025 · Cited by 12
“There is a large amount of experimental evidence of the beneficial effects of various forms of niacin in a number of neurodegenerative diseases (Green et al., 2008; Gong et al., 2013; Xie et al., 2019).”
Soliman, S. M., & Massoud, R. A. (2012) · Computational and Theoretical Chemistry · doi:10.1016/j.comptc.2012.02.022 · Cited by 11
Zeidler, J. D., Chini, C. C. S., Kanamori, K. S., Kashyap, S., Espíndola‐Netto, J. M., Thompson, K. D., Warner, G. M., Cabral, F. S., Peclat, T., Gomez, L. S., et al. (2022) · iScience · doi:10.1016/j.isci.2022.105431 · Cited by 11
“, 2003), in vivo (Green et al., 2008; Hathorn et al., 2011; Turunc Bayrakdar et al., 2014) and that it may possess anti-inflammatory activity (Hiromatsu et al.”
BackgroundSekiya, M., Sakakibara, Y., Hirota, Y., Ito, N., Chikamatsu, S., Takei, K., Nishijima, R., & Iijima, K. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106694 · Cited by 10
“…AD mice (Gong et al., 2013), APP/PS1 mice (Hou et al., 2021; Sorrentino et al., 2017; Xie et al., 2019; Xing et al., 2019; Yao et al., 2017), 5xFAD mice (Kim et al., 2020), and 3xTg-AD mice (Green et al., 2008; Liu et al., 2013), alleviating cognitive deficits and brain pathologies in these models.”
BackgroundGenetic Editing and Pharmacogenetics in Current And Future Therapy Of Neurocognitive Disorders
Prendecki, M., Kowalska, M., Totoń, E., & Kozubski, W. P. (2020) · Current Alzheimer Research · doi:10.2174/1567205017666200422152440 · Cited by 10
Wang, K., & Zhang, W. (2021) · Synapse · doi:10.1002/syn.22196 · Cited by 11
Is systemic activation of Sirt1 beneficial for ageing-associated metabolic disorders?
Tang, B. L., & Chua, C. E. L. (2009) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2009.11.016 · Cited by 10
Jarero-Basulto, J. J., Gasca-Martínez, Y., Rivera-Cervantes, M. C., Gasca‐Martínez, D., González, N., Beas‐Zárate, C., & Gudiño‐Cabrera, G. (2024) · NeuroSci · doi:10.3390/neurosci5020010 · Cited by 11
“A Tubulin is a protein that can undergo a series of PTMs (e.g., detyrosination, polyglutamylation, and acetylation) that affect its functionality and MT stability [49,50], triggering cellular stress.”
RetractedZhang, C., Shao, Q., Zhang, Y., Liu, W., Kang, J., Jin, Z., Huang, N., & Ning, B. (2024) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14826 · Cited by 11
Sirtuins in Brain and Neurodegenerative Disease
Szegő, É. M., Outeiro, T. F., & Kazantsev, A. G. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-813499-3.00013-7 · Cited by 9
Nutrients in Alzheimer’s Disease: The Interaction of Diet, Drugs and Disease
Liyanage, S. I., Vilekar, P., & Weaver, D. F. (2019) · Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques · doi:10.1017/cjn.2018.353 · Cited by 11
Meng, Y., Song, C., Ren, Z., Li, X., Yang, X., Ai, N., Yang, Y., Wang, D., Zhan, M., Wang, J., et al. (2021) · Cell Death and Disease · doi:10.1038/s41419-021-04395-z · Cited by 9
“Nicotinamide was often regarded as an inhibitor of PARP and Sirtuin pathways [12, 18]; however, there is limited evidence to directly support this role [11, 19–21].”
BackgroundAltay, Ö., Yang, H., Yıldırım, S., Bayram, C., Bolat, İ., Öner, S., Tozlu, Ö. Ö., Arslan, M. E., Hacımüftüoğlu, A., Shoaie, S., et al. (2024) · Biomedicines · doi:10.3390/biomedicines12040927 · Cited by 9
“For instance, nicotinamide has been shown to restore cognitive deficits in Alzheimer’s disease models by modulating tau phosphorylation and enhancing mitochondrial function and autophagy, processes vital for neuronal health [42,43].”
BackgroundNiacin, an Old Drug, has New Effects on Central Nervous System Disease
Chen, J., & Chopp, M. (2010) · The Open Drug Discovery Journal · Cited by 9
Neira-Peña, T., Espina-Marchant, P., Rojas-Mancilla, E., Esmar, D., Kraus, C., Muñoz, V., Perez, R. S., Rivera, B., Bustamante, D., Valdés, J. L., et al. (2014) · Springer eBooks · doi:10.1007/978-1-4614-5836-4_115 · Cited by 9
Witt, E. A., & Reissner, K. J. (2019) · Psychopharmacology · doi:10.1007/s00213-019-05404-y · Cited by 9
“…models, NAM is known to produce behavioral changes as well, including improved shortterm and long-term memory in Alzheimer’s disease model mice (Green et al. 2008), improved reference memory acquisition and reversal learning in post-cortical contusion injury rats (Peterson et al. 2012), and…”
Spencer, K. D., Bline, H., Chen, H. J., Verosky, B. G., Hilt, M. E., Jaggers, R. M., Gur, T., Mathé, E. A., & Bailey, M. T. (2024) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2024.07.024 · Cited by 9
“It is possible, however, that nicotinamide played a beneficial role, since nicotinamide has been linked to improvements in several neurological conditions, including Alzheimer ’ s disease, Parkinson ’ s disease, and Huntington ’ s disease (Fricker et al., 2018; Green et al., 2008).”
