The Role of Astrocytes in the Relationship Between Amyloid-ß Accumulation and Synaptic Dysfunction in Alzheimer’s Disease
DOI:
https://doi.org/10.47611/jsrhs.v13i1.6191Keywords:
Astrocytes, Amyloid-B, Synaptic Dysfunction, Alzheimer's DiseaseAbstract
Alzheimer’s disease is a progressive neurodegenerative disorder and is the most common cause of dementia worldwide. The disease is characterized by the accumulation of Amyloid-ß plaques, aggregation of tau protein resulting in neurofibrillary tangles, and the dysfunction of neuronal synapses, all of which lead to cognitive impairment and memory loss. Although previous research has focused more on the neuronal aspect of Alzheimer’s disease, recent research has implicated the role of glial cells, most notably astrocytes, to have a significant impact on the disease’s pathogenesis. Astrocytes are the most abundant type of glial cell in the central nervous system and are important in maintaining neuron homeostasis through their various functions in gliotransmission, phagocytosis, and synaptic regulation. The main objective of this review is to examine the role of astrocytes in Alzheimer's disease, specifically in the relationship between Amyloid-ß accumulation and synaptic dysfunction. After reviewing the literature, it can be concluded that Amyloid-ß accumulation induces several changes in astrocytic functions that promote the malfunction of synaptic transmission, thus resulting in synaptic dysfunction in Alzheimer’s Disease. As there has been no cure or highly efficient treatment for Alzheimer’s disease thus far, further research into the role of astrocytes in the relationship between Amyloid-ß accumulation and synaptic dysfunction in the disease could provide alternative pathways and targets for therapeutic treatment.
Downloads
References or Bibliography
Acosta, C., Anderson, H. D., & Anderson, C. M. (2017). Astrocyte dysfunction in Alzheimer disease. Journal of Neuroscience Research, 95(12), 2430–2447. https://doi.org/10.1002/jnr.24075
Agulhon, C., Fiacco, T. A., & McCarthy, K. D. (2010). Hippocampal short- and long-term plasticity are not modulated by astrocyte ca 2+ signaling. Science, 327(5970), 1250–1254. https://doi.org/10.1126/science.1184821
Alifragis, P., & Marsh, J. (2018). Synaptic dysfunction in Alzheimer's disease: The effects of amyloid beta on synaptic vesicle dynamics as a novel target for therapeutic intervention. Neural Regeneration Research, 13(4), 616. https://doi.org/10.4103/1673-5374.230276
Barnes, J. R., Mukherjee, B., Rogers, B. C., Nafar, F., Gosse, M., & Parsons, M. P. (2020). The relationship between glutamate dynamics and activity-dependent synaptic plasticity. The Journal of Neuroscience, 40(14), 2793–2807. https://doi.org/10.1523/jneurosci.1655-19.2020
Blasko, I., Veerhuis, R., Stampfer-Kountchev, M., Saurwein-Teissl, M., Eikelenboom, P., & Grubeck-Loebenstein, B. (2000). Costimulatory effects of interferon-γ and interleukin-1β or tumor necrosis factor α on the synthesis of AΒ1-40 and AΒ1-42 by human astrocytes. Neurobiology of Disease, 7(6), 682–689. https://doi.org/10.1006/nbdi.2000.0321
Bosson, A., Paumier, A., Boisseau, S., Jacquier-Sarlin, M., Buisson, A., & Albrieux, M. (2017). TRPA1 channels promote astrocytic ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide. Molecular Neurodegeneration, 12(1). https://doi.org/10.1186/s13024-017-0194-8
