CoChat
Sign Up
Cited by 91Alzheimer's disease research and treatmentsMitochondrial Function and PathologyNeuroinflammation and Neurodegeneration Mechanisms

Interleukin-1β mediates alterations in mitochondrial fusion/fission proteins and memory impairment induced by amyloid-β oligomers

Open access
Batista, Andre F., Rody, Tayná, Forny-Germano, Leticia, Cerdeiro, Suzana, Bellio, Maria, Ferreira, Sergio T., Munoz, Douglas P., De Felice, Fernanda G.·2021·Journal of Neuroinflammation
DOI 10.1186/s12974-021-02099-xPMC PMC7897381
Open this paper in CoChat — free accountOpen PDF

Abstract

Background: The lack of effective treatments for Alzheimer’s disease (AD) reflects an incomplete understanding of disease mechanisms. Alterations in proteins involved in mitochondrial dynamics, an essential process for mitochondrial integrity and function, have been reported in AD brains. Impaired mitochondrial dynamics causes mitochondrial dysfunction and has been associated with cognitive impairment in AD. Here, we investigated a possible link between pro-inflammatory interleukin-1 (IL-1), mitochondrial dysfunction, and cognitive impairment in AD models. Methods: We exposed primary hippocampal cell cultures to amyloid-β oligomers (AβOs) and carried out AβO infusions into the lateral cerebral ventricle of cynomolgus macaques to assess the impact of AβOs on proteins that regulate mitochondrial dynamics. Where indicated, primary cultures were pre-treated with mitochondrial division inhibitor 1 (mdivi-1), or with anakinra, a recombinant interleukin-1 receptor (IL-1R) antagonist used in the treatment of rheumatoid arthritis. Cognitive impairment was investigated in C57BL/6 mice that received an intracerebroventricular (i.c.v.) infusion of AβOs in the presence or absence of mdivi-1. To assess the role of interleukin-1 beta (IL-1β) in AβO-induced alterations in mitochondrial proteins and memory impairment, interleukin receptor-1 knockout (Il1r1−/−) mice received an i.c.v. infusion of AβOs. Results: We report that anakinra prevented AβO-induced alteration in mitochondrial dynamics proteins in primary hippocampal cultures. Altered levels of proteins involved in mitochondrial fusion and fission were observed in the brains of cynomolgus macaques that received i.c.v. infusions of AβOs. The mitochondrial fission inhibitor, mdivi-1, alleviated synapse loss and cognitive impairment induced by AβOs in mice. In addition, AβOs failed to cause alterations in expression of mitochondrial dynamics proteins or memory impairment in Il1r1−/− mice. Conclusion: These findings indicate that IL-1β mediates the impact of AβOs on proteins involved in mitochondrial dynamics and that strategies aimed to prevent pathological alterations in those proteins may counteract synapse loss and cognitive impairment in AD.

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/s12974-021-02099-x

Cites

16 of 16 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?

  • Fragmented mitochondria are often associated with decreased ATP production and compromised membrane potential, ultimately contributing to cellular dysfunction and pathological conditions.

    “Fragmented mitochondria are often associated with decreased ATP production and compromised membrane potential, ultimately contributing to cellular dysfunction and pathological conditions (Motori et al., 2013; Joshi et al., 2019; Batista et al., 2021).”

    From Aging promotes an increase in mitochondrial fragmentation in astrocytes (2024) · cites this paper as Batista et al., 2021

    The Discussion (page unavailable) links disrupted mitochondrial dynamics to impaired function and reports that reducing fragmentation alleviated loss of mitochondrial membrane potential in an Alzheimer’s mouse model. It also describes mitochondria’s role in energy production, but does not specifically say that fragmentation is associated with decreased ATP production. The paper’s disease-model evidence does not establish the full claim across pathological conditions generally. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

