Efecto de la sobreexpresión de CCL1 (I-309) en las espinas dendríticas de neuronas del hipocampo

Lorena L. Adames-Torres; Alanna S. Madrid L; Kevin G. Mata A.; Julio A. Flores-Cuadra; Gabrielle B.  Britton; Alcibiades E.  Villarreal; María B. Carreira F.

doi:10.48204/j.scientia.v35n1.a6658

Submitted January 3, 2025

Published 2025-01-06

Artículos

Vol. 35 No. 1 (2025): Scientia

Effect of CCL1 (I-309) overexpression on dendritic spines of hippocampal neurons

Lorena L. Adames-Torres ⁺⁻
Alanna S. Madrid L ⁺⁻
Kevin G. Mata A. ⁺⁻
Julio A. Flores-Cuadra ⁺⁻
Gabrielle B. Britton ⁺⁻
Alcibiades E. Villarreal ⁺⁻
María B. Carreira F. ⁺⁻

DOI https://doi.org/10.48204/j.scientia.v35n1.a6658

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DOI: 10.48204/j.scientia.v35n1.a6658

Published: 2025-01-06

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Adames-Torres , L. L., Madrid L , A. S., Mata A. , K. G., Flores-Cuadra , J. A., Britton , G. B., Villarreal , A. E., & Carreira F. , M. B. (2025). Effect of CCL1 (I-309) overexpression on dendritic spines of hippocampal neurons . Scientia, 35(1), 71–85. https://doi.org/10.48204/j.scientia.v35n1.a6658

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Abstract

Abnormal accumulation of ?-amyloid (A?), hyperphosphorylated tau protein, and neuroinflammation are factors that affect neuronal function in Alzheimer´s Disease (AD). AD-associated neuroinflammation could cause synaptic damage itself or exacerbate the damage caused by A? accumulation. The cytokine CCL1 (I-309) has been detected increased in the peripheral blood serum of people with Mild Cognitive Impairment (MCI) and AD, so it is proposed that it may be useful as a biomarker for the diagnosis of MCI and AD. The general objective of this study was to evaluate the effect of overexpression of the CCL1(I-309) in the dendritic spines of neurons located in the hippocampus. Sprague Dawley (N=6) were used as an animal model, in which stereotaxic surgeries were performed to inoculate CCL1 overexpression. Golgi staining was performed on the brains of the rats, a cryostat was used to make the histological sections and the density of dendritic spines was evaluated by optical microscopy. The one-way ANOVA did not show significant differences (p>0.05) between the CCL1 overexpression group when compared to the control group and the A?_1-42+ CCL1 overexpression group. It was concluded that CCL1 overexpression does not significantly modify the density of dendritic spines in the hippocampus.