Bowser, D. N., & Khakh, B. S. (2007). Vesicular ATP is the predominant cause of intercellular calcium waves in astrocytes. Journal of General Physiology, 129(6), 485–491. https://doi.org/10.1085/jgp.200709780
Chen, G.-fang, Xu, T.-hai, Yan, Y., Zhou, Y.-ren, Jiang, Y., Melcher, K., & Xu, H. E. (2017). Amyloid beta: Structure, biology and structure-based therapeutic development. Acta Pharmacologica Sinica, 38(9), 1205–1235. https://doi.org/10.1038/aps.2017.28
Chen, Y., Fu, A. K. Y., & Ip, N. Y. (2019). Synaptic dysfunction in Alzheimer's disease: Mechanisms and therapeutic strategies. Pharmacology & Therapeutics, 195, 186–198. https://doi.org/10.1016/j.pharmthera.2018.11.006
Cho, H. J., Kim, S.-K., Jin, S. M., Hwang, E.-M., Kim, Y. S., Huh, K., & Mook-Jung, I. (2007). IFN-γ-induced BACE1 expression is mediated by activation of JAK2 and ERK1/2 signaling pathways and direct binding of STAT1 to BACE1 promoter in astrocytes. Glia, 55(3), 253–262. https://doi.org/10.1002/glia.20451
Chun, H., & Lee, C. J. (2018). Reactive astrocytes in Alzheimer's disease: A double-edged sword. Neuroscience Research, 126, 44–52. https://doi.org/10.1016/j.neures.2017.11.012
Chung, W.-S., Allen, N. J., & Eroglu, C. (2015). Astrocytes control synapse formation, function, and elimination. Cold Spring Harbor Perspectives in Biology, 7(9). https://doi.org/10.1101/cshperspect.a020370
Cirrito, J. R., Yamada, K. A., Finn, M. B., Sloviter, R. S., Bales, K. R., May, P. C., Schoepp, D. D., Paul, S. M., Mennerick, S., & Holtzman, D. M. (2005). Synaptic activity regulates interstitial fluid amyloid-β levels in vivo. Neuron, 48(6), 913–922. https://doi.org/10.1016/j.neuron.2005.10.028
Cole, S. L., & Vassar, R. (2007). The Alzheimer's disease beta-secretase enzyme, BACE1. Molecular Neurodegeneration, 2(1), 22. https://doi.org/10.1186/1750-1326-2-22
Couturier, J., Stancu, I.-C., Schakman, O., Pierrot, N., Huaux, F., Kienlen-Campard, P., Dewachter, I., & Octave, J.-N. (2016). Activation of phagocytic activity in astrocytes by reduced expression of the inflammasome component ASC and its implication in a mouse model of Alzheimer disease. Journal of Neuroinflammation, 13(1). https://doi.org/10.1186/s12974-016-0477-y
Das, S., Li, Z., Noori, A., Hyman, B. T., & Serrano-Pozo, A. (2020). Meta-analysis of mouse transcriptomic studies supports a context-dependent astrocyte reaction in acute CNS injury versus neurodegeneration. Journal of Neuroinflammation, 17(1). https://doi.org/10.1186/s12974-020-01898-y
De Mena, L., Smith, M. A., Martin, J., Dunton, K. L., Ceballos-Diaz, C., Jansen-West, K. R., Cruz, P. E., Dillon, K. D., Rincon-Limas, D. E., Golde, T. E., Moore, B. D., & Levites, Y. (2020). ASS40 displays amyloidogenic properties in the non-transgenic mouse brain but does not exacerbate ASS42 toxicity in drosophila. Alzheimer's Research & Therapy, 12(1). https://doi.org/10.1186/s13195-020-00698-z
Dorostkar, M. M., Zou, C., Blazquez-Llorca, L., & Herms, J. (2015). Analyzing dendritic spine pathology in Alzheimer’s disease: Problems and opportunities. Acta Neuropathologica, 130(1), 1-19. https://doi.org/10.1007/s00401-015-1449-5
El-Amouri, S. S., Zhu, H., Yu, J., Marr, R., Verma, I. M., & Kindy, M. S. (2008). NEPRILYSIN: An enzyme candidate to slow the progression of Alzheimer's disease. The American Journal of Pathology, 172(5), 1342–1354. https://doi.org/10.2353/ajpath.2008.070620
