CoChat
Sign Up
Cited by 205Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchDementia and Cognitive Impairment Research

Calcium/calmodulin-dependent kinase II and Alzheimer’s disease

Open access
Ghosh, Anshua, Giese, Karl Peter·2015·Molecular Brain
DOI 10.1186/s13041-015-0166-2PMC PMC4657223
Open this paper in CoChat — free accountOpen PDF

Abstract

CaMKII is a remarkably complex protein kinase, known to have a fundamental role in synaptic plasticity and memory formation. Further, CaMKII has also been suggested to be a tau kinase. CaMKII dysregulation may therefore be a modulator of toxicity in Alzheimer's disease, a dementia characterised by aberrant calcium signalling, synapse and neuronal loss, and impaired memory. Here, we first examine the evidence for CaMKII dysregulation in Alzheimer's patients and draw parallels to findings in disease models which recapitulate key aspects of the disease. We then put forward the hypothesis that these changes critically contribute to neurodegeneration and memory impairment in Alzheimer's disease.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1186/s13041-015-0166-2

Cites

18 of 18 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Compared to unaffected Sst supertypes, vulnerable Sst supertypes collectively downregulated specific kinases and E3 ubiquitin ligases.

    “Compared to unaffected Sst supertypes, the vulnerable Sst supertypes collectively downregulated specific kinases (from the tyrosine kinase56 and calcium2+/calmodulin-dependent kinase57 families) (Fig. 5h, green) and E3 ubiquitin ligases (from the homologous to the E6-AP carboxyl terminus (HECT) family58) (Fig. 5h, blue).”

    From Integrated multimodal cell atlas of Alzheimer’s disease (2024) · cites this paper as [57]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 77