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Al-Ghraiybah, N. F., Wang, J., Alkhalifa, A. E., Roberts, A. B., Raj, R., Yang, E., & Kaddoumi, A. (2022). Glial Cell-Mediated Neuroinflammation in Alzheimer’s Disease. In International Journal of Molecular Sciences (Vol. 23, Issue 18). MDPI. https://doi.org/10.3390/ijms231810572
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Borbély, E., Horváth, J., Furdan, S., Bozsó, Z., Penke, B., & Fülöp, L. (2014). Simultaneous changes of spatial memory and spine density after intrahippocampal administration of fibrillar a ? 1-42 to the rat brain. BioMed Research International, 2014. https://doi.org/10.1155/2014/345305
Breijyeh, Z., & Karaman, R. (2020). Comprehensive Review on Alzheimer ’ s Disease?: Molecules, 25(24).
Brosseron, F., Kleemann, K., Kolbe, C. C., Santarelli, F., Castro-Gomez, S., Tacik, P., Latz, E., Jessen, F., & Heneka, M. T. (2021). Interrelations of Alzheimer´s disease candidate biomarkers neurogranin, fatty acid-binding protein 3 and ferritin to neurodegeneration and neuroinflammation. Journal of Neurochemistry, 157(6), 2210–2224. https://doi.org/10.1111/jnc.15175
Chidambaram, S. B., Rathipriya, A. G., Bolla, S. R., Bhat, A., Ray, B., Mahalakshmi, A. M., Manivasagam, T., Thenmozhi, A. J., Essa, M. M., Guillemin, G. J., Chandra, R., & Sakharkar, M. K. (2019). Dendritic spines: Revisiting the physiological role. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 92, 161–193. https://doi.org/10.1016/J.PNPBP.2019.01.005
Dorostkar, M. M., Zou, C., Blazquez-Llorca, L., & Herms, J. (2015). Analyzing dendritic spine pathology in Alzheimer’s disease: problems and opportunities. In Acta Neuropathologica (Vol. 130, Issue 1). Springer Verlag. https://doi.org/10.1007/s00401-015-1449-5
Facchinetti, R., Bronzuoli, M., & Scudei, C. (2018). An animal model disease based on the intrahippocampal injection of amyloide B-peptido (1- 42). In Neurotrophic Factors: Methods and Protocols, Methods in Molecular Biology.
Götz, J., Bodea, L. G., & Goedert, M. (2018). Rodent models for Alzheimer disease. In Nature Reviews Neuroscience (Vol. 19, Issue 10, pp. 583–598). Nature Publishing Group. https://doi.org/10.1038/s41583-018-0054-8
Gupta, V. B., Hone, E., Pedrini, S., Doecke, J., O’Bryant, S., James, I., Bush, A. I., Rowe, C. C., Villemagne, V. L., Ames, D., Masters, C. L., & Martins, R. N. (2017). Altered levels of blood proteins in Alzheimer’s disease longitudinal study: Results from Australian Imaging Biomarkers Lifestyle Study of Ageing cohort. Alzheimer’s and Dementia: Diagnosis, Assessment and Disease Monitoring, 8, 60–72. https://doi.org/10.1016/j.dadm.2017.04.003
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Kasza, Á., Penke, B., Frank, Z., Bozsó, Z., Szegedi, V., Hunya, Á., Németh, K., Kozma, G., & Fülöp, L. (2017). Studies for improving a rat model of Alzheimer’s disease: ICV administration of well-characterized ?-amyloid 1-42 oligomers induce dysfunction in spatial memory. Molecules, 22(11). https://doi.org/10.3390/molecules22112007
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McLarnon, J. G. (2014). Correlated inflammatory responses and neurodegeneration in peptide-injected animal models of Alzheimer’s disease. BioMed Research International, 2014. https://doi.org/10.1155/2014/923670
Monson, N. L., Ireland, S. J., Ligocki, A. J., Chen, D., Rounds, W. H., Li, M., Huebinger, R. M., Munro Cullum, C., Greenberg, B. M., Stowe, A. M., & Zhang, R. (2014). Elevated CNS inflammation in patients with preclinical Alzheimer’s disease. Journal of Cerebral Blood Flow and Metabolism, 34(1), 30–33. https://doi.org/10.1038/jcbfm.2013.183
O’Bryant, S. E., Xiao, G., Barber, R., Huebinger, R., Wilhelmsen, K., Edwards, M., Graff-Radford, N., Doody, R., & Diaz-Arrastia, R. (2011). A blood-based screening tool for Alzheimer’s disease that spans serum and plasma: Findings from TARC and ADNI. PLoS ONE, 6(12). https://doi.org/10.1371/journal.pone.0028092
Paxinos, G., & Watson, C. (2006). The Rat Brain in Stereotaxic Coordinates (6th Edititon). Academic Express.
Petralia, M. C., Battaglia, G., Bruno, V., Pennisi, M., Mangano, K., Lombardo, S. D., Fagone, P., Cavalli, E., Saraceno, A., Nicoletti, F., & Basile, M. S. (2020). The role of macrophage migration inhibitory factor in Alzheimer?s disease: Conventionally pathogenetic or unconventionally protective? In Molecules (Vol. 25, Issue 2). MDPI AG. https://doi.org/10.3390/molecules25020291
Pilati, N., Barker, M., Panteleimonitis, S., Donga, R., & Hamann, M. (2008). A rapid method combining Golgi and Nissl staining to study neuronal morphology and cytoarchitecture. Journal of Histochemistry and Cytochemistry, 56(6), 539–550. https://doi.org/10.1369/jhc.2008.950246
Ramírez, E., Mendieta, L., Flores, G., & Limón, I. D. (2018). Neurogenesis and morphological-neural alterations closely related to amyloid ?-peptide (25–35)-induced memory impairment in male rats. Neuropeptides, 67, 9–19. https://doi.org/10.1016/j.npep.2017.11.001
Splittgerber, R. (2019). Neurons and neuroglia. In Snell´s Clinical Neuroanatomy (8th ed., pp. 48–51). Wolters Kluwer.
Taupin, P. (2009). Adult Neurogenesis, Neural Stem Cells and Alzheimer’s Disease: Developments, Limitations, Problems and Promises. In Current Alzheimer Research (Vol. 6).
Tzavellas, N. P., Tsamis, K. I., Katsenos, A. P., Davri, A. S., Simos, Y. V., Nikas, I. P., Bellos, S., Lekkas, P., Kanellos, F. S., Konitsiotis, S., Labrakakis, C., Vezyraki, P., & Peschos, D. (2024). Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression? In Cells (Vol. 13, Issue 5). https://doi.org/10.3390/cells13050434
Villarreal, A. E., O’Bryant, S. E., Edwards, M., Grajales, S., & Britton, G. B. (2016). Serum-based protein profiles of Alzheimer’s disease and mild cognitive impairment in elderly Hispanics. Neurodegenerative Disease Management, 6(3), 203–213. https://doi.org/10.2217/nmt-2015-0009
World Health Organization. (n.d.). Global action plan on the public health response to dementia. http://apps.who.int/bookorders.
Xia, Z., Peng, W., Cheng, S., Zhong, B., Sheng, C., Zhang, C., Gong, W., Cheng, S., Li, J., & Wang, Z. (2017). Naoling decoction restores cognitive function by inhibiting the neuroinflammatory network in a rat model of Alzheimer’s disease. In Oncotarget (Vol. 8, Issue 26). www.impactjournals.com/oncotarget/
Zhou, F., Sun, Y., Xie, X., & Zhao, Y. (2023). Blood and CSF chemokines in Alzheimer’s disease and mild cognitive impairment: a systematic review and meta-analysis. In Alzheimer’s Research and Therapy (Vol. 15, Issue 1). BioMed Central Ltd. https://doi.org/10.1186/s13195-023-01254-1