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: 75

  1. [1]Masters CL Bateman R Blennow K Rowe CC Sperling RA Cummings JL Alzheimer's disease Nat Rev Dis Primers. 2015 1 15056 10.1038/nrdp.2015.56 27188934 · DOI · Paper page
  2. [3]Barsoum MJ Yuan H Gerencser AA Liot G Kushnareva Y Graber S Nitric oxide-induced mitochondrial fission is regulated by dynamin-related GTPases in neurons EMBO J. 2006 25 16 3900 3911 10.1038/sj.emboj.7601253 16874299 PMC1553198 · DOI
  3. [4]Martin-Maestro P Gargini R Garcia E Perry G Avila J Garcia-Escudero V Slower dynamics and aged mitochondria in sporadic Alzheimer's disease Oxid Med Cell Longev. 2017 2017 9302761 10.1155/2017/9302761 29201274 PMC5672147 · DOI
  4. [5]Wai T Langer T Mitochondrial dynamics and metabolic regulation Trends Endocrinol Metab. 2016 27 2 105 117 10.1016/j.tem.2015.12.001 26754340 · DOI
  5. [6]DuBoff B Feany M Gotz J Why size matters - balancing mitochondrial dynamics in Alzheimer's disease Trends Neurosci. 2013 36 6 325 335 10.1016/j.tins.2013.03.002 23582339 · DOI
  6. [8]Rangaraju V Lauterbach M Schuman EM Spatially stable mitochondrial compartments fuel local translation during plasticity Cell. 2019 176 1-2 73 84 10.1016/j.cell.2018.12.013 30612742 · DOI
  7. [9]Du H Guo L Yan S Sosunov AA McKhann GM Yan SS Early deficits in synaptic mitochondria in an Alzheimer's disease mouse model Proc Natl Acad Sci U S A. 2010 107 43 18670 18675 10.1073/pnas.1006586107 20937894 PMC2972922 · DOI · Paper page
  8. [10]Manczak M Reddy PH Abnormal interaction between the mitochondrial fission protein Drp1 and hyperphosphorylated tau in Alzheimer's disease neurons: implications for mitochondrial dysfunction and neuronal damage Hum Mol Genet. 2012 21 11 2538 2547 10.1093/hmg/dds072 22367970 PMC3349426 · DOI
  9. [11]Zhang L Trushin S Christensen TA Bachmeier BV Gateno B Schroeder A Altered brain energetics induces mitochondrial fission arrest in Alzheimer's Disease Sci Rep. 2016 6 18725 10.1038/srep18725 26729583 PMC4700525 · DOI
  10. [14]Exner N Treske B Paquet D Holmstrom K Schiesling C Gispert S Loss-of-function of human PINK1 results in mitochondrial pathology and can be rescued by parkin J Neurosci. 2007 27 45 12413 12418 10.1523/JNEUROSCI.0719-07.2007 17989306 PMC6673250 · DOI
  11. [15]Mortiboys H Thomas KJ Koopman WJ Klaffke S Abou-Sleiman P Olpin S Mitochondrial function and morphology are impaired in parkin-mutant fibroblasts Ann Neurol. 2008 64 5 555 565 10.1002/ana.21492 19067348 PMC2613566 · DOI
  12. [16]Wang H Lim PJ Karbowski M Monteiro MJ Effects of overexpression of huntingtin proteins on mitochondrial integrity Hum Mol Genet. 2009 18 4 737 752 10.1093/hmg/ddn404 19039036 PMC2722218 · DOI
  13. [17]Shirendeb U Reddy AP Manczak M Calkins MJ Mao P Tagle DA Abnormal mitochondrial dynamics, mitochondrial loss and mutant huntingtin oligomers in Huntington's disease: implications for selective neuronal damage Hum Mol Genet. 2011 20 7 1438 1455 10.1093/hmg/ddr024 21257639 PMC3049363 · DOI
  14. [18]Manczak M Calkins MJ Reddy PH Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage Hum Mol Genet. 2011 20 13 2495 2509 10.1093/hmg/ddr139 21459773 PMC3109997 · DOI
  15. [19]Calkins MJ Manczak M Mao P Shirendeb U Reddy PH Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease Hum Mol Genet. 2011 20 23 4515 4529 10.1093/hmg/ddr381 21873260 PMC3209824 · DOI · Paper page
  16. [21]Paula-Lima AC Adasme T SanMartin C Sebollela A Hetz C Carrasco MA Amyloid beta-peptide oligomers stimulate RyR-mediated Ca2+ release inducing mitochondrial fragmentation in hippocampal neurons and prevent RyR-mediated dendritic spine remodeling produced by BDNF Antioxid Redox Signal. 2011 14 7 1209 1223 10.1089/ars.2010.3287 20712397 · DOI
