Role of Calcium Homeostasis in Alzheimer’s Disease
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Alzheimer's disease (AD) is a neurodegenerative disease associated with senile plaques (SP) and neurofibrillary tangles (NFTs) in the brain. With aging of the population, AD has become the most common form of dementia. However, the mechanisms leading to AD are still under investigation, and there are currently no specific drugs for its treatment. Therefore, further study on the pathogenesis of AD to develop new drugs for AD treatment remains a top priority. Several studies have suggested that intracellular calcium homeostasis is dysregulated in AD, and this has been implicated in the deposition of amyloid β (Aβ), hyperphosphorylation of tau protein, abnormal synaptic plasticity, and apoptosis, all of which are involved in the occurrence and development of AD. In addition, some based on pathways linking calcium homeostasis and AD have achieved results in AD treatment. This review comprehensively explores the relationship between calcium homeostasis and the pathogenesis of AD to provide a theoretical basis for the future exploration of AD and the development of novel therapeutic drugs.
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CASQ1 is a ligand for calcium and studies suggest targeting calcium receptors may be beneficial in AD.
“CASQ1 is a ligand for calcium (DB11093) and studies suggest that targeting calcium receptors may be beneficial in AD88.”
From Proteogenomic analysis of human cerebrospinal fluid identifies neurologically relevant regulation and implicates causal proteins for Alzheimer’s disease (2024) · cites this paper as [88]
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Knopman, D. S., Jones, D. T., & Greicius, M. D. (2021) · Alzheimer's & Dementia · doi:10.1002/alz.12213 · Cited by 524 · see citing works
Fresh Evidence Points to an Old Suspect: Calcium
Marx, J. (2007) · Science · doi:10.1126/science.318.5849.384 · Cited by 71 · cited 6× · see citing works
“Aβ has also been proposed to destroy brain cells by forming channels in neuronal membranes to deregulate calcium homeostasis, as mentioned earlier.(26) Moreover, Aβ oligomers-”
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- [1]Clive Ballard S, Gauthier S, Corbett A, Brayne C, Aarsland D, Jones E. Alzheimer’s disease. Lancet. 2011; 377(9770): 1019– 1031. doi: 10.1016/S0140-6736(10)61349-9 21371747 · DOI · Paper page
- [2]Bezprozvanny I, Mattson MP. Neuronal calcium mishandling and the pathogenesis of Alzheimer’s disease. Trends Neurosci. 2008; 31(9): 454– 463. doi: 10.1016/j.tins.2008.06.005 18675468 PMC2566585 · DOI · Paper page
- [3]Ryan C, Ashkavand Z, Norman KR. The role of mitochondrial calcium homeostasis in Alzheimer’s and related diseases. Int J Mol Sci. 2020; 21(23): 9153. doi: 10.3390/ijms21239153 PMC7730848 33271784 · DOI
- [4]Si-Jia L. Two-dimensional nanomaterials against β-amyloid in the treatment of Alzheimer’s disease. Chin J Biochem Mol Biol. 2021; 37(05): e45.
- [6]Noemi Esteras N, Abramov AY. Mitochondrial calcium deregulation in the mechanism of beta-amyloid and tau pathology. Cells. 2020; 9(9): 2135. doi: 10.3390/cells9092135 PMC7564294 32967303 · DOI
- [7]Luísa Cortes L, Malva J, Rego AC, Pereira CF. Calcium signaling in aging and neurodegenerative diseases 2019. Int J Mol Sci. 2021; 21(3): 1125. doi: 10.3390/ijms21031125 PMC7037616 32046230 · DOI
- [8]Dibyadeep Datta D, Leslie SN, Wang M. Age-related calcium dysregulation linked with tau pathology and impaired cognition in non-human primates. Alzheimer’s Dement. 2021; 17(6): 920– 932. doi: 10.1002/alz.12325 33829643 PMC8195842 · DOI
- [9]Starkov A, Beal FMB. Portal to Alzheimer’s disease. Nat Med. 2008; 14(10): 1020– 1021. doi: 10.1038/nm1008-1020 18841137 PMC4511481 · DOI
- [10]Alain Lacampagne A, Liu X, Reiken S. Post-translational remodeling of ryanodine receptor induces calcium leak leading to Alzheimer’s disease-like pathologies and cognitive deficits. Acta Neuropathol. 2017; 134(5): 749– 767. doi: 10.1007/s00401-017-1733-7 28631094 · DOI
- [11]Gholami H, Pourbadie N. Preventing effect of L-type calcium channel blockade on electrophysiological alterations in dentate gyrus granule cells induced by entorhinal amyloid pathology. PLoS One. 2015; 10(2): e117555. PMC4331091 25689857
- [12]Bei-Ling LU. Advances in calcium signaling and Alzheimer’s disease. Chin J Gerontol. 2017; 37(10): 2567– 2570.
