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Journal of Neuroinflammation
Published in: Journal of Neuroinflammation 1/2022

Open Access 01-12-2022 | Alzheimer's Disease | Review

Mitochondrial dysfunction in microglia: a novel perspective for pathogenesis of Alzheimer’s disease

Authors: Yun Li, Xiaohuan Xia, Yi Wang, Jialin C. Zheng

Published in: Journal of Neuroinflammation | Issue 1/2022

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Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease in the elderly globally. Emerging evidence has demonstrated microglia-driven neuroinflammation as a key contributor to the onset and progression of AD, however, the mechanisms that mediate neuroinflammation remain largely unknown. Recent studies have suggested mitochondrial dysfunction including mitochondrial DNA (mtDNA) damage, metabolic defects, and quality control (QC) disorders precedes microglial activation and subsequent neuroinflammation. Therefore, an in-depth understanding of the relationship between mitochondrial dysfunction and microglial activation in AD is important to unveil the pathogenesis of AD and develop effective approaches for early AD diagnosis and treatment. In this review, we summarized current progress in the roles of mtDNA, mitochondrial metabolism, mitochondrial QC changes in microglial activation in AD, and provide comprehensive thoughts for targeting microglial mitochondria as potential therapeutic strategies of AD.
Literature
1.
2.
3.
Gaugler J, James B, Johnson T, Reimer J, Solis M, Weuve J, Buckley RF, Hohman TJ. 2022 Alzheimer’s disease facts and figures. Alzheimers Dement. 2022;18(4):700–89.CrossRef
4.
Brookmeyer R, et al. Forecasting the global burden of Alzheimer’s disease. Alzheimers Dement. 2007;3(3):186–91.PubMedCrossRef
5.
6.
Pradeepkiran JA, Reddy PH. Structure based design and molecular docking studies for phosphorylated tau inhibitors in Alzheimer’s disease. Cells. 2019;8(3):260.PubMedCentralCrossRef
7.
Busche MA, Hyman BT. Synergy between amyloid-β and tau in Alzheimer’s disease. Nat Neurosci. 2020;23(10):1183–93.PubMedCrossRef
8.
Sperling RA, et al. Toward defining the preclinical stages of Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7(3):280–92.PubMedPubMedCentralCrossRef
9.
10.
Ding L, et al. Glutaminase in microglia: a novel regulator of neuroinflammation. Brain Behav Immun. 2021;92:139–56.PubMedCrossRef
11.
Pascoal TA, et al. Microglial activation and tau propagate jointly across Braak stages. Nat Med. 2021;27(9):1592–9.PubMedCrossRef
12.
Leng F, Edison P. Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here? Nat Rev Neurol. 2021;17(3):157–72.PubMedCrossRef
13.
Rajmohan R, Reddy PH. Amyloid-beta and phosphorylated tau accumulations cause abnormalities at synapses of Alzheimer’s disease neurons. J Alzheimers Dis. 2017;57(4):975–99.PubMedPubMedCentralCrossRef
14.
Gao G, et al. Glutaminase C regulates microglial activation and pro-inflammatory exosome release: relevance to the pathogenesis of Alzheimer’s disease. Front Cell Neurosci. 2019;13:264.PubMedPubMedCentralCrossRef
15.
Yan SD, et al. RAGE and amyloid-beta peptide neurotoxicity in Alzheimer’s disease. Nature. 1996;382(6593):685–91.PubMedCrossRef
16.
Chausse B, et al. Selective inhibition of mitochondrial respiratory complexes controls the transition of microglia into a neurotoxic phenotype in situ. Brain Behav Immun. 2020;88:802–14.PubMedCrossRef
17.
Zengeler KE, Lukens JR. Innate immunity at the crossroads of healthy brain maturation and neurodevelopmental disorders. Nat Rev Immunol. 2021;21(7):454–68.PubMedPubMedCentralCrossRef
18.
19.