  17. [22]De Felice FG Ferreira ST Inflammation, defective insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting type 2 diabetes to Alzheimer disease Diabetes. 2014 63 7 2262 2272 10.2337/db13-1954 24931033 · DOI
  18. [25]Parajuli B Sonobe Y Horiuchi H Takeuchi H Mizuno T Suzumura A Oligomeric amyloid beta induces IL-1beta processing via production of ROS: implication in Alzheimer's disease Cell Death Dis. 2013 4 e975 10.1038/cddis.2013.503 24357806 PMC3877570 · DOI · Paper page
  19. [27]Martini AC Gomez-Arboledas A Forner S Rodriguez-Ortiz CJ McQuade A Danhash E Amyloid-beta impairs TOM1-mediated IL-1R1 signaling Proc Natl Acad Sci U S A. 2019 116 42 21198 21206 10.1073/pnas.1914088116 31570577 PMC6800331 · DOI
  20. [28]Ghosh S Wu MD Shaftel SS Kyrkanides S LaFerla FM Olschowka JA Sustained interleukin-1beta overexpression exacerbates tau pathology despite reduced amyloid burden in an Alzheimer's mouse model J Neurosci. 2013 33 11 5053 5064 10.1523/JNEUROSCI.4361-12.2013 23486975 PMC3637949 · DOI · Paper page
  21. [31]Griffin WS Stanley LC Ling C White L MacLeod V Perrot LJ Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease Proc Natl Acad Sci U S A. 1989 86 19 7611 7615 10.1073/pnas.86.19.7611 2529544 PMC298116 · DOI · Paper page
  22. [32]Cacabelos R Barquero M Garcia P Alvarez XA Varela de Seijas E. Cerebrospinal fluid interleukin-1 beta (IL-1 beta) in Alzheimer's disease and neurological disorders Methods Find Exp Clin Pharmacol. 1991 13 7 455 458 1784142
  23. [33]Schneider H Pitossi F Balschun D Wagner A del Rey A Besedovsky HO A neuromodulatory role of interleukin-1beta in the hippocampus Proc Natl Acad Sci U S A. 1998 95 13 7778 7783 10.1073/pnas.95.13.7778 9636227 PMC22755 · DOI · Paper page
  24. [34]Ledo JH Azevedo EP Clarke JR Ribeiro FC Figueiredo CP Foguel D Amyloid-beta oligomers link depressive-like behavior and cognitive deficits in mice Mol Psychiatry. 2013 18 10 1053 1054 10.1038/mp.2012.168 23183490 PMC3781315 · DOI
  25. [35]Mertens M Singh JA Anakinra for rheumatoid arthritis: a systematic review J Rheumatol. 2009 36 6 1118 1125 10.3899/jrheum.090074 19447938 · DOI
  26. [36]Cvetkovic RS Keating G Anakinra BioDrugs. 2002 16 4 303 311 10.2165/00063030-200216040-00005 12196041 · DOI
  27. [37]Bordt EA Clerc P Roelofs BA Saladino AJ Tretter L Adam-Vizi V The putative Drp1 inhibitor mdivi-1 is a reversible mitochondrial complex I inhibitor that modulates reactive oxygen species Dev Cell. 2017 40 6 583 594 10.1016/j.devcel.2017.02.020 28350990 PMC5398851 · DOI
  28. [38]Koch B Traven A Mdivi-1 and mitochondrial fission: recent insights from fungal pathogens Curr Genet. 2019 65 4 837 845 10.1007/s00294-019-00942-6 30783741 PMC6620241 · DOI · Paper page
  29. [39]Koch B Barugahare AA Lo TL Huang C Schittenhelm RB Powell DR A metabolic checkpoint for the yeast-to-hyphae developmental switch regulated by endogenous nitric oxide signaling Cell Rep. 2018 25 8 2244 2258 10.1016/j.celrep.2018.10.080 30463019 · DOI · Paper page
  30. [40]So EC Hsing CH Liang CH Wu SN The actions of mdivi-1, an inhibitor of mitochondrial fission, on rapidly activating delayed-rectifier K(+) current and membrane potential in HL-1 murine atrial cardiomyocytes Eur J Pharmacol. 2012 683 1-3 1 9 10.1016/j.ejphar.2012.02.012 22374256 · DOI
  31. [41]Dai W Wang G Chwa J Oh ME Abeywardana T Yang Y Mitochondrial division inhibitor (mdivi-1) decreases oxidative metabolism in cancer Br J Cancer. 2020 122 9 1288 1297 10.1038/s41416-020-0778-x 32147668 PMC7188673 · DOI