- [13]Luisa Galla L, Redolfi N, Pozzan T, Pizzo P, Greotti E. Intracellular calcium dysregulation by the Alzheimer’s disease-linked protein presenilin 2. Int J Mol Sci. 2020; 21(3): 770. doi: 10.3390/ijms21030770 PMC7037278 31991578 · DOI
- [14]Li-ying JYLZ. Research progress of antidepressants targeting NMDAR. Chin J Med Chem. 2020; 30(8): 502– 508.
- [15]Sushma S, Mondal AC. Role of GPCR signaling and calcium dysregulation in Alzheimer’s disease. Mol Cell Neurosci. 2019; 101: 103414. doi: 10.1016/j.mcn.2019.103414 31655116 · DOI
- [16]Angulo L, Henzi THSA, Neymotin SA. Amyloid pathology–produced unexpected modifications of calcium homeostasis in hippocampal subicular dendrites. Alzheimers Dement. 2020; 16(2): 251– 261. doi: 10.1016/j.jalz.2019.07.017 31668966 · DOI
- [17]Jia-Yin JIN. Research progress on the involvement of inositol 1;4;5-trisphosphate receptors in the occurrence of neurodegenerative diseases. Prog Physiol Sci. 2020; 51(06): 453– 458.
- [18]Cahalan MD. STIMulating store-operated Ca2+ entry. Nat Cell Biol. 2009; 11(6): 669– 677. doi: 10.1038/ncb0609-669 19488056 PMC2721799 · DOI
- [19]Senthil Selvaraj YSJA, Sun Y, Watt JA. Neurotoxin-induced ER stress in mouse dopaminergic neurons involves downregulation of TRPC1 and inhibition of AKT/mTOR signaling. J Clin Invest. 2012; 122(4): 1354– 1367. doi: 10.1172/JCI61332 22446186 PMC3314472 · DOI
- [20]Bezprozvanny I. Calcium signaling and neurodegenerative diseases. Trends Mol Med. 2009; 15(3): 89– 100. doi: 10.1016/j.molmed.2009.01.001 19230774 PMC3226745 · DOI
- [21]Khachaturian ZS. Calcium Hypothesis of Alzheimer’s disease and brain aging: a framework for integrating new evidence into a comprehensive theory of pathogenesis. Alzheimers Dement. 2017; 13(2): 178– 182. doi: 10.1016/j.jalz.2016.12.006 28061328 · DOI · Paper page
- [22]Yoo AS, Cheng I, Chung S, et al. Presenilin-mediated modulation of capacitative calcium entry. Neuron. 2000; 27(3): 561– 572. doi: 10.1016/S0896-6273(00)00066-0 11055438 · DOI
- [23]Thinakaran GTAS, Sisodia SS. Presenilins and Alzheimer disease: the calcium conspiracy. Nat Neurosci. 2006; 9(11): 1354– 1355. doi: 10.1038/nn1106-1354 17066063 · DOI
- [24]Tu H, Nelson O, Bezprozvanny A. Presenilins form ER Ca2+ leak channels. a function disrupted by familial Alzheimer’s disease-linked mutations. Cell. 2006; 126(5): 981– 993. doi: 10.1016/j.cell.2006.06.059 16959576 PMC3241869 · DOI
- [25]Lu GAI. The mechanism of calcium ion in regulating Aβ amyloid accumulation. Chin J Gerontol. 2016; 36(5): 1249– 1251.