  1. [1]Alzheimer A Stelzmann RA Schnitzlein HN Murtagh FR An English translation of Alzheimer’s 1907 paper, “Uber eine eigenartige Erkankung der Hirnrinde” Clin Anat 1995 8 6 429 31 10.1002/ca.980080612 8713166 · DOI · Paper page
  2. [2]Glenner GG Wong CW Alzheimer’s disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein Biochem Biophys Res Commun 1984 120 3 885 890 10.1016/S0006-291X(84)80190-4 6375662 · DOI · Paper page
  3. [3]Glenner GG Wong CW Alzheimer‘s disease and Down’s syndrome: sharing of a unique cerebrovascular amyloid fibril protein Biochem Biophys Res Commun 1984 122 3 1131 1135 10.1016/0006-291X(84)91209-9 6236805 · DOI · Paper page
  4. [4]Masters CL Simms G Weinman NA Multhaup G McDonald BL Beyreuther K Amyloid plaque core protein in Alzheimer disease and Down syndrome Proc Natl Acad Sci U S A 1985 82 12 4245 9 10.1073/pnas.82.12.4245 3159021 PMC397973 · DOI · Paper page
  5. [5]Goedert M Wischik CM Crowther RA Walker JE Klug A Cloning and sequencing of the cDNA encoding a core protein of the paired helical filament of Alzheimer disease: identification as the microtubule-associated protein tau Proc Natl Acad Sci U S A 1988 85 11 4051 5 10.1073/pnas.85.11.4051 3131773 PMC280359 · DOI · Paper page
  6. [6]Grundke-Iqbal I Iqbal K Tung YC Quinlan M Wisniewski HM Binder LI Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology Proc Natl Acad Sci U S A 1986 83 13 4913 7 10.1073/pnas.83.13.4913 3088567 PMC323854 · DOI · Paper page
  7. [7]Ihara Y Nukina N Miura R Ogawara M Phosphorylated tau protein is integrated into paired helical filaments in Alzheimer’s disease J Biochem 1986 99 6 1807 10 2427509
  8. [8]Kosik KS Joachim CL Selkoe DJ Microtubule-associated protein tau (tau) is a major antigenic component of paired helical filaments in Alzheimer disease Proc Natl Acad Sci U S A 1986 83 11 4044 4048 10.1073/pnas.83.11.4044 2424016 PMC323662 · DOI
  9. [12]DeKosky ST Scheff SW Synapse loss in frontal cortex biopsies in Alzheimer’s disease: correlation with cognitive severity Ann Neurol 1990 27 5 457 464 10.1002/ana.410270502 2360787 · DOI · Paper page
  10. [14]Scheff SW Price DA Schmitt FA DeKosky ST Mufson EJ Synaptic alterations in CA1 in mild Alzheimer disease and mild cognitive impairment Neurology 2007 68 18 1501 8 10.1212/01.wnl.0000260698.46517.8f 17470753 · DOI · Paper page
  11. [15]Terry RD Masliah E Salmon DP Butters N DeTeresa R Hill R Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment Ann Neurol 1991 30 4 572 80 10.1002/ana.410300410 1789684 · DOI · Paper page
  12. [16]Masliah E Mallory M Hansen L DeTeresa R Terry RD Quantitative synaptic alterations in the human neocortex during normal aging Neurology 1993 43 1 192 7 10.1212/WNL.43.1_Part_1.192 8423884 · DOI
  13. [17]Moolman DL Vitolo OV Vonsattel JP Shelanski ML Dendrite and dendritic spine alterations in Alzheimer models J Neurocytol 2004 33 3 377 87 10.1023/B:NEUR.0000044197.83514.64 15475691 · DOI · Paper page
  14. [21]Shankar GM Li S Mehta TH Garcia-Munoz A Shepardson NE Smith I Amyloid-beta protein dimers isolated directly from Alzheimer’s brains impair synaptic plasticity and memory Nat Med 2008 14 8 837 42 10.1038/nm1782 18568035 PMC2772133 · DOI · Paper page
  15. [22]Li S Hong S Shepardson NE Walsh DM Shankar GM Selkoe D Soluble oligomers of amyloid Beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake Neuron 2009 62 6 788 801 10.1016/j.neuron.2009.05.012 19555648 PMC2702854 · DOI · Paper page
  16. [23]Marcello E Epis R Di Luca M Amyloid flirting with synaptic failure: towards a comprehensive view of Alzheimer’s disease pathogenesis Eur J Pharmacol 2008 585 1 109 118 10.1016/j.ejphar.2007.11.083 18377893 · DOI
  17. [24]LaFerla FM Calcium dyshomeostasis and intracellular signalling in Alzheimer’s disease Nat Rev Neurosci 2002 3 11 862 872 10.1038/nrn960 12415294 · DOI
  18. [25]Bezprozvanny I Mattson MP Neuronal calcium mishandling and the pathogenesis of Alzheimer’s disease Trends Neurosci 2008 31 9 454 463 10.1016/j.tins.2008.06.005 18675468 PMC2566585 · DOI · Paper page
  19. [26]Mattson MP Cheng B Davis D Bryant K Lieberburg I Rydel RE Beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity J Neurosci 1992 12 2 376 89 1346802 PMC6575616
  20. [27]Demuro A Parker I Stutzmann GE Calcium signaling and amyloid toxicity in Alzheimer disease J Biol Chem 2010 285 17 12463 12468 10.1074/jbc.R109.080895 20212036 PMC2857063 · DOI
  21. [29]Hanson PI Schulman H Neuronal Ca2+/calmodulin-dependent protein kinases Annu Rev Biochem 1992 61 559 601 10.1146/annurev.bi.61.070192.003015 1323238 · DOI
  22. [30]Bronstein J Nishimura R Lasher R Cole R de Vellis J Farber D Calmodulin kinase II in pure cultured astrocytes J Neurochem 1988 50 1 45 9 10.1111/j.1471-4159.1988.tb13227.x 2826689 · DOI
