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

Enviado enero 3, 2025

Publicado 2025-01-06

Artículos

Vol. 35 Núm. 1 (2025): Scientia

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

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DOI: 10.48204/j.scientia.v35n1.a6658

Publicado: 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). Efecto de la sobreexpresión de CCL1 (I-309) en las espinas dendríticas de neuronas del hipocampo . Scientia, 35(1), 71–85. https://doi.org/10.48204/j.scientia.v35n1.a6658

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Esta obra está bajo una licencia internacional Creative Commons Atribución-NoComercial-CompartirIgual 4.0.

Resumen

La acumulación irregular de la proteína ?-amiloide (A?), la proteína tau hiperfosforilada y la neuroinflamación son factores que afectan la función neuronal en la Enfermedad de Alzheimer (EA). La neuroinflamación asociada a la EA podría causar el daño sináptico por sí mismo o exacerbar el daño causado por la acumulación de A?. Se ha detectado un aumento de la citocina CCL1 (I-309) en el suero de sangre periférica de personas con Deterioro Cognitivo Leve (DCL) y con la EA, por lo que se propone que puede ser útil como un biomarcador diagnóstico del DCL y la EA. El objetivo general de este estudio fue evaluar el efecto de la sobreexpresión de la proteína CCL1 (I-309) en las espinas dendríticas de las neuronas localizadas en el hipocampo. Se utilizó ratas Sprague Dawley (N=6) como modelo animal, a quienes se les realizó cirugías estereotáxicas para inocular la sobreexpresión de CCL1. Se realizó la tinción de Golgi a los cerebros de las ratas, se utilizó un criostato para realizar los cortes histológicos y se evaluó la densidad de las espinas dendríticas mediante microscopia óptica. El ANOVA de una vía no mostró diferencias significativas (p>0.05) entre el grupo con sobreexpresión de CCL1 al compararlo con el grupo control y con el grupo con sobreexpresión A?_1-42+CCL1. Se concluyó que la sobreexpresión de CCL1 no modifica significativamente la densidad de espinas dendríticas en el hipocampo.

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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
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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
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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.
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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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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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