- [27]Jing NIE. The role of presenilin in the pathogenesis of Alzheimer’s disease. West China J Pharm Sci. 2017; 32(01): 99– 103.
- [28]Ping SUN. Progress of neuronal calcium dyshomeostasis in the pathogenesis of Alzheimer’s disease. Prog Mod Biomed. 2009; 9(06): 1183– 1185.
- [29]Lippa CF, Saunders AM, Smith TW. Familial and sporadic Alzheimer’s disease: neuropathology cannot exclude a final common pathway. Neurology. 1996; 46(2): 406– 412. doi: 10.1212/WNL.46.2.406 8614503 · DOI
- [30]De Strooper B, Saftig P, Craessaerts K. Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein. Nature. 1998; 391(6665): 387– 390. doi: 10.1038/34910 9450754 · DOI · Paper page
- [31]Ying Gao Y, Ren R-J, Zhong Z-L. Mutation profile of APP. PSEN1; and PSEN2 in Chinese Familial Alzheimer’s Disease. Neurobiol Aging. 2019; 77: 154– 157. doi: 10.1016/j.neurobiolaging.2019.01.018 30822634 · DOI
- [32]Chun-Kit B, Tong CSLW. Familial Alzheimer’s disease-associated presenilin 1 mutants promote γ-secretase cleavage of STIM1 to impair store-operated Ca2+ entry. Sci Signal. 2016; 9(444): a89. PMC5384262 27601731
- [33]Olga Simakova O, Arispe NJ. Early and late cytotoxic effects of external application of the Alzheimer’s Abeta result from the initial formation and function of Abeta ion channels. Biochemistry. 2006; 45(18): 5907– 5915. doi: 10.1021/bi060148g 16669633 · DOI
- [34]Kuchibhotla KV, Goldman ST, Lattarulo CR, et al. Abeta plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks. Neuron. 2008; 59(2): 214– 225. doi: 10.1016/j.neuron.2008.06.008 18667150 PMC2578820 · DOI · Paper page
- [35]Maria Calvo-Rodriguez M, Hou SS, Snyder AC. Increased mitochondrial calcium levels associated with neuronal death in a mouse model of Alzheimer’s disease. Nat Commun. 2020; 11(1): 2146. doi: 10.1038/s41467-020-16074-2 32358564 PMC7195480 · DOI
- [36]Laura Texidó L, Martín-Satué M, Alberdi E, Solsona C, Matute C. Amyloid β peptide oligomers directly activate NMDA receptors. Cell Calcium. 2011; 49(3): 184– 190. doi: 10.1016/j.ceca.2011.02.001 21349580 · DOI
- [37]Hartmann H, Eckert A, Muller WE. Apolipoprotein E and cholesterol affect neuronal calcium signalling: the possible relationship to beta-amyloid neurotoxicity. Biochem Biophys Res Commun. 1994; 200(3): 1185– 1192. doi: 10.1006/bbrc.1994.1576 8185566 · DOI
- [38]LaFerla FM. Calcium dyshomeostasis and intracellular signalling in Alzheimer’s disease. Nat Rev Neurosci. 2002; 3(11): 862– 872. doi: 10.1038/nrn960 12415294 · DOI
- [39]Ohm TG. Apolipoprotein E and beta A4-amyloid: signals and effects. Biochem Soc Symp. 2001; 67: 121– 129. 11447828
- [40]Mattson MP. Pathways towards and away from Alzheimer’s disease. Nature. 2004; 430(7000): 631– 639. doi: 10.1038/nature02621 15295589 PMC3091392 · DOI · Paper page
- [41]Peterson C. Altered calcium uptake in cultured skin fibroblasts from patients with Alzheimer’s disease. N Engl J Med. 1985; 312(16): 1063– 1065. 3982463
- [42]Deary IJ, Hendrickson AE. Calcium and Alzheimer’s disease. Lancet. 1986; 1(8491): 1219. doi: 10.1016/S0140-6736(86)91205-5 2871461 · DOI
- [43]Green KN, Smith IF, Laferla FM. Role of calcium in the pathogenesis of Alzheimer’s disease and transgenic models. Subcell Biochem. 2007; 45: 507– 521. 18193650
- [44]Yanyan YXLX. Experimental research progress on traditional Chinese medicine in treatment of Alzheimer’s disease by regulating and controlling calcium ions in steady state. Chin Arch Trad Chin Med. 2018; 36(01): 49– 52.