  32. [42]Lambert MP Velasco PT Chang L Viola KL Fernandez S Lacor PN Monoclonal antibodies that target pathological assemblies of Abeta J Neurochem. 2007 100 1 23 35 10.1111/j.1471-4159.2006.04157.x 17116235 · DOI · Paper page
  33. [43]Brito-Moreira J Lourenco MV Oliveira MM Ribeiro FC Ledo JH Diniz LP Interaction of amyloid-beta (Abeta) oligomers with neurexin 2alpha and neuroligin 1 mediates synapse damage and memory loss in mice J Biol Chem. 2017 292 18 7327 7337 10.1074/jbc.M116.761189 28283575 PMC5418035 · DOI · Paper page
  34. [44]Figueiredo CP Clarke JR Ledo JH Ribeiro FC Costa CV Melo HM Memantine rescues transient cognitive impairment caused by high-molecular-weight abeta oligomers but not the persistent impairment induced by low-molecular-weight oligomers J Neurosci. 2013 33 23 9626 9634 10.1523/JNEUROSCI.0482-13.2013 23739959 PMC6619709 · DOI
  35. [45]Seixas da Silva GS Melo HM Lourenco MV Lyra ESNM de Carvalho MB Alves-Leon SV Amyloid-beta oligomers transiently inhibit AMP-activated kinase and cause metabolic defects in hippocampal neurons J Biol Chem. 2017 292 18 7395 7406 10.1074/jbc.M116.753525 28302722 PMC5418041 · DOI
  36. [46]Sebollela A Freitas-Correa L Oliveira FF Paula-Lima AC Saraiva LM Martins SM Amyloid-beta oligomers induce differential gene expression in adult human brain slices J Biol Chem. 2012 287 10 7436 7445 10.1074/jbc.M111.298471 22235132 PMC3293600 · DOI
  37. [47]De Felice FG Wu D Lambert MP Fernandez SJ Velasco PT Lacor PN Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers Neurobiol Aging. 2008 29 9 1334 1347 10.1016/j.neurobiolaging.2007.02.029 17403556 PMC3142933 · DOI · Paper page
  38. [48]Manczak M Reddy PH Mitochondrial division inhibitor 1 protects against mutant huntingtin-induced abnormal mitochondrial dynamics and neuronal damage in Huntington's disease Hum Mol Genet. 2015 24 25 7308 25 10.1093/hmg/ddv429 26464486 PMC4664169 · DOI
  39. [49]Rappold PM Cui M Grima JC Fan RZ de Mesy-Bentley KL Chen L Drp1 inhibition attenuates neurotoxicity and dopamine release deficits in vivo Nat Commun. 2014 5 5244 10.1038/ncomms6244 25370169 PMC4223875 · DOI
  40. [51]Brewer GJ Isolation and culture of adult rat hippocampal neurons J Neurosci Methods. 1997 71 2 143 155 10.1016/S0165-0270(96)00136-7 9128149 · DOI
  41. [53]Batista AF Forny-Germano L Clarke JR Lyra ESNM Brito-Moreira J Boehnke SE The diabetes drug liraglutide reverses cognitive impairment in mice and attenuates insulin receptor and synaptic pathology in a non-human primate model of Alzheimer's disease J Pathol. 2018 245 1 85 100 10.1002/path.5056 29435980 PMC5947670 · DOI
  42. [54]Diniz LP Tortelli V Matias I Morgado J Bergamo Araujo AP Melo HM Astrocyte transforming growth factor beta 1 protects synapses against Abeta oligomers in Alzheimer's disease model J Neurosci. 2017 37 28 6797 6809 10.1523/JNEUROSCI.3351-16.2017 28607171 PMC6596548 · DOI · Paper page
  43. [56]Lourenco MV Clarke JR Frozza RL Bomfim TR Forny-Germano L Batista AF TNF-alpha mediates PKR-dependent memory impairment and brain IRS-1 inhibition induced by Alzheimer's beta-amyloid oligomers in mice and monkeys Cell Metab. 2013 18 6 831 843 10.1016/j.cmet.2013.11.002 24315369 · DOI
  44. [57]Clarke JR Lyra ESNM Figueiredo CP Frozza RL Ledo JH Beckman D Alzheimer-associated Abeta oligomers impact the central nervous system to induce peripheral metabolic deregulation EMBO Mol Med. 2015 7 2 190 210 10.15252/emmm.201404183 25617315 PMC4328648 · DOI · Paper page
