Function of the microglia in neuroinflammation of Alzheimer's disease:a brief review

doi:10.16352/j.issn.1001-6325.2022.08.1310

Abstract

Abstract: Different types of activated imbroglio exist in the brain of the patients with Alzheimer's disease (AD). As the neuroinflammation reaction progresses, significant changes take place in the morphology and function of those cells. They could play a pathogenic role by altering the phagocytic function of cells, including intracellular toxic reactions or directly participate in immune response. Several clinical trials have been conducted to promote targeted therapy focusing on the role that microglia played in neuroinflammation reactions of AD. More large scale studies are necessary to elucidate the function and mechanism of microglia in the neuroinflammation reaction of AD.

Key words: Alzheimer's disease, microglia, neuroinflammation

CLC Number:

R741.02

WANG Yuan-zhuo, ZHENG Qing-yue, ZHANG Han-lin, QIU Wen-ying, WANG Tao, MA Chao. Function of the microglia in neuroinflammation of Alzheimer's disease:a brief review[J]. Basic & Clinical Medicine, 2022, 42(8): 1310-1313.

References 25

[1]	Long J, Holtzman D. Alzheimer disease:an update on pathobiology and treatment strategies[J]. Cell,2019,179:312-339.
[2]	Braak H, Thal DR, Ghebremedhin E, et al. Stages of the pathologic process in Alzheimer disease:age categories from 1 to 100 years[J]. J Neuropathol Exp Neurol,2011,70:960-969.
[3]	Parbo P, Ismail R, Sommerauer M, et al. Does inflammation precede tau aggregation in early Alzheimer's disease? A PET study[J]. Neurobiol Dis,2018,117:211-216.
[4]	Singh-Bains MK, Linke V, Austria MDR, et al. Altered microglia and neurovasculature in the Alzheimer's disease cerebellum[J]. Neurobiol Dis,2019,132.doi:10.1016/j.nbd.2019.104589.
[5]	Carmona-Abellan M, Martinez-Valbuena I, Marcilla I, et al. Microglia is associated with p-Tau aggregates in the olfactory bulb of patients with neurodegenerative diseases[J]. Neurol Sci,2020. doi:10.1007/s10072-020-04686-x.
[6]	Hopperton KE, Mohammad D, Trépanier MO, et al. Markers of microglia in post-mortem brain samples from patients with Alzheimer's disease:a systematic review[J]. Mol Psychiatry,2018,23:177-198.
[7]	Lue LF, Schmitz CT, Serrano G, et al. TREM2 protein expression changes correlate with Alzheimer's disease neurodegenerative pathologies in post-mortem temporal cortices[J]. Brain Pathol,2015,25:469-480.
[8]	Streit WJ, Khoshbouei H, Bechmann I. Dystrophic microglia in late-onset alzheimer's disease[J]. Glia,2020,68:845-854.
[9]	Toomey CE, Heywood W, Benson BC, et al. Investigation of pathology, expression and proteomic profiles in human TREM2 variant postmortem brains with and without Alzheimer's disease[J]. Brain Pathology,2020,30:794-810.
[10]	Zhou Y, Song WM, Andhey PS, et al. Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer's disease[J]. Nat Med,2020,26:131-142.
[11]	Sierra A, Gottfried-Blackmore AC, Mcewen BS, et al. Microglia derived from aging mice exhibit an altered inflammatory profile[J]. Glia, 2007, 55:412-424.
[12]	Ofengeim D, Mazzitelli S, Ito Y, et al. RIPK1 mediates a disease-associated microglial response in Alzheimer's disease[J]. Proc Natl Acad Sci U S A,2017,114:e8788-e8797.
[13]	Crapser JD, Spangenberg EE, Barahona RA, et al. Microglia facilitate loss of perineuronal nets in the Alzheimer's disease brain[J]. EBioMedicine,2020,58. doi:10.1016/j.ebiom.2020.102919.
[14]	Hemonnot AL, Hua J, Ulmann L, et al. Microglia in Alzheimer disease:well-known targets and new opportunities[J]. Front Aging Neurosci,2019,11:233. doi:10.3389/fnagi.2019.00233.
[15]	Lian H, Litvinchuk A, Chiang AC, et al. Astrocyte-microglia cross talk through complement activation modulates amyloid pathology in mouse models of Alzheimer's disease[J]. J Neurosci,2016,36:577-589.
[16]	Angelova DM, Brown DR. Microglia and the aging brain:are senescent microglia the key to neurodegeneration?[J]. J Neurochem,2019,151:676-688.
[17]	Cummings JL, Tong G, Ballard C. Treatment combina-tions for Alzheimer's disease:current and future pharmacotherapy options[J]. J Alzheimers Dis,2019,67:779-794.
[18]	Dobrowolska Zakaria JA, Vassar RJ. A promising, novel, and unique BACE1 inhibitor emerges in the quest to prevent Alzheimer's disease[J]. EMBO Mol Med,2018,10. doi:10.15252/emmm.201809717.
[19]	Heneka MT, Carson MJ, El Khoury J, et al. Neuroinflammation in Alzheimer's disease[J]. Lancet Neurol, 2015, 14:388-405.
[20]	Maher-Edwards G, De'Ath J, Barnett C, et al. A 24-week study to evaluate the effect of rilapladib on cognition and cerebrospinal fluid biomarkers of Alzheimer's disease[J]. Alzheimers Dement (NY),2015,1:131-140.
[21]	Huang F, Wang K, Shen J. Lipoprotein-associated phospholipase A2:the story continues[J]. Med Res Rev,2020,40:79-134.
[22]	Gopalakrishnan V, Spencer CN, Nezi L, et al. Gut microbiome modulates response to anti-PD-1 immunotherapy in melanoma patients[J]. Science,2018,359:97-103.
[23]	Mullard A. Microglia-targeted candidates push the Alzheimer drug envelope[J]. Nat Rev Drug Discov,2018,17:303-305.
[24]	Wang J, Tan L, Wang HF, et al. Anti-inflammatory drugs and risk of Alzheimer's disease:an updated syste-matic review and meta-analysis[J]. J Alzheimers Dis,2015,44:385-396.
[25]	Omar SH, Scott CJ, Hamlin AS, et al. Olive biophenols reduces Alzheimer's pathology in sh-sy5y cells and appswe mice[J]. Int J Mol Sci,2018,20. doi:10.3390/ijms20010125.