- [45]Xi-Ju HE. Research progress of transient receptor potential channels in neurons. J Hubei Univ Med. 2014; 33(01): 81– 84.
- [46]Xiaoyuan HOU. Interplay between calcium signaling and reactive oxygen species. Chin J Cell Biol. 2019; 41(09): 1837– 1844.
- [47]Ru-Yi LIN. Progress of the relationship between Ca2+ dysregulation and Alzheimer’s disease development. Chin Bull Life Sci. 2012; 24(2): 297– 303.
- [48]Pooja Jadiya P, Kolmetzky DW, Tomar D. Impaired mitochondrial calcium efflux contributes to disease progression in models of Alzheimer’s disease. Nat Commun. 2019; 10(1): 3885. doi: 10.1038/s41467-019-11813-6 31467276 PMC6715724 · DOI · Paper page
- [49]Kodis J, Choi SCES. N-methyl-D-aspartate receptor–mediated calcium influx connects amyloid-b oligomers to ectopic neuronal cell cycle reentry in Alzheimer’s disease. Alzheimers Dement. 2018; 14(10): 1302– 1312. doi: 10.1016/j.jalz.2018.05.017 30293574 PMC8363206 · DOI
- [50]Tanzi RE. Of calcium, caspases, and cognitive decline. Nat Med. 1998; 4(10): 1127– 1128. doi: 10.1038/2622 9771743 · DOI
- [51]David Riascos DDLA, de Leon D, Baker-Nigh A. Age-related loss of calcium buffering and selective neuronal vulnerability in Alzheimer’s disease. Acta Neuropathol. 2011; 122(5): 565– 576. doi: 10.1007/s00401-011-0865-4 21874328 PMC3245740 · DOI
- [52]Ling ZHANG. Research progress on the pathogenesis of Alzheimer’s disease and its immunotherapy. Mod pract med. 2019; 31(02): 147– 148.
- [53]Min Y, Xu W, Xihan G. Progress on loss-of-function hypothesis of presenilin-1 mutations in Alzheimer diseases. J Zhejiang Univ. 2020; 49(4): 487– 499. PMC8800746 32985163
- [54]Pei-Chang CYWY. Regulation of amyloidogenesis and clearance of β-amyloid in Alzheimer’s disease. Chin J Biochem Mol Biol. 2021; 37(2): 176– 181.
- [55]Bennett BD, Denis P, Haniu M. A furin-like convertase mediates propeptide cleavage of BACE. the Alzheimer’s beta-secretase. J Biol Chem. 2000; 275(48): 37712– 37717. doi: 10.1074/jbc.M005339200 10956649 · DOI
- [56]Li liu RMGK. Palmitate induces transcriptional regulation of BACE1 and presenilin by STAT3 in neurons mediated by astrocytes. Exp Neurol. 2013; 248: 482– 490. 23968646 PMC3787872
- [57]María florencia Ogara MF, Belluscio LM, de la Fuente V. CDK5-mediated phosphorylation of p19INK4d avoids DNA damage-induced neurodegeneration in mouse hippocampus and prevents loss of cognitive functions. Biochimica et Biophysica Acta (BBA) - Mol Cell Res. 2014; 1843(7): 1309– 1324. doi: 10.1016/j.bbamcr.2014.03.026 24703879 · DOI
- [58]Joe Atherton J, Kurbatskaya K, Bondulich M. Calpain cleavage and inactivation of the sodium calcium exchanger-3 occur downstream of Aβ in Alzheimer’s disease. Aging Cell. 2014; 13(1): 49– 59. doi: 10.1111/acel.12148 23919677 PMC4326873 · DOI
- [59]Gui-hai CHEN. The expression of calcium/ calmodulin-dependent protein kinase II in the senile plaques in Alzheimer disease. Chin J Neurosci. 2004; 20(6): 441– 445.