  45. [58]Bido S Soria FN Fan RZ Bezard E Tieu K Mitochondrial division inhibitor-1 is neuroprotective in the A53T-alpha-synuclein rat model of Parkinson's disease Sci Rep. 2017 7 1 7495 10.1038/s41598-017-07181-0 28790323 PMC5548731 · DOI
  46. [59]Li YH Xu F Thome R Guo MF Sun ML Song GB Mdivi-1, a mitochondrial fission inhibitor, modulates T helper cells and suppresses the development of experimental autoimmune encephalomyelitis J Neuroinflammation. 2019 16 1 149 10.1186/s12974-019-1542-0 31324254 PMC6642537 · DOI
  47. [60]Livak KJ Schmittgen TD Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method Methods. 2001 25 4 402 408 10.1006/meth.2001.1262 11846609 · DOI · Paper page
  48. [61]Forny-Germano L Lyra E Silva NM Batista AF Brito-Moreira J Gralle M Boehnke SE Alzheimer's disease-like pathology induced by amyloid-beta oligomers in nonhuman primates J Neurosci. 2014 34 41 13629 13643 10.1523/JNEUROSCI.1353-14.2014 25297091 PMC6608380 · DOI
  49. [62]Wilkins HM Swerdlow RH Relationships between mitochondria and neuroinflammation: implications for Alzheimer's disease Curr Top Med Chem. 2016 16 8 849 857 10.2174/1568026615666150827095102 26311426 PMC5480219 · DOI
  50. [63]Harland M Torres S Liu J Wang X Neuronal mitochondria modulation of LPS-induced neuroinflammation J Neurosci. 2020 40 8 1756 1765 10.1523/JNEUROSCI.2324-19.2020 31937559 PMC7046320 · DOI
  51. [64]Nair S Sobotka KS Joshi P Gressens P Fleiss B Thornton C Lipopolysaccharide-induced alteration of mitochondrial morphology induces a metabolic shift in microglia modulating the inflammatory response in vitro and in vivo Glia. 2019 67 6 1047 1061 10.1002/glia.23587 30637805 · DOI
  52. [65]Fiocco U Vezzu M Cozzi L Todesco S IL-1Ra (recombinant human IL-1 receptor antagonist) in the treatment of rheumatoid arthritis: the efficacy Reumatismo. 2004 56 1 Suppl 1 62 73 15201942
  53. [66]Bomfim TR Forny-Germano L Sathler LB Brito-Moreira J Houzel JC Decker H An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer's disease- associated Abeta oligomers J Clin Invest. 2012 122 4 1339 1353 10.1172/JCI57256 22476196 PMC3314445 · DOI
  54. [67]Reddy PH Manczak M Yin X Mitochondria-division inhibitor 1 protects against Amyloid-beta induced mitochondrial fragmentation and synaptic damage in Alzheimer's disease J Alzheimers Dis. 2017 58 1 147 162 10.3233/JAD-170051 28409745 PMC5444307 · DOI · Paper page
  55. [68]Reddy AP Reddy PH Mitochondria-targeted molecules as potential drugs to treat patients with Alzheimer's disease Prog Mol Biol Transl Sci. 2017 146 173 201 10.1016/bs.pmbts.2016.12.010 28253985 · DOI
  56. [69]Reddy PH Inhibitors of mitochondrial fission as a therapeutic strategy for diseases with oxidative stress and mitochondrial dysfunction J Alzheimers Dis. 2014 40 2 245 256 10.3233/JAD-132060 24413616 PMC3972337 · DOI
  57. [71]Park J Choi H Min JS Park SJ Kim JH Park HJ Mitochondrial dynamics modulate the expression of pro-inflammatory mediators in microglial cells J Neurochem. 2013 127 2 221 232 10.1111/jnc.12361 23815397 · DOI
  58. [72]Fan LF He PY Peng YC Du QH Ma YJ Jin JX Mdivi-1 ameliorates early brain injury after subarachnoid hemorrhage via the suppression of inflammation-related blood-brain barrier disruption and endoplasmic reticulum stress-based apoptosis Free Radic Biol Med. 2017 112 336 349 10.1016/j.freeradbiomed.2017.08.003 28790012 · DOI
  59. [73]Katoh M Wu B Nguyen HB Thai TQ Yamasaki R Lu H Polymorphic regulation of mitochondrial fission and fusion modifies phenotypes of microglia in neuroinflammation Sci Rep. 2017 7 1 4942 10.1038/s41598-017-05232-0 28694451 PMC5503944 · DOI