Farrant, M., & Nusser, Z. (2005). Variations on an inhibitory theme: Phasic and tonic activation of Gabaa receptors. Nature Reviews Neuroscience, 6(3), 215–229. https://doi.org/10.1038/nrn1625
Fiacco, T. A., Agulhon, C., Taves, S. R., Petravicz, J., Casper, K. B., Dong, X., Chen, J., & McCarthy, K. D. (2007). Selective stimulation of astrocyte calcium in situ does not affect neuronal excitatory synaptic activity. Neuron, 54(4), 611–626. https://doi.org/10.1016/j.neuron.2007.04.032
Fiala, M., & Veerhuis, R. (2010). Biomarkers of inflammation and amyloid-β phagocytosis in patients at risk of Alzheimer disease. Experimental Gerontology, 45(1), 57–63. https://doi.org/10.1016/j.exger.2009.08.003
Grochowska, K. M., Yuanxiang, P. A., Bär, J., Raman, R., Brugal, G., Sahu, G., Schweizer, M., Bikbaev, A., Schilling, S., Demuth, H. U., & Kreutz, M. R. (2017). Posttranslational modification impact on the mechanism by which amyloid‐β induces synaptic dysfunction. EMBO Reports, 18(6), 962–981. https://doi.org/10.15252/embr.201643519
Guthrie, P. B., Knappenberger, J., Segal, M., Bennett, M. V., Charles, A. C., & Kater, S. B. (1999). ATP released from astrocytes mediates glial calcium waves. The Journal of Neuroscience, 19(2), 520–528. https://doi.org/10.1523/jneurosci.19-02-00520.1999
Hamilton, N. B., & Attwell, D. (2010). Do astrocytes really exocytose neurotransmitters? Nature Reviews Neuroscience, 11(4), 227–238. https://doi.org/10.1038/nrn2803
Han, K.-S., Woo, J., Park, H., Yoon, B.-J., Choi, S., & Lee, C. J. (2013). Channel-mediated astrocytic glutamate release via bestrophin-1 targets synaptic nmdars. Molecular Brain, 6(1). https://doi.org/10.1186/1756-6606-6-4
Harada, K., Kamiya, T., & Tsuboi, T. (2016). Gliotransmitter release from astrocytes: Functional, developmental, and pathological implications in the brain. Frontiers in Neuroscience, 9. https://doi.org/10.3389/fnins.2015.00499
Haughey, N. J., & Mattson, M. P. (2003). Alzheimer's amyloid β-peptide enhances ATP/gap junction-mediated calcium-wave propagation in astrocytes. NeuroMolecular Medicine, 3(3), 173–180. https://doi.org/10.1385/nmm:3:3:173
Henneberger, C., Papouin, T., Oliet, S. H., & Rusakov, D. A. (2010). Long-term potentiation depends on release of D-serine from astrocytes. Nature, 463(7278), 232–236. https://doi.org/10.1038/nature08673
Holcomb, L. A., Gordon, M. N., Jantzen, P., Hsiao, K., Duff, K., & Morgan, D. (1999). Behavioral Changes in Transgenic Mice Expressing Both Amyloid Precursor Protein and Presenilin-1 Mutations: Lack of Association with Amyloid Deposits. Behavior Genetics, 29(3), 177–185. https://doi.org/10.1023/a:1021691918517
Hong, H. S., Hwang, E. M., Sim, H. J., Cho, H.-J., Boo, J. H., Oh, S. S., Kim, S. U., & Mook-Jung, I. (2003). Interferon γ stimulates β-secretase expression and sappβ production in astrocytes. Biochemical and Biophysical Research Communications, 307(4), 922–927. https://doi.org/10.1016/s0006-291x(03)01270-1
Huang, S., Tong, H., Lei, M., Zhou, M., Guo, W., Li, G., Tang, X., Li, Z., Mo, M., Zhang, X., Chen, X., Cen, L., Wei, L., Xiao, Y., Li, K., Huang, Q., Yang, X., Liu, W., Zhang, L., … Xu, P. (2018). Astrocytic glutamatergic transporters are involved in AΒ-induced synaptic dysfunction. Brain Research, 1678, 129–137. https://doi.org/10.1016/j.brainres.2017.10.011