- [60]Georges Mairet-Coello G, Courchet J, Pieraut S, Courchet V, Maximov A, Polleux F. The CAMKK2-AMPK kinase pathway mediates the synaptotoxic effects of Ab oligomers through tau phosphorylation. Neuron. 2013; 78(1): 94– 108. doi: 10.1016/j.neuron.2013.02.003 23583109 PMC3784324 · DOI · Paper page
- [61]Wen-Ming YANG. Research progress on genes related to Alzheimer’s disease. Chin J Gerontol. 2013; 33(2): 455– 459.
- [62]Tanzi E, Bertram LB. Alzheimer’s disease: the latest suspect. Nature. 2008; 454(7205): 706– 708. doi: 10.1038/454706a 18685694 · DOI
- [63]Ute Dreses-Werringloer U, Lambert J-C, Vingtdeux V, et al. A polymorphism in CALHM1 influences Ca2+ homeostasis. Ab levels. and Alzheimer’s disease risk. Cell. 2008; 133(7): 1149– 1161. doi: 10.1016/j.cell.2008.05.048 18585350 PMC2577842 · DOI
- [64]Green N, LaFerla FML. Linking calcium to Abeta and Alzheimer’s disease. Neuron. 2008; 59(2): 190– 194. doi: 10.1016/j.neuron.2008.07.013 18667147 · DOI
- [65]Yang ZHOU. Research progress on genetics and signaling pathways of Alzheimer’s disease. Acta Univ Med Anhui. 2019; 54(06): 994– 1000.
- [66]Lars Bertram L, Schjeide B-M-M, Hooli B. No association between CALHM1 and Alzheimer’s disease risk. Cell. 2008; 135(6): 993– 994. doi: 10.1016/j.cell.2008.11.030 19070563 PMC2841134 · DOI
- [67]Joana S, Cristóvão VKMI, Hugo M, Botelho CGRD, Tobias Madl GFBR. The neuronal S100B protein is a calcium-tuned suppressor of amyloid-aggregation. Sci Adv. 2018; 4: 1– 13. PMC6025902 29963623
- [68]Meng-ting LI, Zhao-Yang Z, Wen-Rong H, et al. Research progress in the pathogenesis of Alzheimer’s disease. World Latest Med Info. 2020; 20(76): 39–41; 44.
- [69]Ji-Yun WU. Effect of calcium signaling on Alzheimer diseases pathogenesis. J Jinggangshan Univ. 2010; 31(04): 107– 109.
- [70]Nathalie Pierrot N, Santos SF, Feyt C, Morel M, Brion J-P, Octave J-N. Calcium-mediated transient phosphorylation of tau and amyloid precursor protein followed by intraneuronal amyloid-beta accumulation. J Biol Chem. 2006; 281(52): 39907– 39914. doi: 10.1074/jbc.M606015200 17085446 · DOI
- [71]Gong CX. Phosphoprotein phosphatase activities in Alzheimer disease brain. J Neurochem. 1993; 61(3): 921– 927. doi: 10.1111/j.1471-4159.1993.tb03603.x 8395566 · DOI · Paper page
- [72]Hartigan JA, Johnson GVW. Transient increases in intracellular calcium result in prolonged site-selective increases in Tau phosphorylation through a glycogen synthase kinase 3beta-dependent pathway. J Biol Chem. 1999; 274(30): 21395– 21401. doi: 10.1074/jbc.274.30.21395 10409701 · DOI · Paper page
- [73]Thibault O, Hadley R, Landfield PW. Elevated postsynaptic [Ca2+] i and L-type calcium channel activity in aged hippocampal neurons: relationship to impaired synaptic plasticity. J Neurosci. 2001; 21(24): 9744– 9756. doi: 10.1523/JNEUROSCI.21-24-09744.2001 11739583 PMC6763040 · DOI
- [74]Fei XU. The relationship between Tau protein. Aβ protein and Alzheimer’s disease and their effects. J Clin Med Pract. 2008; 3: 118– 120.