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[1] Akimoto, N., Ifuku, M., Mori, Y., & Noda, M. (2013). Effects of chemokine (C-C motif) ligand 1 on microglial function. Biochemical and Biophysical Research Communications, 436(3), 455–461. https://doi.org/10.1016/j.bbrc.2013.05.126

[2] Al-Ghraiybah, N. F., Wang, J., Alkhalifa, A. E., Roberts, A. B., Raj, R., Yang, E., & Kaddoumi, A. (2022). Glial Cell-Mediated Neuroinflammation in Alzheimer’s Disease. In International Journal of Molecular Sciences (Vol. 23, Issue 18). MDPI. https://doi.org/10.3390/ijms231810572

[3] Bale, T. L., Abel, T., Akil, H., Carlezon, W. A., Moghaddam, B., Nestler, E. J., Ressler, K. J., & Thompson, S. M. (2019). The critical importance of basic animal research for neuropsychiatric disorders. Neuropsychopharmacology, 44(8), 1349–1353. https://doi.org/10.1038/s41386-019-0405-9

[4] Borbély, E., Horváth, J., Furdan, S., Bozsó, Z., Penke, B., & Fülöp, L. (2014). Simultaneous changes of spatial memory and spine density after intrahippocampal administration of fibrillar a ? 1-42 to the rat brain. BioMed Research International, 2014. https://doi.org/10.1155/2014/345305

[5] Breijyeh, Z., & Karaman, R. (2020). Comprehensive Review on Alzheimer ’ s Disease?: Molecules, 25(24).