McAvoy K, Kawamata H. Glial mitochondrial function and dysfunction in health and neurodegeneration. Mol Cell Neurosci. 2019;101: 103417.PubMedCrossRef
20.
Salminen A, et al. Impaired mitochondrial energy metabolism in Alzheimer’s disease: impact on pathogenesis via disturbed epigenetic regulation of chromatin landscape. Prog Neurobiol. 2015;131:1–20.PubMedCrossRef
21.
22.
Lee A, et al. Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondrial fission and mitophagy. Nat Commun. 2022;13(1):4444.PubMedPubMedCentralCrossRef
23.
24.
John A, Reddy PH. Synaptic basis of Alzheimer’s disease: focus on synaptic amyloid beta P-tau and mitochondria. Ageing Res Rev. 2021;65: 101208.PubMedCrossRef
25.
Morton H, et al. Defective mitophagy and synaptic degeneration in Alzheimer’s disease: focus on aging, mitochondria and synapse. Free Radic Biol Med. 2021;172:652–67.PubMedCrossRef
26.
Cadonic C, Sabbir MG, Albensi BC. Mechanisms of mitochondrial dysfunction in Alzheimer’s disease. Mol Neurobiol. 2016;53(9):6078–90.PubMedCrossRef
27.
28.
Zhang X, et al. Association of mitochondrial variants and haplogroups identified by whole exome sequencing with Alzheimer’s disease. Alzheimers Dement. 2022;18(2):294–306.PubMedCrossRef
29.
Vaillant-Beuchot L, et al. Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer’s disease models and human brains. Acta Neuropathol. 2021;141(1):39–65.PubMedCrossRef
30.
31.
Baik SH, et al. A breakdown in metabolic reprogramming causes microglia dysfunction in Alzheimer’s disease. Cell Metab. 2019;30(3):493–507.PubMedCrossRef
32.
Lin MT, Beal MF. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature. 2006;443(7113):787–95.PubMedCrossRef
33.
34.
Tang S, Huang T. Characterization of mitochondrial DNA heteroplasmy using a parallel sequencing system. Biotechniques. 2010;48(4):287–96.PubMedCrossRef
35.
Cruz ACP, et al. Frequency and association of mitochondrial genetic variants with neurological disorders. Mitochondrion. 2019;46:345–60.PubMedCrossRef
36.
Coskun PE, Beal MF, Wallace DC. Alzheimer’s brains harbor somatic mtDNA control-region mutations that suppress mitochondrial transcription and replication. Proc Natl Acad Sci USA. 2004;101(29):10726–31.PubMedPubMedCentralCrossRef
37.
Rodríguez-Santiago B, Casademont J, Nunes V. Is mitochondrial DNA depletion involved in Alzheimer’s disease? Eur J Hum Genet. 2001;9(4):279–85.PubMedCrossRef
38.
Wei W, et al. Mitochondrial DNA point mutations and relative copy number in 1363 disease and control human brains. Acta Neuropathol Commun. 2017;5(1):13.PubMedPubMedCentralCrossRef
39.
40.
Klein HU, et al. Characterization of mitochondrial DNA quantity and quality in the human aged and Alzheimer’s disease brain. Mol Neurodegener. 2021;16(1):75.PubMedPubMedCentralCrossRef
41.
Swerdlow RH, et al. Exploratory analysis of mtDNA haplogroups in two Alzheimer’s longitudinal cohorts. Alzheimers Dement. 2020;16(8):1164–72.PubMedCrossRef
42.
Blanch M, et al. Altered mitochondrial DNA methylation pattern in Alzheimer disease-related pathology and in Parkinson disease. Am J Pathol. 2016;186(2):385–97.PubMedCrossRef
43.
Roubertoux PL, et al. Mitochondrial DNA modifies cognition in interaction with the nuclear genome and age in mice. Nat Genet. 2003;35(1):65–9.PubMedCrossRef
44.
45.