- [75]Tiwari SS, Mizuno KMAG, Ghosh A. Alzheimer-related decrease in CYFIP2 links amyloid production to tau hyperphosphorylation and memory loss. Brain. 2016; 139(10): 2751– 2765. doi: 10.1093/brain/aww205 27524794 PMC5035822 · DOI · Paper page
- [76]Anshua Ghosh A, Giese KP. Calcium/calmodulin-dependent kinase II and Alzheimer’s disease. Ghosh Giese Mol Brain. 2015; 8(1): 78. doi: 10.1186/s13041-015-0166-2 26603284 PMC4657223 · DOI · Paper page
- [77]Rui DING. The role of calpain in Alzheimer’s disease. Foreign Med Sci. 2007; 28(06): 257– 261.
- [78]Kai-wen GUO. Advance in mechanisms of calpain involved in hyperphosphorylation and truncation of tau protein. Chinese J Rehabilitation Theory Pract. 2020; 26(10): 1182– 1185.
- [79]Mahaman Y, Huang F, Kessete Afewerky H, Maibouge TMS, Ghose B, Wang X. Involvement of calpain in the neuropathogenesis of Alzheimer’s disease. Med Res Rev. 2018; 39(2): 608– 630. doi: 10.1002/med.21534 30260518 PMC6585958 · DOI
- [80]Yi D. Irisin: anew target for exercise to improve decline in Alzheimer’s Disease. China Sport Sci Technol. 2020; 9(56): 30– 36.
- [81]Zhao-Peng ZHOU. Research progress of synaptic plasticity after cerebral ischemia. Guangdong Med J. 2018; 39(23): 3573– 3577.
- [82]Chengyu GUO. Research progress of calcium homeostasis in neurodegenerative diseases. J Pract Med. 2020; 36(02): 263– 267.
- [83]Chun-Lei Z. New discovery of Alzheimer’s disease pathology——Mutated genes in patients may play an important role. World Sci. 2009; 12: 35.
- [84]Cassia Overk C, Masliah E. Perspective on the calcium dyshomeostasis hypothesis in the pathogenesis of selective neuronal degeneration in animal models of AD. Alzheimers Dement. 2017; 13(2): 183– 185. doi: 10.1016/j.jalz.2017.01.005 28130011 PMC5935121 · DOI
- [85]Na WJW. Research progress of learning and memory and neurotoxicity mediated by NMDA receptor. Chinese J Gen Pract. 2020; 18(06): 994– 997.
- [86]Yanjun Zhao Y, Sivaji S, Chiang MC, Ali H. Amyloid beta peptides block new synapse assembly by nogo receptor-mediated inhibition of T-type calcium channels. Neuron. 2017; 96(2): 355– 372. doi: 10.1016/j.neuron.2017.09.041 29024660 PMC6101033 · DOI
- [87]Tariot PN, Farlow MR, Grossberg GT, et al. Memantine treatment in patients with moderate to severe alzheimer disease already receiving donepezil: a randomized controlled trial. JAMA. 2004; 291(3): 317– 324. doi: 10.1001/jama.291.3.317 14734594 · DOI · Paper page
- [88]Farlow R, Salloway SSPN, Tariot PN. Effectiveness and tolerability of high-dose (23 mg/d) versus standard-dose (10 mg/d) donepezil in moderate to severe Alzheimer’s disease: a 24-week randomized double-blind study. Clin Ther. 2010; 32(7): 1234– 1251. doi: 10.1016/j.clinthera.2010.06.019 20678673 PMC3068609 · DOI
- [89]Ross Penninkilampi R, Brothers HM, Eslick GD. Safety and efficacy of anti-amyloid-β immunotherapy in Alzheimer’s disease: a systematic review and meta analysis. J Neuroimmune Pharmacol. 2017; 12(1): 194– 203. doi: 10.1007/s11481-016-9722-5 28025724 · DOI
- [90]Jian-liang HFF. Tau-targeting immunotherapies for Alzheimer ′s disease: research advances. Int J Pharm Res. 2020; 47(10): 774– 780.