Jahn, R., & Fasshauer, D. (2012). Molecular machines governing exocytosis of synaptic vesicles. Nature, 490(7419), 201–207. https://doi.org/10.1038/nature11320
Jiang, Q., Lee, C. Y. D., Mandrekar, S., Wilkinson, B., Cramer, P., Zelcer, N., Mann, K., Lamb, B., Willson, T. M., Collins, J. L., Richardson, J. C., Smith, J. D., Comery, T. A., Riddell, D., Holtzman, D. M., Tontonoz, P., & Landreth, G. E. (2008). ApoE promotes the proteolytic degradation of AΒ. Neuron, 58(5), 681–693. https://doi.org/10.1016/j.neuron.2008.04.010
Jo, S., Yarishkin, O., Hwang, Y. J., Chun, Y. E., Park, M., Woo, D. H., Bae, J. Y., Kim, T., Lee, J., Chun, H., Park, H. J., Lee, D. Y., Hong, J., Kim, H. Y., Oh, S.-J., Park, S. J., Lee, H., Yoon, B.-E., Kim, Y. S., … Lee, C. J. (2014). GABA from reactive astrocytes impairs memory in mouse models of Alzheimer's disease. Nature Medicine, 20(8), 886–896. https://doi.org/10.1038/nm.3639
Jones, R. S., Minogue, A. M., Connor, T. J., & Lynch, M. A. (2012). Amyloid-β-induced astrocytic phagocytosis is mediated by CD36, CD47 and rage. Journal of Neuroimmune Pharmacology, 8(1), 301–311. https://doi.org/10.1007/s11481-012-9427-3
Jourdain, P., Bergersen, L. H., Bhaukaurally, K., Bezzi, P., Santello, M., Domercq, M., Matute, C., Tonello, F., Gundersen, V., & Volterra, A. (2007). Glutamate exocytosis from astrocytes controls synaptic strength. Nature Neuroscience, 10(3), 331–339. https://doi.org/10.1038/nn1849
Jung, E. S., An, K., Hong, H. S., Kim, J. H., & Mook-Jung, I. (2012). Astrocyte-originated ATP protects Aβ(1-42)-induced impairment of synaptic plasticity. The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(9), 3081–3087. https://doi.org/10.1523/JNEUROSCI.6357-11.2012
Kajiwara, Y., Wang, E., Wang, M., Sin, W. C., Brennand, K. J., Schadt, E., Naus, C. C., Buxbaum, J., & Zhang, B. (2018). Gja1 (Connexin43) is a key regulator of Alzheimer's disease pathogenesis. Acta Neuropathologica Communications, 6(1). https://doi.org/10.1186/s40478-018-0642-x
Kamenetz, F., Tomita, T., Hsieh, H., Seabrook, G., Borchelt, D., Iwatsubo, T., Sisodia, S., & Malinow, R. (2003). App Processing and synaptic function. Neuron, 37(6), 925–937. https://doi.org/10.1016/s0896-6273(03)00124-7
Kervern, M., Angeli, A., Nicole, O., Léveillé, F., Parent, B., Villette, V., Buisson, A., & Dutar, P. (2012). Selective impairment of some forms of synaptic plasticity by oligomeric amyloid-β peptide in the mouse hippocampus: Implication of extrasynaptic NMDA receptors. Journal of Alzheimer's Disease, 32(1), 183–196. https://doi.org/10.3233/jad-2012-120394
Kim, Y., Park, J., & Choi, Y. K. (2019). The role of astrocytes in the central nervous system focused on BK channel and heme oxygenase metabolites: A Review. Antioxidants, 8(5), 121. https://doi.org/10.3390/antiox8050121
Koffie, R. M., Meyer-Luehmann, M., Hashimoto, T., Adams, K. W., Mielke, M. L., Garcia-Alloza, M., Micheva, K. D., Smith, S. J., Kim, M. L., Lee, V. M., Hyman, B. T., & Spires-Jones, T. L. (2009). Oligomeric amyloid β associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques. Proceedings of the National Academy of Sciences, 106(10), 4012–4017. https://doi.org/10.1073/pnas.0811698106
