Gabriela Martínez-Ramírez
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Gabriela Martínez-Ramírez has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Daniel Ortuño-Sahagún
Laboratorio de Neuroinmunobiología Molecular, Instituto de Neurociencias Traslacionales, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara
1 shared publication - Enrique Becerril-Villanueva
Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz
1 shared publication - Enrique Estudillo
Laboratorio de Reprogramación Celular, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City 14269, Mexico
1 shared publication - Gilberto Pérez-Sánchez
Laboratorio de Psicoinmunología, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Mexico City 14370, Mexico
1 shared publication - Javier Villafranco
Laboratorio de Psicoinmunología, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Mexico City 14370, Mexico
1 shared publication - Karla Cristina Razón-Hernández
Laboratorio de Neurociencias, Subdirección de Medicina Experimental, Instituto Nacional de Pediatría, Mexico City 04530, Mexico
1 shared publication
Latest Publications
- Open Access
- 31 December 2025
- Published by MDPI AG in Brain Sciences
- Vol. 16 (1) , 63
Microglial Activation in Cerebrovascular Accidents and the Manifestation of Major Depressive Disorder: A Comprehensive Review
Emerging evidence highlights a strong association between cerebrovascular accident (CVA) and major depressive disorder (MDD), mediated by immune dysregulation. Elevated levels of proinflammatory cytokines, reduced adaptive immune responses, altered immune cell composition, and increased microglial activation characterize this bidirectional relationship. Microglial activation appears to be a central molecular mechanism linking CVA and MDD, underscoring the immune system’s crucial role in disease pathogenesis. This interplay suggests that immune-driven processes not only exacerbate neurological damage but also contribute to psychiatric manifestations. Based on current literature, the role of proinflammatory processes, particularly microglial activation, in the relationship between CVA and MDD warrants special attention. In this context, the participation of myeloid differentiation factor 88 (MyD88), a cytosolic adaptor protein, appears to play a key role in proinflammatory signaling pathways driving microglial activation. Thus, focusing on MyD88 emerges as a promising complementary strategy for future research and for advancing our understanding of the mechanisms underlying microglial homeostasis dysregulation and its link to the pathophysiology of MDD and CVA.
- 31 December 2025
- Published by MDPI AG in Brain Sciences
- Vol. 16 (1) , 63
Open AccessMicroglial Activation in Cerebrovascular Accidents and the Manifestation of Major Depressive Disorder: A Comprehensive Review
Emerging evidence highlights a strong association between cerebrovascular accident (CVA) and major depressive disorder (MDD), mediated by immune dysregulation. Elevated levels of proinflammatory cytokines, reduced adaptive immune responses, altered immune cell composition, and increased microglial activation characterize this bidirectional relationship. Microglial activation appears to be a central molecular mechanism linking CVA and MDD, underscoring the immune system’s crucial role in disease pathogenesis. This interplay suggests that immune-driven processes not only exacerbate neurological damage but also contribute to psychiatric manifestations. Based on current literature, the role of proinflammatory processes, particularly microglial activation, in the relationship between CVA and MDD warrants special attention. In this context, the participation of myeloid differentiation factor 88 (MyD88), a cytosolic adaptor protein, appears to play a key role in proinflammatory signaling pathways driving microglial activation. Thus, focusing on MyD88 emerges as a promising complementary strategy for future research and for advancing our understanding of the mechanisms underlying microglial homeostasis dysregulation and its link to the pathophysiology of MDD and CVA.