- [91]Moussa CE-H. Beta-secretase inhibitors in Phase I and Phase II clinical trials for Alzheimer’s disease. Expert Opin Investig Drugs. 2017; 26(10): 1131– 1136. doi: 10.1080/13543784.2017.1369527 28817311 · DOI
- [92]Ji-Yu YANG. Alzheimers disease and its drug treatment progress. Sichuan J Physiol Sci. 2017; 39(02): 101– 103.
- [93]Daverey A, Agrawal SK. Neuroprotective effects of Riluzole and Curcumin in human astrocytes and spinal cord white matter hypoxia. Neurosci Lett. 2020; 738: 135351. doi: 10.1016/j.neulet.2020.135351 32891672 · DOI
- [94]Dost FS, Kaya D, Ontan MS. Theracurmin supplementation may be a therapeutic option for older patients with Alzheimer’s disease: a 6-month retrospective follow-up study. Curr Alzheimer Res. 2021; 18(14): 1087– 1092. doi: 10.2174/1567205019666211221125255 34939543 · DOI
- [95]Kastanenka V, Bussiere TBNS, Shakerdge N. Immunotherapy with aducanumab restores calcium homeostasis in Tg2576 mice. J Neurosci. 2016; 36(50): 12549– 12558. doi: 10.1523/JNEUROSCI.2080-16.2016 27810931 PMC5157102 · DOI
- [96]Maria Calvo-Rodriguez M, Bacskai BJ. Mitochondria and calcium in Alzheimer’s disease: from cell signaling to neuronal cell death. Trends Neurosci. 2020; 44(2): 136– 151. doi: 10.1016/j.tins.2020.10.004 33160650 · DOI · Paper page
- [97]Hyun Jik Lee YHJG, Jung YH, Choi GE. Urolithin A suppresses high glucose-induced neuronal amyloidogenesis by modulating TGM2-dependent ER-mitochondria contacts and calcium homeostasis. Cell Death Differ. 2020; 28(1): 184– 202. doi: 10.1038/s41418-020-0593-1 32704090 PMC7852667 · DOI
- [98]Alessandra Bisi RLAM, Arribas RL, Micucci M. Polycyclic maleimide-based derivatives as first dual modulators of neuronal calcium channels and GSK-3b for Alzheimer’s disease treatment. Eur J Med Chem. 2019; 163: 394– 402. doi: 10.1016/j.ejmech.2018.12.003 30530190 · DOI
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Aducanumab—Hope or Disappointment for Alzheimer’s Disease
Wojtunik-Kulesza, K., Rudkowska, M., & Orzeł-Sajdłowska, A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24054367 · Cited by 73 · see citing works
- Authors
- Ge, M., Zhang, J., Chen, S., Huang, Y., Chen, W., He, L., & Zhang, Y.
- Affiliations
- Zhejiang Chinese Medical University (CN)
- Corresponding author
- Zhang, Yuyan
- Venue
- Neuropsychiatric Disease and Treatment
- Publisher
- Informa UK Limited
- Published
- 2022-03
- Volume
- Volume 18
- Pages
- 487-498
- ISSN
- 1176-6328 (ISSN-L)
- 1178-2021
- PMC
- PMC8901263
- OpenAlex
- W4214936098
- Cited by
- 124
- References
- 2
- Citations by year
- 2026: 23 · 2025: 35 · 2024: 39 · 2023: 23 · 2022: 4
- FWCI
- 3.41
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Neuropsychiatric Disease and Treatment (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
- Funders
- National Natural Science Foundation of China (81774230)
- Natural Science Foundation of Zhejiang Province (LY21H270012)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- Alzheimer's disease, calcium homeostasis, intracellular calcium dysregulation, amyloid-beta deposition, tau hyperphosphorylation, neurofibrillary tangles, amyloid plaques, synaptic plasticity, apoptosis, AD pathogenesis
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