  60. [74]Ho DH Je AR Lee H Son I Kweon HS Kim HG LRRK2 kinase activity induces mitochondrial fission in microglia via Drp1 and modulates neuroinflammation Exp Neurobiol. 2018 27 3 171 180 10.5607/en.2018.27.3.171 30022868 PMC6050415 · DOI
  61. [76]Lesne SE Sherman MA Grant M Kuskowski M Schneider JA Bennett DA Brain amyloid-beta oligomers in ageing and Alzheimer's disease Brain. 2013 136 Pt 5 1383 1398 10.1093/brain/awt062 23576130 PMC3634198 · DOI
  62. [77]Wang X Su B Zheng L Perry G Smith MA Zhu X The role of abnormal mitochondrial dynamics in the pathogenesis of Alzheimer's disease J Neurochem. 2009 109 Suppl 1 153 159 10.1111/j.1471-4159.2009.05867.x 19393022 PMC2720030 · DOI
  63. [78]Wang W Yin J Ma X Zhao F Siedlak SL Wang Z Inhibition of mitochondrial fragmentation protects against Alzheimer's disease in rodent model Hum Mol Genet. 2017 26 21 4118 4131 10.1093/hmg/ddx299 28973308 PMC5886251 · DOI · Paper page
  64. [79]Wang X Su B Fujioka H Zhu X Dynamin-like protein 1 reduction underlies mitochondrial morphology and distribution abnormalities in fibroblasts from sporadic Alzheimer's disease patients Am J Pathol. 2008 173 2 470 482 10.2353/ajpath.2008.071208 18599615 PMC2475784 · DOI · Paper page
  65. [80]Wang X Su B Siedlak SL Moreira PI Fujioka H Wang Y Amyloid-beta overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins Proc Natl Acad Sci U S A. 2008 105 49 19318 19323 10.1073/pnas.0804871105 19050078 PMC2614759 · DOI · Paper page
  66. [81]Cai Q Tammineni P Mitochondrial aspects of synaptic dysfunction in Alzheimer's disease J Alzheimers Dis. 2017 57 4 1087 1103 10.3233/JAD-160726 27767992 PMC5398949 · DOI
  67. [82]Sebastian D Palacin M Zorzano A Mitochondrial dynamics: coupling mitochondrial fitness with healthy aging Trends Mol Med. 2017 23 3 201 215 10.1016/j.molmed.2017.01.003 28188102 · DOI
  68. [83]Stephenson J Nutma E van der Valk P Amor S Inflammation in CNS neurodegenerative diseases Immunology. 2018 154 2 204 219 10.1111/imm.12922 29513402 PMC5980185 · DOI · Paper page
  69. [85]Zhou R Yazdi AS Menu P Tschopp J A role for mitochondria in NLRP3 inflammasome activation Nature. 2011 469 7329 221 225 10.1038/nature09663 21124315 · DOI · Paper page
  70. [86]Tyagi A Nguyen CU Chong T Michel CR Fritz KS Reisdorph N SIRT3 deficiency-induced mitochondrial dysfunction and inflammasome formation in the brain Sci Rep. 2018 8 1 17547 10.1038/s41598-018-35890-7 30510203 PMC6277395 · DOI
  71. [87]Fang EF, Hou Y, Palikaras K, Adriaanse BA, Kerr JS, Yang B, et al. Mitophagy inhibits amyloid-beta and tau pathology and reverses cognitive deficits in models of Alzheimer's disease. Nat Neurosci. 2019. PMC6693625 30742114
  72. [88]Sandhir R Halder A Sunkaria A Mitochondria as a centrally positioned hub in the innate immune response Biochim Biophys Acta Mol Basis Dis. 2017 1863 5 1090 1097 10.1016/j.bbadis.2016.10.020 27794419 · DOI · Paper page
  73. [90]Iyer SS He Q Janczy JR Elliott EI Zhong Z Olivier AK Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation Immunity. 2013 39 2 311 323 10.1016/j.immuni.2013.08.001 23954133 PMC3779285 · DOI
  74. [91]Shimada K Crother TR Karlin J Dagvadorj J Chiba N Chen S Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis Immunity. 2012 36 3 401 414 10.1016/j.immuni.2012.01.009 22342844 PMC3312986 · DOI · Paper page
  75. [92]Nakahira K Haspel JA Rathinam VA Lee SJ Dolinay T Lam HC Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome Nat Immunol. 2011 12 3 222 230 10.1038/ni.1980 21151103 PMC3079381 · DOI · Paper page