Khan SM, et al. Alzheimer’s disease cybrids replicate beta-amyloid abnormalities through cell death pathways. Ann Neurol. 2000;48(2):148–55.PubMedCrossRef
46.
47.
Liao Y, et al. HDAC3 inhibition ameliorates ischemia/reperfusion-induced brain injury by regulating the microglial cGAS-STING pathway. Theranostics. 2020;10(21):9644–62.PubMedPubMedCentralCrossRef
48.
Strobel S, et al. Astrocyte- and microglia-specific mitochondrial DNA deletions levels in sporadic Alzheimer’s disease. J Alzheimers Dis. 2019;67(1):149–57.PubMedCrossRef
49.
50.
Simpson DSA, Oliver PL. ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease. Antioxidants (Basel). 2020;9(8):743.CrossRef
51.
Gong T, et al. DAMP-sensing receptors in sterile inflammation and inflammatory diseases. Nat Rev Immunol. 2020;20(2):95–112.PubMedCrossRef
52.
53.
Milenkovic D, et al. The enigma of the respiratory chain supercomplex. Cell Metab. 2017;25(4):765–76.PubMedCrossRef
54.
Walker JE. The ATP synthase: the understood, the uncertain and the unknown. Biochem Soc Trans. 2013;41(1):1–16.PubMedCrossRef
55.
56.
57.
Hu Y, et al. mTOR-mediated metabolic reprogramming shapes distinct microglia functions in response to lipopolysaccharide and ATP. Glia. 2020;68(5):1031–45.PubMedCrossRef
58.
Gordon BA, et al. Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer’s disease: a longitudinal study. Lancet Neurol. 2018;17(3):241–50.PubMedPubMedCentralCrossRef
59.
Croteau E, et al. A cross-sectional comparison of brain glucose and ketone metabolism in cognitively healthy older adults, mild cognitive impairment and early Alzheimer’s disease. Exp Gerontol. 2018;107:18–26.PubMedCrossRef
60.
Johnson ECB, et al. Large-scale proteomic analysis of Alzheimer’s disease brain and cerebrospinal fluid reveals early changes in energy metabolism associated with microglia and astrocyte activation. Nat Med. 2020;26(5):769–80.PubMedPubMedCentralCrossRef
61.
Brooks WM, et al. Gene expression profiles of metabolic enzyme transcripts in Alzheimer’s disease. Brain Res. 2007;1127(1):127–35.PubMedCrossRef
62.
63.
Bubber P, et al. Mitochondrial abnormalities in Alzheimer brain: mechanistic implications. Ann Neurol. 2005;57(5):695–703.PubMedCrossRef
64.
Gibson GE, Sheu KF, Blass JP. Abnormalities of mitochondrial enzymes in Alzheimer disease. J Neural Transm (Vienna). 1998;105(8–9):855–70.CrossRef
65.
Dumont M, et al. Mitochondrial dihydrolipoyl succinyltransferase deficiency accelerates amyloid pathology and memory deficit in a transgenic mouse model of amyloid deposition. Free Radic Biol Med. 2009;47(7):1019–27.PubMedPubMedCentralCrossRef
66.
Sancheti H, et al. Reversal of metabolic deficits by lipoic acid in a triple transgenic mouse model of Alzheimer’s disease: a 13C NMR study. J Cereb Blood Flow Metab. 2014;34(2):288–96.PubMedCrossRef
67.
68.
Terada T, et al. Mitochondrial complex I abnormalities is associated with tau and clinical symptoms in mild Alzheimer’s disease. Mol Neurodegener. 2021;16(1):28.PubMedPubMedCentralCrossRef
69.
Kilbride SM, et al. High-level inhibition of mitochondrial complexes III and IV is required to increase glutamate release from the nerve terminal. Mol Neurodegener. 2011;6(1):53.PubMedPubMedCentralCrossRef
70.
Cardoso SM, et al. Cytochrome c oxidase is decreased in Alzheimer’s disease platelets. Neurobiol Aging. 2004;25(1):105–10.PubMedCrossRef
71.