  23. [31]Liu XB Jones EG Localization of alpha type II calcium calmodulin-dependent protein kinase at glutamatergic but not gamma-aminobutyric acid (GABAergic) synapses in thalamus and cerebral cortex Proc Natl Acad Sci U S A 1996 93 14 7332 7336 10.1073/pnas.93.14.7332 8692993 PMC38984 · DOI · Paper page
  24. [32]Lamsa K Irvine EE Giese KP Kullmann DM NMDA receptor-dependent long-term potentiation in mouse hippocampal interneurons shows a unique dependence on Ca(2+)/calmodulin-dependent kinases J Physiol 2007 584 Pt 3 885 94 10.1113/jphysiol.2007.137380 17884930 PMC2276991 · DOI · Paper page
  25. [33]Fink CC Bayer KU Myers JW Ferrell JE Jr Schulman H Meyer T Selective regulation of neurite extension and synapse formation by the beta but not the alpha isoform of CaMKII Neuron 2003 39 2 283 97 10.1016/S0896-6273(03)00428-8 12873385 · DOI · Paper page
  26. [34]Okamoto K Bosch M Hayashi Y The roles of CaMKII and F-actin in the structural plasticity of dendritic spines: a potential molecular identity of a synaptic tag? Physiology 2009 24 357 366 10.1152/physiol.00029.2009 19996366 · DOI
  27. [36]Hell JW CaMKII: claiming center stage in postsynaptic function and organization Neuron 2014 81 2 249 265 10.1016/j.neuron.2013.12.024 24462093 PMC4570830 · DOI
  28. [37]Borgesius NZ van Woerden GM Buitendijk GH Keijzer N Jaarsma D Hoogenraad CC BetaCaMKII plays a nonenzymatic role in hippocampal synaptic plasticity and learning by targeting alphaCaMKII to synapses J Neurosci 2011 31 28 10141 8 10.1523/JNEUROSCI.5105-10.2011 21752990 PMC6623068 · DOI · Paper page
  29. [38]Lee SJ Escobedo-Lozoya Y Szatmari EM Yasuda R Activation of CaMKII in single dendritic spines during long-term potentiation Nature 2009 458 7236 299 304 10.1038/nature07842 19295602 PMC2719773 · DOI · Paper page
  30. [39]Irvine EE von Hertzen LS Plattner F Giese KP AlphaCaMKII autophosphorylation: a fast track to memory Trends Neurosci 2006 29 8 459 65 10.1016/j.tins.2006.06.009 16806507 · DOI
  31. [40]Lengyel I Voss K Cammarota M Bradshaw K Brent V Murphy KP Autonomous activity of CaMKII is only transiently increased following the induction of long-term potentiation in the rat hippocampus Eur J Neurosci 2004 20 11 3063 72 10.1111/j.1460-9568.2004.03748.x 15579161 · DOI
  32. [41]Giese KP Fedorov NB Filipkowski RK Silva AJ Autophosphorylation at Thr286 of the alpha calcium-calmodulin kinase II in LTP and learning Science 1998 279 5352 870 3 10.1126/science.279.5352.870 9452388 · DOI · Paper page
  33. [43]Irvine EE Danhiez A Radwanska K Nassim C Lucchesi W Godaux E Properties of contextual memory formed in the absence of alphaCaMKII autophosphorylation Mol Brain. 2011 4 8 10.1186/1756-6606-4-8 21276220 PMC3038913 · DOI
  34. [45]Need AC Giese KP Handling and environmental enrichment do not rescue learning and memory impairments in alphaCamKII(T286A) mutant mice Genes Brain Behav 2003 2 3 132 139 10.1034/j.1601-183X.2003.00020.x 12931786 · DOI
  35. [46]Lucchesi W Mizuno K Giese KP Novel insights into CaMKII function and regulation during memory formation Brain Res Bull 2011 85 1-2 2 8 10.1016/j.brainresbull.2010.10.009 21070840 · DOI
  36. [48]Amada N Aihara K Ravid R Horie M Reduction of NR1 and phosphorylated Ca2+/calmodulin-dependent protein kinase II levels in Alzheimer’s disease Neuroreport 2005 16 16 1809 13 10.1097/01.wnr.0000185015.44563.5d 16237332 · DOI
  37. [49]Tannenberg RK Scott HL Tannenberg AE Dodd PR Selective loss of synaptic proteins in Alzheimer’s disease: evidence for an increased severity with APOE varepsilon4 Neurochem Int 2006 49 7 631 9 10.1016/j.neuint.2006.05.004 16814428 · DOI
  38. [50]McKee AC Kosik KS Kennedy MB Kowall NW Hippocampal neurons predisposed to neurofibrillary tangle formation are enriched in type II calcium/calmodulin-dependent protein kinase J Neuropathol Exp Neurol 1990 49 1 49 63 10.1097/00005072-199001000-00006 2153760 · DOI
  39. [51]Wang YJ Chen GH Hu XY Lu YP Zhou JN Liu RY The expression of calcium/calmodulin-dependent protein kinase II-alpha in the hippocampus of patients with Alzheimer’s disease and its links with AD-related pathology Brain Res 2005 1031 1 101 8 10.1016/j.brainres.2004.10.061 15621017 · DOI
  40. [52]Ferrer I Blanco R Carmona M Puig B Phosphorylated mitogen-activated protein kinase (MAPK/ERK-P), protein kinase of 38 kDa (p38-P), stress-activated protein kinase (SAPK/JNK-P), and calcium/calmodulin-dependent kinase II (CaM kinase II) are differentially expressed in tau deposits in neurons and glial cells in tauopathies J Neural Transm 2001 108 12 1397 415 10.1007/s007020100016 11810404 · DOI