Kofuji, P., & Araque, A. (2021). G-protein-coupled receptors in astrocyte–neuron communication. Neuroscience, 456, 71–84. https://doi.org/10.1016/j.neuroscience.2020.03.025
Konishi, H., Okamoto, T., Hara, Y., Komine, O., Tamada, H., Maeda, M., Osako, F., Kobayashi, M., Nishiyama, A., Kataoka, Y., Takai, T., Udagawa, N., Jung, S., Ozato, K., Tamura, T., Tsuda, M., Yamanaka, K., Ogi, T., Sato, K., & Kiyama, H. (2020). Astrocytic phagocytosis is a compensatory mechanism for microglial dysfunction. The EMBO Journal, 39(22). https://doi.org/10.15252/embj.2020104464
Kullmann, D. M., & Lamsa, K. P. (2007). Long-term synaptic plasticity in hippocampal interneurons. Nature Reviews Neuroscience, 8(9), 687–699. https://doi.org/10.1038/nrn2207
Lee, S., Yoon, B.-E., Berglund, K., Oh, S.-J., Park, H., Shin, H.-S., Augustine, G. J., & Lee, C. J. (2010). Channel-mediated tonic GABA release from glia. Science, 330(6005), 790–796. https://doi.org/10.1126/science.1184334
Li, S., & Selkoe, D. J. (2020). A mechanistic hypothesis for the impairment of synaptic plasticity by soluble AΒ oligomers from alzheimer’s brain. Journal of Neurochemistry, 154(6), 583–597. https://doi.org/10.1111/jnc.15007
Li, S., Hong, S., Shepardson, N. E., Walsh, D. M., Shankar, G. M., & Selkoe, D. (2009). Soluble oligomers of amyloid β protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake. Neuron, 62(6), 788–801. https://doi.org/10.1016/j.neuron.2009.05.012
Liang, J., Kulasiri, D., & Samarasinghe, S. (2017). Computational investigation of amyloid-β-induced location- and subunit-specific disturbances of NMDAR at hippocampal dendritic spine in Alzheimer's disease. PLOS ONE, 12(8). https://doi.org/10.1371/journal.pone.0182743
Liu, L., Wong, T. P., Pozza, M. F., Lingenhoehl, K., Wang, Y., Sheng, M., Auberson, Y. P., & Wang, Y. T. (2004). Role of NMDA receptor subtypes in governing the direction of hippocampal synaptic plasticity. Science, 304(5673), 1021–1024. https://doi.org/10.1126/science.1096615
Liu, Q.-song, Xu, Q., Arcuino, G., Kang, J., & Nedergaard, M. (2004). Astrocyte-mediated activation of neuronal kainate receptors. Proceedings of the National Academy of Sciences, 101(9), 3172–3177. https://doi.org/10.1073/pnas.0306731101
Lööv, C., Mitchell, C. H., Simonsson, M., & Erlandsson, A. (2015). Slow degradation in phagocytic astrocytes can be enhanced by lysosomal acidification. Glia, 63(11), 1997–2009. https://doi.org/10.1002/glia.22873
Mahmoud, S., Gharagozloo, M., Simard, C., & Gris, D. (2019). Astrocytes maintain glutamate homeostasis in the CNS by controlling the balance between glutamate uptake and release. Cells, 8(2), 184. https://doi.org/10.3390/cells8020184
Martins, R. N., Taddei, K., Kendall, C., Evin, G., Bates, K. A., & Harvey, A. R. (2001). Altered expression of apolipoprotein E, amyloid precursor protein and presenilin-1 is associated with chronic reactive gliosis in rat cortical tissue. Neuroscience, 106(3), 557–569. https://doi.org/10.1016/s0306-4522(01)00289-5
Martín, R., Bajo-Grañeras, R., Moratalla, R., Perea, G., & Araque, A. (2015). Circuit-specific signaling in astrocyte-neuron networks in basal ganglia pathways. Science, 349(6249), 730–734. https://doi.org/10.1126/science.aaa7945
Masters, C. L., Bateman, R., Blennow, K., Rowe, C. C., Sperling, R. A., & Cummings, J. L. (2015). Alzheimer's disease. Nature Reviews Disease Primers, 1(1). https://doi.org/10.1038/nrdp.2015.56