Cited by

Sorted by citations

Authors
Batista, A. F., Rody, T., Forny-Germano, L., Cerdeiro, S., Bellio, M., Ferreira, S. T., Munoz, D. P., & De Felice, F. G.
Affiliations
  • Universidade Federal do Rio de Janeiro (BR)
  • Queen's University (CA)
ORCID
Venue
Journal of Neuroinflammation
Publisher
Springer Science and Business Media LLC
Published
2021-02-21
Volume
18
Issue
1
Pages
54-54
ISSN
1742-2094 (ISSN-L)
DOI
10.1186/s12974-021-02099-x
PMC
PMC7897381
OpenAlex
W3130988710
Cited by
91
References
16
Citations by year
2026: 17 · 2025: 18 · 2024: 17 · 2023: 16 · 2022: 14 · 2021: 9
FWCI
8.56
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Neuroinflammation (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Canada Research Chair Program
  • John Simon Guggenheim Memorial Foundation
  • Instituto Nacional de Ciência e Tecnologia de Neurociência Translacional
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico
  • Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro
  • Canadian Institutes for Health Research
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
IL-1β, amyloid-beta oligomers, Alzheimer's disease, mitochondrial dynamics, mitochondrial fusion, mitochondrial fission, Mdivi-1, anakinra, IL1R1, cognitive impairment, memory impairment, synaptic loss, hippocampal neurons, neuroinflammation, intracerebroventricular infusion, cynomolgus macaques
MeSH terms
Animals, Female, Hippocampus, Macaca fascicularis, Male, Memory Disorders, Mice, Inbred C57BL, Peptide Fragments, Amyloid beta-Peptides, Mice, Knockout, Mice, Rats, Membrane Potential, Mitochondrial, Interleukin-1beta, Mitochondrial Dynamics

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