  41. [53]Simonian NA Elvhage T Czernik AJ Greengard P Hyman BT Calcium/calmodulin-dependent protein kinase II immunostaining is preserved in Alzheimer’s disease hippocampal neurons Brain Res 1994 657 1-2 294 9 10.1016/0006-8993(94)90979-2 7820630 · DOI
  42. [55]Mah VH Eskin TA Kazee AM Lapham L Higgins GA In situ hybridization of calcium/calmodulin dependent protein kinase II and tau mRNAs; species differences and relative preservation in Alzheimer’s disease Brain Res Mol Brain Res 1992 12 1-3 85 94 10.1016/0169-328X(92)90071-I 1312209 · DOI
  43. [56]Murray KD Gall CM Jones EG Isackson PJ Differential regulation of brain-derived neurotrophic factor and type II calcium/calmodulin-dependent protein kinase messenger RNA expression in Alzheimer’s disease Neuroscience 1994 60 1 37 48 10.1016/0306-4522(94)90202-X 8052419 · DOI
  44. [57]Liang WS Dunckley T Beach TG Grover A Mastroeni D Ramsey K Altered neuronal gene expression in brain regions differentially affected by Alzheimer’s disease: a reference data set Physiol Genomics 2008 33 2 240 56 10.1152/physiolgenomics.00242.2007 18270320 PMC2826117 · DOI · Paper page
  45. [58]Solomon B Koppel R Jossiphov J Immunostaining of calmodulin and aluminium in Alzheimer’s disease-affected brains Brain Res Bull 2001 55 2 253 256 10.1016/S0361-9230(01)00466-X 11470324 · DOI
  46. [59]Reese LC Laezza F Woltjer R Taglialatela G Dysregulated phosphorylation of Ca(2+) /calmodulin-dependent protein kinase II-alpha in the hippocampus of subjects with mild cognitive impairment and Alzheimer’s disease J Neurochem 2011 119 4 791 804 10.1111/j.1471-4159.2011.07447.x 21883216 PMC4021864 · DOI
  47. [60]Cavazzin C Bonvicini C Nocera A Racchi M Kasahara J Tardito D Expression and phosphorylation of delta-CaM kinase II in cultured Alzheimer fibroblasts Neurobiol Aging 2004 25 9 1187 96 10.1016/j.neurobiolaging.2003.12.003 15312964 · DOI
  48. [61]Esteras N Munoz U Alquezar C Bartolome F Bermejo-Pareja F Martin-Requero A Altered calmodulin degradation and signaling in non-neuronal cells from Alzheimer’s disease patients Curr Alzheimer Res 2012 9 3 267 77 10.2174/156720512800107564 22044025 · DOI
  49. [63]Gu Z Liu W Yan Z {beta}-Amyloid impairs AMPA receptor trafficking and function by reducing Ca2+/calmodulin-dependent protein kinase II synaptic distribution J Biol Chem 2009 284 16 10639 10649 10.1074/jbc.M806508200 19240035 PMC2667751 · DOI
  50. [64]Wang DM Yang YJ Zhang L Zhang X Guan FF Zhang LF The alterations of Ca2+/calmodulin/CaMKII/CaV1.2 signaling in experimental models of Alzheimer’s disease and vascular dementia Neurosci Lett 2013 538 60 5 10.1016/j.neulet.2013.02.001 23403102 · DOI
  51. [65]Wang DM Yang YJ Zhang L Zhang X Guan FF Zhang LF Naringin Enhances CaMKII Activity and Improves Long-Term Memory in a Mouse Model of Alzheimer’s Disease Int J Mol Sci 2013 14 3 5576 86 10.3390/ijms14035576 23478434 PMC3634479 · DOI
  52. [69]Cooke SF Bliss TV Plasticity in the human central nervous system Brain 2006 129 Pt 7 1659 1673 10.1093/brain/awl082 16672292 · DOI
  53. [70]Jiang X Chai GS Wang ZH Hu Y Li XG Ma ZW Spatial training preserves associative memory capacity with augmentation of dendrite ramification and spine generation in Tg2576 mice Sci Rep. 2015 5 9488 10.1038/srep09488 25820815 PMC4377552 · DOI
  54. [71]Zhao D Watson JB Xie CW Amyloid beta prevents activation of calcium/calmodulin-dependent protein kinase II and AMPA receptor phosphorylation during hippocampal long-term potentiation J Neurophysiol 2004 92 5 2853 2858 10.1152/jn.00485.2004 15212428 · DOI
  55. [72]Zeng Y Zhao D Xie CW Neurotrophins enhance CaMKII activity and rescue amyloid-beta-induced deficits in hippocampal synaptic plasticity J Alzheimers Dis 2010 21 3 823 831 20634586 PMC3125154
  56. [73]Gandy S Czernik AJ Greengard P Phosphorylation of Alzheimer disease amyloid precursor peptide by protein kinase C and Ca2+/calmodulin-dependent protein kinase II Proc Natl Acad Sci U S A 1988 85 16 6218 6221 10.1073/pnas.85.16.6218 3137567 PMC281937 · DOI
  57. [74]Lee MS Kao SC Lemere CA Xia W Tseng HC Zhou Y APP processing is regulated by cytoplasmic phosphorylation J Cell Biol 2003 163 1 83 95 10.1083/jcb.200301115 14557249 PMC2173445 · DOI
  58. [75]Ramelot TA Nicholson LK Phosphorylation-induced structural changes in the amyloid precursor protein cytoplasmic tail detected by NMR J Mol Biol 2001 307 3 871 884 10.1006/jmbi.2001.4535 11273707 · DOI
  59. [76]Vieira SI Rebelo S Esselmann H Wiltfang J Lah J Lane R Retrieval of the Alzheimer’s amyloid precursor protein from the endosome to the TGN is S655 phosphorylation state-dependent and retromer-mediated Mol Neurodegener. 2010 5 40 10.1186/1750-1326-5-40 20937087 PMC2994555 · DOI