Matos, M., Augusto, E., Oliveira, C. R., & Agostinho, P. (2008). Amyloid-beta peptide decreases glutamate uptake in cultured astrocytes: Involvement of oxidative stress and mitogen-activated protein kinase cascades. Neuroscience, 156(4), 898–910. https://doi.org/10.1016/j.neuroscience.2008.08.022
McManus, R. M., Finucane, O. M., Wilk, M. M., Mills, K. H., & Lynch, M. A. (2017). FTY720 attenuates infection-induced enhancement of AΒ accumulation in APP/PS1 mice by modulating astrocytic activation. Journal of Neuroimmune Pharmacology, 12(4), 670–681. https://doi.org/10.1007/s11481-017-9753-6
Medeiros, R., Prediger, R. D., Passos, G. F., Pandolfo, P., Duarte, F. S., Franco, J. L., Dafre, A. L., Di Giunta, G., Figueiredo, C. P., Takahashi, R. N., Campos, M. M., & Calixto, J. B. (2007). Connecting TNF- signaling pathways to inos expression in a mouse model of Alzheimer's disease: Relevance for the behavioral and synaptic deficits induced by amyloid protein. Journal of Neuroscience, 27(20), 5394–5404. https://doi.org/10.1523/jneurosci.5047-06.2007
Min, R., & Nevian, T. (2012). Astrocyte signaling controls spike timing–dependent depression at neocortical synapses. Nature Neuroscience, 15(5), 746–753. https://doi.org/10.1038/nn.3075
Morris, G. P., Clark, I. A., & Vissel, B. (2014). Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's disease. Acta Neuropathologica Communications, 2(1). https://doi.org/10.1186/s40478-014-0135-5
Mucke, L., & Selkoe, D. J. (2012). Neurotoxicity of amyloid -protein: Synaptic and network dysfunction. Cold Spring Harbor Perspectives in Medicine, 2(7). https://doi.org/10.1101/cshperspect.a006338
Mucke, L., & Selkoe, D. J. (2012). Neurotoxicity of amyloid -protein: Synaptic and network dysfunction. Cold Spring Harbor Perspectives in Medicine, 2(7). https://doi.org/10.1101/cshperspect.a006338
Nagy, J. I., Li, W., Hertzberg, E. L., & Marotta, C. A. (1996). Elevated connexin43 immunoreactivity at sites of amyloid plaques in alzheimer's disease. Brain Research, 717(1-2), 173–178. https://doi.org/10.1016/0006-8993(95)01526-4
Nanclares, C., Baraibar, A. M., Araque, A., & Kofuji, P. (2021). Dysregulation of astrocyte–neuronal communication in alzheimer’s disease. International Journal of Molecular Sciences, 22(15), 7887. https://doi.org/10.3390/ijms22157887
Nielsen, H. M., Mulder, S. D., Beliën, J. A., Musters, R. J., Eikelenboom, P., & Veerhuis, R. (2010). Astrocytic AΒ1-42 uptake is determined by AΒ-aggregation state and the presence of amyloid-associated proteins. Glia, 58(10), 1235–1246. https://doi.org/10.1002/glia.21004
Orellana, J. A., Froger, N., Ezan, P., Jiang, J. X., Bennett, M. V., Naus, C. C., Giaume, C., & Sáez, J. C. (2011). ATP and glutamate released via astroglial connexin 43 hemichannels mediate neuronal death through activation of Pannexin 1 hemichannels. Journal of Neurochemistry, 118(5), 826–840. https://doi.org/10.1111/j.1471-4159.2011.07210.x
Panatier, A., & Robitaille, R. (2016). Astrocytic mGluR5 and the tripartite synapse. Neuroscience, 323, 29–34. https://doi.org/10.1016/j.neuroscience.2015.03.063
Panatier, A., Vallée, J., Haber, M., Murai, K. K., Lacaille, J.-C., & Robitaille, R. (2011). Astrocytes are endogenous regulators of basal transmission at central synapses. Cell, 146(5), 785–798. https://doi.org/10.1016/j.cell.2011.07.022