[6] Brosseron, F., Kleemann, K., Kolbe, C. C., Santarelli, F., Castro-Gomez, S., Tacik, P., Latz, E., Jessen, F., & Heneka, M. T. (2021). Interrelations of Alzheimer´s disease candidate biomarkers neurogranin, fatty acid-binding protein 3 and ferritin to neurodegeneration and neuroinflammation. Journal of Neurochemistry, 157(6), 2210–2224. https://doi.org/10.1111/jnc.15175

[7] Chidambaram, S. B., Rathipriya, A. G., Bolla, S. R., Bhat, A., Ray, B., Mahalakshmi, A. M., Manivasagam, T., Thenmozhi, A. J., Essa, M. M., Guillemin, G. J., Chandra, R., & Sakharkar, M. K. (2019). Dendritic spines: Revisiting the physiological role. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 92, 161–193. https://doi.org/10.1016/J.PNPBP.2019.01.005

[8] Dorostkar, M. M., Zou, C., Blazquez-Llorca, L., & Herms, J. (2015). Analyzing dendritic spine pathology in Alzheimer’s disease: problems and opportunities. In Acta Neuropathologica (Vol. 130, Issue 1). Springer Verlag. https://doi.org/10.1007/s00401-015-1449-5

[9] Facchinetti, R., Bronzuoli, M., & Scudei, C. (2018). An animal model disease based on the intrahippocampal injection of amyloide B-peptido (1- 42). In Neurotrophic Factors: Methods and Protocols, Methods in Molecular Biology.

[10] Götz, J., Bodea, L. G., & Goedert, M. (2018). Rodent models for Alzheimer disease. In Nature Reviews Neuroscience (Vol. 19, Issue 10, pp. 583–598). Nature Publishing Group. https://doi.org/10.1038/s41583-018-0054-8

[11] Gupta, V. B., Hone, E., Pedrini, S., Doecke, J., O’Bryant, S., James, I., Bush, A. I., Rowe, C. C., Villemagne, V. L., Ames, D., Masters, C. L., & Martins, R. N. (2017). Altered levels of blood proteins in Alzheimer’s disease longitudinal study: Results from Australian Imaging Biomarkers Lifestyle Study of Ageing cohort. Alzheimer’s and Dementia: Diagnosis, Assessment and Disease Monitoring, 8, 60–72. https://doi.org/10.1016/j.dadm.2017.04.003

[12] Ito, M., Komai, K., Mise-Omata, S., Iizuka-Koga, M., Noguchi, Y., Kondo, T., Sakai, R., Matsuo, K., Nakayama, T., Yoshie, O., Nakatsukasa, H., Chikuma, S., Shichita, T., & Yoshimura, A. (2019). Brain regulatory T cells suppress astrogliosis and potentiate neurological recovery. Nature, 565(7738), 246–250. https://doi.org/10.1038/s41586-018-0824-5

[13] Kasza, Á., Penke, B., Frank, Z., Bozsó, Z., Szegedi, V., Hunya, Á., Németh, K., Kozma, G., & Fülöp, L. (2017). Studies for improving a rat model of Alzheimer’s disease: ICV administration of well-characterized ?-amyloid 1-42 oligomers induce dysfunction in spatial memory. Molecules, 22(11). https://doi.org/10.3390/molecules22112007

[14] Leng, F., & Edison, P. (2021). Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here? In Nature Reviews Neurology (Vol. 17, Issue 3, pp. 157–172). Nature Research. https://doi.org/10.1038/s41582-020-00435-y

[15] Liu, C., Cui, G., Zhu, M., Kang, X., & Guo, H. (2014). Neuroinflammation in Alzheimer’s disease: Chemokines produced by astrocytes and chemokine receptors. International Journal of Clinical and Experimental Pathology, 7(12), 8342–8355. https://doi.org/D - nlm: pmc4314046 oto – notnlmMcgeer, P. L., & Mcgeer, E. G. (n.d.). Inflammation of the brain in Alzheimer’s disease: implications for therapy. http://www.jleukbio.org

[16] McLarnon, J. G. (2014). Correlated inflammatory responses and neurodegeneration in peptide-injected animal models of Alzheimer’s disease. BioMed Research International, 2014. https://doi.org/10.1155/2014/923670