Coussee E, et al. G37R SOD1 mutant alters mitochondrial complex I activity, Ca2+ uptake and ATP production. Cell Calcium. 2011;49(4):217–25.PubMedCrossRef
72.
Holland R, et al. Inflammatory microglia are glycolytic and iron retentive and typify the microglia in APP/PS1 mice. Brain Behav Immun. 2018;68:183–96.PubMedCrossRef
73.
74.
75.
76.
77.
Ye J, et al. Electron transport chain inhibitors induce microglia activation through enhancing mitochondrial reactive oxygen species production. Exp Cell Res. 2016;340(2):315–26.PubMedCrossRef
78.
Hammond TR, et al. Single-cell RNA sequencing of microglia throughout the mouse lifespan and in the injured brain reveals complex cell-state changes. Immunity. 2019;50(1):253-271.e6.PubMedCrossRef
79.
Gimeno-Bayón J, et al. Glucose pathways adaptation supports acquisition of activated microglia phenotype. J Neurosci Res. 2014;92(6):723–31.PubMedCrossRef
80.
Ebert D, Haller RG, Walton ME. Energy contribution of octanoate to intact rat brain metabolism measured by 13C nuclear magnetic resonance spectroscopy. J Neurosci. 2003;23(13):5928–35.PubMedPubMedCentralCrossRef
81.
Zhang Y, et al. An RNA-sequencing transcriptome and splicing database of glia, neurons, and vascular cells of the cerebral cortex. J Neurosci. 2014;34(36):11929–47.PubMedPubMedCentralCrossRef
82.
Flowers A, et al. Proteomic analysis of aged microglia: shifts in transcription, bioenergetics, and nutrient response. J Neuroinflamm. 2017;14(1):96.CrossRef
83.
Trépanier MO, et al. N-3 polyunsaturated fatty acids in animal models with neuroinflammation: an update. Eur J Pharmacol. 2016;785:187–206.PubMedCrossRef
84.
Albrecht J, et al. Glutamine in the central nervous system: function and dysfunction. Front Biosci. 2007;12:332–43.PubMedCrossRef
85.
86.
Churchward MA, Tchir DR, Todd KG. Microglial function during glucose deprivation: inflammatory and neuropsychiatric implications. Mol Neurobiol. 2018;55(2):1477–87.PubMedCrossRef
87.
Nagy AM, et al. Versatility of microglial bioenergetic machinery under starving conditions. Biochim Biophys Acta Bioenerg. 2018;1859(3):201–14.PubMedCrossRef
88.
Ryu JK, et al. Microglial activation and cell death induced by the mitochondrial toxin 3-nitropropionic acid: in vitro and in vivo studies. Neurobiol Dis. 2003;12(2):121–32.PubMedCrossRef
89.
Kausar S, Wang F, Cui H. The role of mitochondria in reactive oxygen species generation and its implications for neurodegenerative diseases. Cells. 2018;7(12):274.PubMedCentralCrossRef
90.
McIntosh A, et al. Iron accumulation in microglia triggers a cascade of events that leads to altered metabolism and compromised function in APP/PS1 mice. Brain Pathol. 2019;29(5):606–21.PubMedPubMedCentralCrossRef
91.
Rubio-Araiz A, et al. Anti-TLR2 antibody triggers oxidative phosphorylation in microglia and increases phagocytosis of β-amyloid. J Neuroinflamm. 2018;15(1):247.CrossRef
92.
Vlassenko AG, et al. Spatial correlation between brain aerobic glycolysis and amyloid-β (Aβ ) deposition. Proc Natl Acad Sci USA. 2010;107(41):17763–7.PubMedPubMedCentralCrossRef
93.
Voloboueva LA, et al. Inflammatory response of microglial BV-2 cells includes a glycolytic shift and is modulated by mitochondrial glucose-regulated protein 75/mortalin. FEBS Lett. 2013;587(6):756–62.PubMedPubMedCentralCrossRef
94.