Pangršič, T., Potokar, M., Stenovec, M., Kreft, M., Fabbretti, E., Nistri, A., Pryazhnikov, E., Khiroug, L., Giniatullin, R., & Zorec, R. (2007). Exocytotic release of ATP from cultured astrocytes. Journal of Biological Chemistry, 282(39), 28749–28758. https://doi.org/10.1074/jbc.m700290200
Parpura , V., Fang , Y., Basarsky , T., Jahn , R., & Haydon , P. G. (1995). Expression of synaptobrevin II, Cellubrevin and syntaxin but not snap-25 in cultured astrocytes. FEBS Letters, 377(3), 489–492. https://doi.org/10.1016/0014-5793(95)01401-2
Pham, C., Hérault, K., Oheim, M., Maldera, S., Vialou, V., Cauli, B., & Li, D. (2021). Astrocytes respond to a neurotoxic AΒ fragment with state-dependent ca2+ alteration and multiphasic transmitter release. Acta Neuropathologica Communications, 9(1). https://doi.org/10.1186/s40478-021-01146-1
Poskanzer, K. E., & Yuste, R. (2016). Astrocytes regulate cortical state switching in vivo. Proceedings of the National Academy of Sciences, 113(19). https://doi.org/10.1073/pnas.1520759113
Puzzo, D., Privitera, L., Leznik, E., Fa, M., Staniszewski, A., Palmeri, A., & Arancio, O. (2008). Picomolar amyloid- positively modulates synaptic plasticity and memory in Hippocampus. Journal of Neuroscience, 28(53), 14537–14545. https://doi.org/10.1523/jneurosci.2692-08.2008
Role of microglia and astrocytes in Alzheimer's disease. (2004). The Role of Glia in Neurotoxicity, 319–332. https://doi.org/10.1201/9781420039740-23
Rossner, S., Lange-Dohna, C., Zeitschel, U., & Perez-Polo, J. R. (2005). Alzheimer's disease beta-secretase BACE1 is not a neuron-specific enzyme. Journal of Neurochemistry, 92(2), 226–234. https://doi.org/10.1111/j.1471-4159.2004.02857.x
Saido, T. C., Iwatsubo, T., Mann, D. M. A., Shimada, H., Ihara, Y., & Kawashima, S. (1995). Dominant and differential deposition of distinct β-amyloid peptide species, AΒN3(PE), in senile plaques. Neuron, 14(2), 457–466. https://doi.org/10.1016/0896-6273(95)90301-1
Schiavo, G. G., Benfenati, F., Poulain, B., Rossetto, O., de Laureto, P. P., DasGupta, B. R., & Montecucco, C. (1992). Tetanus and botulinum-B neurotoxins block neurotransmitter release by proteolytic cleavage of Synaptobrevin. Nature, 359(6398), 832–835. https://doi.org/10.1038/359832a0
Scimemi, A., Meabon, J. S., Woltjer, R. L., Sullivan, J. M., Diamond, J. S., & Cook, D. G. (2013). Amyloid- 1-42 slows clearance of synaptically released glutamate by mislocalizing astrocytic GLT-1. Journal of Neuroscience, 33(12), 5312–5318. https://doi.org/10.1523/jneurosci.5274-12.2013
Selkoe, D. J., & Hardy, J. (2016). The amyloid hypothesis of Alzheimer's disease at 25 Years. EMBO Molecular Medicine, 8(6), 595–608. https://doi.org/10.15252/emmm.201606210
Shrivastava, A. N., Kowalewski, J. M., Renner, M., Bousset, L., Koulakoff, A., Melki, R., Giaume, C., & Triller, A. (2013). Β-amyloid and ATP-induced diffusional trapping of astrocyte and neuronal metabotropic glutamate type-5 receptors. Glia, 61(10), 1673–1686. https://doi.org/10.1002/glia.22548
Smit, T., Deshayes, N. A., Borchelt, D. R., Kamphuis, W., Middeldorp, J., & Hol, E. M. (2021). Reactive astrocytes as treatment targets in Alzheimer's disease—systematic review of studies using the appswe ps1de9 mouse model. Glia, 69(8), 1852–1881. https://doi.org/10.1002/glia.23981