BackgroundYu, Q., Li, L., Yu, S., Han, J., Cheng, Q., Cui, Z., Chen, H., Li, M., & Lu, Z. (2025) · Neurochemical Research · doi:10.1007/s11064-025-04490-z · Cited by 9
“Oral administration of nicotinamide improved memory in an AD mouse model and reduced brain tau aggregates [112].”
Autophagy–NAD+ axis: emerging insights into neuronal homeostasis and neurodegenerative diseases
Koçak, G., Dimas, M. M., Silva, L., Silva-Amaral, D., Sun, C., Cruddas, S., Barrett, T. G., Martins‐de‐Souza, D., Cunha‐Neto, E., Brocardo, P. S., et al. (2025) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2025.1695486 · Cited by 8
Mezo‐González, C. E., Abdi, A. D., Reyes‐Castro, L. A., Olvera-Hernández, S., Almeida, C., Croyal, M., Aguesse, A., Gavioli, E. C., Zambrano, E., & Bolaños, F. J. (2022) · International Journal of Tryptophan Research · doi:10.1177/11786469221111116 · Cited by 10
Sirtuins Function as the Modulators in Aging-related Diseases in Common or Respectively
Wang, Q., & Guo, S. (2015) · Chinese Medical Journal · doi:10.4103/0366-6999.158375 · Cited by 10
“In mice AD model, studies have found that SIRT1 inhibition can restore cognition by stabilizing tau protein.[59] Deacetylase SIRT2 involves in neuron cells apoptosis by mediation of different proteins.”
BackgroundMelatonin attenuates scopolamine‐induced cognitive dysfunction through SIRT1/IRE1α/XBP1 pathway
Liu, X., Huang, S., Zheng, J., Wan, C., Tian, H., Cai, Y., Wang, Q., & Zhang, S. (2024) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14891 · Cited by 7
Alzheimer’s disease: a jigsaw puzzle comprised of different types of programmed cell death pieces
Wang, Y., Mu, D., Li, Y., Liu, C., Feng, J., Lai, Y., & Lou, G. (2025) · Brain Research · doi:10.1016/j.brainres.2025.149861 · Cited by 7
Hacıoğlu, C., Kar, F., & Kanbak, G. (2021) · Neurochemical Research · doi:10.1007/s11064-020-03216-7 · Cited by 7
Alzheimer’s Disease Pharmacology
Plascencia‐Villa, G., & Perry, G. L. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-820472-6.00018-9 · Cited by 6
Low-Dose Chidamide Treatment Displays Sex-Specific Differences in the 3xTg-AD Mouse
Dennison, J. L., Mendez, A. J., Szeto, A., Lohse, I., Wahlestedt, C., & Volmar, C. (2023) · Biomolecules · doi:10.3390/biom13091324 · Cited by 11
“Previous studies using 3xTg-AD mice have reported improvements in Morris Water Maze and Barnes Maze performance with HDAC inhibitor treatment [30,35,36,38], and either improvement or no change in NOR [30,36].”
Method
Metadata
- Authors
- Green, K. N., Steffan, J. S., Martinez-Coria, H., Sun, X., Schreiber, S. S., Thompson, L. M., & LaFerla, F. M.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- LaFerla, Frank M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-11-05
- Volume
- 28
- Issue
- 45
- Pages
- 11500-11510
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2617713
- OpenAlex
- W2089740883
- Cited by
- 404
- References
- 59
- Citations by year
- 2026: 9 · 2025: 20 · 2024: 25 · 2023: 24 · 2022: 18 · 2021: 23 · 2020: 23 · 2019: 21 · 2018: 21 · 2017: 28 · 2016: 18 · 2015: 18 · 2014: 29 · 2013: 27 · 2012: 28
- FWCI
- 16.52
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- Funders
- Alzheimer's Drug Discovery Foundation
- National Institutes of Health
- National Institute on Aging (AG0212982, R01AG021982)
- National Institute of Neurological Disorders and Stroke (R01NS052789, NS52789)
- 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
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- nicotinamide, Alzheimer's disease, sirtuins, SIRT1, SIRT2, tau phosphorylation, acetylated alpha-tubulin, microtubule stability, histone deacetylase inhibition, 3xTg-AD mice, cognitive impairment, tau clearance, tauopathy, memory loss
- MeSH terms
- Alzheimer Disease, Animals, Behavior, Animal, Butyrates, Cell Line, Transformed, Cognition Disorders, Disease Models, Animal, Enzyme Inhibitors, Humans, Mice, Inbred C57BL, Mice, Transgenic, Microtubule-Associated Proteins, Mutation, Niacinamide, Peptide Fragments, Phosphorylation, Threonine, Time Factors, Transfection, Tubulin, Vitamin B Complex, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Maze Learning, Sirtuins, Immunoprecipitation, Mice, Presenilin-1
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