  60. [77]Hanger DP Betts JC Loviny TL Blackstock WP Anderton BH New phosphorylation sites identified in hyperphosphorylated tau (paired helical filament-tau) from Alzheimer’s disease brain using nanoelectrospray mass spectrometry J Neurochem 1998 71 6 2465 76 10.1046/j.1471-4159.1998.71062465.x 9832145 · DOI
  61. [78]Xiao J Perry G Troncoso J Monteiro MJ Alpha-calcium-calmodulin-dependent kinase II is associated with paired helical filaments of Alzheimer’s disease J Neuropathol Exp Neurol 1996 55 9 954 63 10.1097/00005072-199609000-00002 8800091 · DOI
  62. [79]Yamamoto H Hiragami Y Murayama M Ishizuka K Kawahara M Takashima A Phosphorylation of tau at serine 416 by Ca2+/calmodulin-dependent protein kinase II in neuronal soma in brain J Neurochem 2005 94 5 1438 47 10.1111/j.1471-4159.2005.03307.x 16000144 · DOI
  63. [80]Yoshimura Y Ichinose T Yamauchi T Phosphorylation of tau protein to sites found in Alzheimer’s disease brain is catalyzed by Ca2+/calmodulin-dependent protein kinase II as demonstrated tandem mass spectrometry Neurosci Lett 2003 353 3 185 188 10.1016/j.neulet.2003.09.037 14665412 · DOI
  64. [81]Baudier J Cole RD Phosphorylation of tau proteins to a state like that in Alzheimer’s brain is catalyzed by a calcium/calmodulin-dependent kinase and modulated by phospholipids J Biol Chem 1987 262 36 17577 17583 3121601
  65. [82]Steiner B Mandelkow EM Biernat J Gustke N Meyer HE Schmidt B Phosphorylation of microtubule-associated protein tau: identification of the site for Ca2(+)-calmodulin dependent kinase and relationship with tau phosphorylation in Alzheimer tangles EMBO J 1990 9 11 3539 44 2120043 PMC552103
  66. [83]Hagestedt T Lichtenberg B Wille H Mandelkow EM Mandelkow E Tau protein becomes long and stiff upon phosphorylation: correlation between paracrystalline structure and degree of phosphorylation J Cell Biol 1989 109 4 Pt 1 1643 51 10.1083/jcb.109.4.1643 2507554 PMC2115827 · DOI
  67. [84]Singh TJ Wang JZ Novak M Kontzekova E Grundke-Iqbal I Iqbal K Calcium/calmodulin-dependent protein kinase II phosphorylates tau at Ser-262 but only partially inhibits its binding to microtubules FEBS Lett 1996 387 2-3 145 8 10.1016/0014-5793(96)00485-1 8674537 · DOI
  68. [85]Sengupta A Kabat J Novak M Wu Q Grundke-Iqbal I Iqbal K Phosphorylation of tau at both Thr 231 and Ser 262 is required for maximal inhibition of its binding to microtubules Arch Biochem Biophys 1998 357 2 299 309 10.1006/abbi.1998.0813 9735171 · DOI · Paper page
  69. [86]Wang JZ Grundke-Iqbal I Iqbal K Kinases and phosphatases and tau sites involved in Alzheimer neurofibrillary degeneration Eur J Neurosci 2007 25 1 59 68 10.1111/j.1460-9568.2006.05226.x 17241267 PMC3191918 · DOI
  70. [87]Gardoni F Schrama LH Kamal A Gispen WH Cattabeni F Di Luca M Hippocampal synaptic plasticity involves competition between Ca2+/calmodulin-dependent protein kinase II and postsynaptic density 95 for binding to the NR2A subunit of the NMDA receptor J Neurosci 2001 21 5 1501 9 11222640 PMC6762931
  71. [88]Gardoni F Bellone C Viviani B Marinovich M Meli E Pellegrini-Giampietro DE Lack of PSD-95 drives hippocampal neuronal cell death through activation of an alpha CaMKII transduction pathway Eur J Neurosci 2002 16 5 777 86 10.1046/j.1460-9568.2002.02141.x 12372013 · DOI
  72. [89]Ashpole NM Song W Brustovetsky T Engleman EA Brustovetsky N Cummins TR Calcium/calmodulin-dependent protein kinase II (CaMKII) inhibition induces neurotoxicity via dysregulation of glutamate/calcium signaling and hyperexcitability J Biol Chem 2012 287 11 8495 506 10.1074/jbc.M111.323915 22253441 PMC3318689 · DOI
  73. [90]Bok J Wang Q Huang J Green SH CaMKII and CaMKIV mediate distinct prosurvival signaling pathways in response to depolarization in neurons Mol Cell Neurosci 2007 36 1 13 26 10.1016/j.mcn.2007.05.008 17651987 PMC2040167 · DOI
  74. [91]Churn SB Limbrick D Sombati S DeLorenzo RJ Excitotoxic activation of the NMDA receptor results in inhibition of calcium/calmodulin kinase II activity in cultured hippocampal neurons J Neurosci 1995 15 4 3200 14 7722657 PMC6577768
  75. [92]Lin KF Chang RC Suen KC So KF Hugon J Modulation of calcium/calmodulin kinase-II provides partial neuroprotection against beta-amyloid peptide toxicity Eur J Neurosci 2004 19 8 2047 55 10.1111/j.0953-816X.2004.03245.x 15090032 · DOI
  76. [93]Pike CJ Balazs R Cotman CW Attenuation of beta-amyloid neurotoxicity in vitro by potassium-induced depolarization J Neurochem 1996 67 4 1774 1777 10.1046/j.1471-4159.1996.67041774.x 8858966 · DOI
  77. [95]Ma H Li B Tsien RW Distinct roles of multiple isoforms of CaMKII in signaling to the nucleus Biochim Biophys Acta 2015 1853 9 1953 1957 10.1016/j.bbamcr.2015.02.008 25700840 PMC4522395 · DOI