Smith, J. A., Das, A., Ray, S. K., & Banik, N. L. (2012). Role of pro-inflammatory cytokines released from microglia in Neurodegenerative Diseases. Brain Research Bulletin, 87(1), 10–20. https://doi.org/10.1016/j.brainresbull.2011.10.004
Sondag, C. M., Dhawan, G., & Combs, C. K. (2009). Beta amyloid oligomers and fibrils stimulate differential activation of primary microglia. Journal of Neuroinflammation, 6(1). https://doi.org/10.1186/1742-2094-6-1
Steinert, J. R., Chernova, T., & Forsythe, I. D. (2010). Nitric oxide signaling in brain function, dysfunction, and dementia. The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 16(4), 435–452. https://doi.org/10.1177/1073858410366481
Sturcher-Pierrat , C., & Staufenbiel, M. (2006). Pathogenic mechanisms of alzheimer's disease analyzed in the app23 transgenic mouse model. Annals of the New York Academy of Sciences, 920(1), 134–139. https://doi.org/10.1111/j.1749-6632.2000.tb06915.x
Sun, W., McConnell, E., Pare, J.-F., Xu, Q., Chen, M., Peng, W., Lovatt, D., Han, X., Smith, Y., & Nedergaard, M. (2013). Glutamate-dependent neuroglial calcium signaling differs between young and adult brains. Science, 339(6116), 197–200. https://doi.org/10.1126/science.1226740
Söllvander, S., Nikitidou, E., Brolin, R., Söderberg, L., Sehlin, D., Lannfelt, L., & Erlandsson, A. (2016). Accumulation of amyloid-β by astrocytes results in enlarged endosomes and microvesicle-induced apoptosis of neurons. Molecular Neurodegeneration, 11(1). https://doi.org/10.1186/s13024-016-0098-z
Südhof, T. C. (2018). Towards an understanding of synapse formation. Neuron, 100(2), 276–293. https://doi.org/10.1016/j.neuron.2018.09.040
Valtcheva, S., & Venance, L. (2019). Control of long-term plasticity by glutamate transporters. Frontiers in Synaptic Neuroscience, 11. https://doi.org/10.3389/fnsyn.2019.00010
Wei, W., Nguyen, L. N., Kessels, H. W., Hagiwara, H., Sisodia, S., & Malinow, R. (2009). Amyloid beta from axons and dendrites reduces local spine number and plasticity. Nature Neuroscience, 13(2), 190–196. https://doi.org/10.1038/nn.2476
Xiao, Q., Yan, P., Ma, X., Liu, H., Perez, R., Zhu, A., Gonzales, E., Burchett, J. M., Schuler, D. R., Cirrito, J. R., Diwan, A., & Lee, J.-M. (2014). Enhancing astrocytic lysosome biogenesis facilitates a clearance and attenuates amyloid plaque pathogenesis. Journal of Neuroscience, 34(29), 9607–9620. https://doi.org/10.1523/jneurosci.3788-13.2014
Zhao, J., Fu, Y., Yasvoina, M., Shao, P., Hitt, B., O'Connor, T., Logan, S., Maus, E., Citron, M., Berry, R., Binder, L., & Vassar, R. (2007). -site amyloid precursor protein cleaving enzyme 1 levels become elevated in neurons around amyloid plaques: Implications for Alzheimer's disease pathogenesis. Journal of Neuroscience, 27(14), 3639–3649. https://doi.org/10.1523/jneurosci.4396-06.2007
Zhao, J., O'Connor, T., & Vassar, R. (2011). The contribution of activated astrocytes to AΒ production: Implications for alzheimer's disease pathogenesis. Journal of Neuroinflammation, 8(1). https://doi.org/10.1186/1742-2094-8-150
Published
How to Cite
Issue
Section
Copyright (c) 2024 Afsheen Fatima; Arij Daou
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
Copyright holder(s) granted JSR a perpetual, non-exclusive license to distriute & display this article.