Wu B, et al. Glutaminase 1 regulates the release of extracellular vesicles during neuroinflammation through key metabolic intermediate alpha-ketoglutarate. J Neuroinflamm. 2018;15(1):79.CrossRef
95.
Hollinger KR, et al. Glutamine antagonist JHU-083 normalizes aberrant hippocampal glutaminase activity and improves cognition in APOE4 mice. J Alzheimers Dis. 2020;77(1):437–47.PubMedPubMedCentralCrossRef
96.
97.
Bernier LP, York EM, MacVicar BA. Immunometabolism in the brain: how metabolism shapes microglial function. Trends Neurosci. 2020;43(11):854–69.PubMedCrossRef
98.
Wai T, Langer T. Mitochondrial dynamics and metabolic regulation. Trends Endocrinol Metab. 2016;27(2):105–17.PubMedCrossRef
99.
van der Bliek AM, Shen Q, Kawajiri S. Mechanisms of mitochondrial fission and fusion. Cold Spring Harb Perspect Biol. 2013;5(6):a011072–a011072.PubMedPubMedCentral
100.
101.
Liang J, et al. Exercise-induced benefits for Alzheimer’s disease by stimulating mitophagy and improving mitochondrial function. Front Aging Neurosci. 2021;13: 755665.PubMedPubMedCentralCrossRef
102.
Palikaras K, Lionaki E, Tavernarakis N. Mechanisms of mitophagy in cellular homeostasis, physiology and pathology. Nat Cell Biol. 2018;20(9):1013–22.PubMedCrossRef
103.
104.
Picca A, et al. Mitochondrial dysfunction, oxidative stress, and neuroinflammation: intertwined roads to neurodegeneration. Antioxidants (Basel). 2020;9(8):647.CrossRef
105.
106.
Archer SL. Mitochondrial dynamics–mitochondrial fission and fusion in human diseases. N Engl J Med. 2013;369(23):2236–51.PubMedCrossRef
107.
108.
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):2495–509.PubMedPubMedCentralCrossRef
109.
110.
Reddy PH, et al. Mutant APP and amyloid beta-induced defective autophagy, mitophagy, mitochondrial structural and functional changes and synaptic damage in hippocampal neurons from Alzheimer’s disease. Hum Mol Genet. 2018;27(14):2502–16.PubMedPubMedCentralCrossRef
111.
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):2538–47.PubMedPubMedCentralCrossRef
112.
Manczak M, et al. Hippocampal mutant APP and amyloid beta-induced cognitive decline, dendritic spine loss, defective autophagy, mitophagy and mitochondrial abnormalities in a mouse model of Alzheimer’s disease. Hum Mol Genet. 2018;27(8):1332–42.PubMedPubMedCentralCrossRef
113.
Kandimalla R, et al. Hippocampal phosphorylated tau induced cognitive decline, dendritic spine loss and mitochondrial abnormalities in a mouse model of Alzheimer’s disease. Hum Mol Genet. 2018;27(1):30–40.PubMedCrossRef
114.
Hou X, et al. Mitophagy alterations in Alzheimer’s disease are associated with granulovacuolar degeneration and early tau pathology. Alzheimers Dement. 2020;17:417.PubMedCentralCrossRef
115.
Kshirsagar S, et al. Protective effects of mitophagy enhancers against amyloid beta-induced mitochondrial and synaptic toxicities in Alzheimer disease. Hum Mol Genet. 2022;31(3):423–39.PubMedCrossRef
116.
Kshirsagar S, et al. Mitophagy enhancers against phosphorylated Tau-induced mitochondrial and synaptic toxicities in Alzheimer disease. Pharmacol Res. 2021;174: 105973.PubMedCrossRef
117.
Fang EF, et al. Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease. Nat Neurosci. 2019;22(3):401–12.PubMedPubMedCentralCrossRef
118.