[17] Monson, N. L., Ireland, S. J., Ligocki, A. J., Chen, D., Rounds, W. H., Li, M., Huebinger, R. M., Munro Cullum, C., Greenberg, B. M., Stowe, A. M., & Zhang, R. (2014). Elevated CNS inflammation in patients with preclinical Alzheimer’s disease. Journal of Cerebral Blood Flow and Metabolism, 34(1), 30–33. https://doi.org/10.1038/jcbfm.2013.183

[18] O’Bryant, S. E., Xiao, G., Barber, R., Huebinger, R., Wilhelmsen, K., Edwards, M., Graff-Radford, N., Doody, R., & Diaz-Arrastia, R. (2011). A blood-based screening tool for Alzheimer’s disease that spans serum and plasma: Findings from TARC and ADNI. PLoS ONE, 6(12). https://doi.org/10.1371/journal.pone.0028092

[19] Paxinos, G., & Watson, C. (2006). The Rat Brain in Stereotaxic Coordinates (6th Edititon). Academic Express.

[20] Petralia, M. C., Battaglia, G., Bruno, V., Pennisi, M., Mangano, K., Lombardo, S. D., Fagone, P., Cavalli, E., Saraceno, A., Nicoletti, F., & Basile, M. S. (2020). The role of macrophage migration inhibitory factor in Alzheimer?s disease: Conventionally pathogenetic or unconventionally protective? In Molecules (Vol. 25, Issue 2). MDPI AG. https://doi.org/10.3390/molecules25020291

[21] Pilati, N., Barker, M., Panteleimonitis, S., Donga, R., & Hamann, M. (2008). A rapid method combining Golgi and Nissl staining to study neuronal morphology and cytoarchitecture. Journal of Histochemistry and Cytochemistry, 56(6), 539–550. https://doi.org/10.1369/jhc.2008.950246

[22] Ramírez, E., Mendieta, L., Flores, G., & Limón, I. D. (2018). Neurogenesis and morphological-neural alterations closely related to amyloid ?-peptide (25–35)-induced memory impairment in male rats. Neuropeptides, 67, 9–19. https://doi.org/10.1016/j.npep.2017.11.001

[23] Splittgerber, R. (2019). Neurons and neuroglia. In Snell´s Clinical Neuroanatomy (8th ed., pp. 48–51). Wolters Kluwer.

[24] Taupin, P. (2009). Adult Neurogenesis, Neural Stem Cells and Alzheimer’s Disease: Developments, Limitations, Problems and Promises. In Current Alzheimer Research (Vol. 6).

[25] Tzavellas, N. P., Tsamis, K. I., Katsenos, A. P., Davri, A. S., Simos, Y. V., Nikas, I. P., Bellos, S., Lekkas, P., Kanellos, F. S., Konitsiotis, S., Labrakakis, C., Vezyraki, P., & Peschos, D. (2024). Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression? In Cells (Vol. 13, Issue 5). https://doi.org/10.3390/cells13050434

[26] Villarreal, A. E., O’Bryant, S. E., Edwards, M., Grajales, S., & Britton, G. B. (2016). Serum-based protein profiles of Alzheimer’s disease and mild cognitive impairment in elderly Hispanics. Neurodegenerative Disease Management, 6(3), 203–213. https://doi.org/10.2217/nmt-2015-0009

[27] World Health Organization. (n.d.). Global action plan on the public health response to dementia. http://apps.who.int/bookorders.

[28] Xia, Z., Peng, W., Cheng, S., Zhong, B., Sheng, C., Zhang, C., Gong, W., Cheng, S., Li, J., & Wang, Z. (2017). Naoling decoction restores cognitive function by inhibiting the neuroinflammatory network in a rat model of Alzheimer’s disease. In Oncotarget (Vol. 8, Issue 26). www.impactjournals.com/oncotarget/

[29] Zhou, F., Sun, Y., Xie, X., & Zhao, Y. (2023). Blood and CSF chemokines in Alzheimer’s disease and mild cognitive impairment: a systematic review and meta-analysis. In Alzheimer’s Research and Therapy (Vol. 15, Issue 1). BioMed Central Ltd. https://doi.org/10.1186/s13195-023-01254-1

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