Cited by

Sorted by citations

Authors
Ghosh, A., & Giese, K. P.
Affiliations
King's College London (GB)
Corresponding author
Giese, Karl Peter
ORCID
Venue
Molecular Brain
Publisher
Springer Science and Business Media LLC
Published
2015-11-24
Volume
8
Issue
1
Pages
78-78
ISSN
1756-6606 (ISSN-L)
DOI
10.1186/s13041-015-0166-2
PMC
PMC4657223
OpenAlex
W2181028377
Cited by
205
References
18
Citations by year
2026: 16 · 2025: 26 · 2024: 22 · 2023: 32 · 2022: 19 · 2021: 18 · 2020: 14 · 2019: 17 · 2018: 19 · 2017: 16 · 2016: 6
FWCI
1.68
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Molecular Brain (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Research Portal (King's College London) (publishedVersion, other-oa)
Funders
Medical Research Council (PhD studentship)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
CaMKII, calcium/calmodulin-dependent protein kinase II, Alzheimer's disease, tau kinases, synaptic plasticity, memory impairment, neurodegeneration, calcium signaling, disease models, neuronal loss
MeSH terms
Alzheimer Disease, Animals, Disease Models, Animal, Humans, Models, Biological, Calcium-Calmodulin-Dependent Protein Kinase Type 2

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