Jassim AH, Inman DM, Mitchell CH. Crosstalk between dysfunctional mitochondria and inflammation in glaucomatous neurodegeneration. Front Pharmacol. 2021;12: 699623.PubMedPubMedCentralCrossRef
119.
Joshi AU, et al. Fragmented mitochondria released from microglia trigger A1 astrocytic response and propagate inflammatory neurodegeneration. Nat Neurosci. 2019;22(10):1635–48.PubMedPubMedCentralCrossRef
120.
Park J, et al. Mitochondrial dynamics modulate the expression of pro-inflammatory mediators in microglial cells. J Neurochem. 2013;127(2):221–32.PubMedCrossRef
121.
Zhou K, et al. Atractylenolide III ameliorates cerebral ischemic injury and neuroinflammation associated with inhibiting JAK2/STAT3/Drp1-dependent mitochondrial fission in microglia. Phytomedicine. 2019;59: 152922.PubMedCrossRef
122.
Zhou L, et al. Echinacoside attenuates inflammatory response in a rat model of cervical spondylotic myelopathy via inhibition of excessive mitochondrial fission. Free Radic Biol Med. 2020;152:697–714.PubMedCrossRef
123.
124.
125.
Yao J, et al. 2-Deoxy-D-glucose treatment induces ketogenesis, sustains mitochondrial function, and reduces pathology in female mouse model of Alzheimer’s disease. PLoS ONE. 2011;6(7): e21788.PubMedPubMedCentralCrossRef
126.
127.
Abd El-Fatah IM, et al. Dimethyl fumarate abridged tauo-/amyloidopathy in a D-Galactose/ovariectomy-induced Alzheimer’s-like disease: modulation of AMPK/SIRT-1, AKT/CREB/BDNF, AKT/GSK-3beta, adiponectin/Adipo1R, and NF-kappaB/IL-1beta/ROS trajectories. Neurochem Int. 2021;148: 105082.PubMedCrossRef
128.
Li M, et al. Mitofusin 2 confers the suppression of microglial activation by cannabidiol: insights from in vitro and in vivo models. Brain Behav Immun. 2022;104:155–70.PubMedCrossRef
129.
Xie C, et al. Amelioration of Alzheimer’s disease pathology by mitophagy inducers identified via machine learning and a cross-species workflow. Nat Biomed Eng. 2022;6(1):76–93.PubMedPubMedCentralCrossRef
130.
Chen C, et al. Melatonin ameliorates cognitive deficits through improving mitophagy in a mouse model of Alzheimer’s disease. J Pineal Res. 2021;71(4): e12774.PubMedCrossRef
131.
Han X, et al. Quercetin hinders microglial activation to alleviate neurotoxicity via the interplay between NLRP3 inflammasome and mitophagy. Redox Biol. 2021;44: 102010.PubMedPubMedCentralCrossRef
132.
133.
Li HW, Zhang L, Qin C. Current state of research on non-human primate models of Alzheimer’s disease. Anim Model Exp Med. 2019;2(4):227–38.CrossRef
134.
Picone P, et al. Nano-structured myelin: new nanovesicles for targeted delivery to white matter and microglia, from brain-to-brain. Mater Today Bio. 2021;12: 100146.PubMedPubMedCentralCrossRef
135.
Jia Y, et al. The brain targeted delivery of programmed cell death 4 specific siRNA protects mice from CRS-induced depressive behavior. Cell Death Dis. 2021;12(11):1077.PubMedPubMedCentralCrossRef
136.
Metadata
Title
Mitochondrial dysfunction in microglia: a novel perspective for pathogenesis of Alzheimer’s disease
Authors
Yun Li
Xiaohuan Xia
Yi Wang
Jialin C. Zheng
Publication date
01-12-2022
Publisher
BioMed Central
Published in
Journal of Neuroinflammation / Issue 1/2022
Electronic ISSN: 1742-2094
DOI
https://doi.org/10.1186/s12974-022-02613-9

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