C1q induces a program of gene expression in amyloid beta injured neurons necessary for neuron survival

Benoit, Marie; Hernandez, Michael; Dinh, Minhan L.; Benavente, Francisca; Vasquez, Osvaldo; Tenner, Andrea J.

doi:10.1016/j.imbio.2012.08.041

Cited by 2 publications

(2 citation statements)

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“…One possible reason for this outcome is the different inflammatory response that characterize each model. C1q, for example, has previously been shown to label cell debris and promote phagocytosis in models of acute brain damage (49,50). Clearance of the damaged cells and debris can aid in the resolution of inflammation and enhance endogenous repair systems, ultimately resulting in a more favorable clinical outcome.…”

Section: Bimentioning

confidence: 99%

Divergent complement system activation in two clinically distinct murine models of multiple sclerosis

Linzey

DiSano²,

Welsh³

et al. 2022

Front. Immunol.

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Multiple sclerosis (MS) is a neurological disease featuring neuroinflammation and neurodegeneration in young adults. So far, most research has focused on the peripheral immune system, which appears to be the driver of acute relapses. Concurrently, the mechanisms underlying neurodegeneration in the progressive forms of the disease remain unclear. The complement system, a molecular component of the innate immunity, has been recently implicated in several neurological disorders, including MS. However, it is still unknown if the complement proteins detected in the central nervous system (CNS) are actively involved in perpetuating chronic inflammation and neurodegeneration. To address this knowledge gap, we compared two clinically distinct mouse models of MS: 1) proteolipid protein (PLP)-induced experimental autoimmune encephalomyelitis (rEAE) resembling a relapsing-remitting disease course, and 2) Theiler’s murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) resembling a progressive disease. Real-time PCR was performed in the spinal cord of rEAE mice, TMEV-IDD mice and age-matched sham controls to quantify gene expression for a broad range of complement components. In both experimental models, we found significantly increased expression of complement factors, such as C1q, C3, CfB, and C3aR. We showed that the complement system, specifically the classical complement pathway, was associated with TMEV-IDD pathogenesis, as the expression of C1q, C3 and C3aR1 were all significantly correlated to a worse disease outcome (all P≤0.0168). In line with this finding, C1q and C3 deposition was observed in the spinal cord of TMEV-IDD mice. Furthermore, C1q deposition was detected in spinal cord regions characterized by inflammation, demyelination, and axonal damage. Conversely, activation of the classical complement cascade seemed to result in protection from rEAE (C1q: P=0.0307). Interestingly, the alternative pathway related to a worse disease outcome in rEAE (CFb: P=0.0006). Overall, these results indicate potential divergent roles for the complement system in MS. The chronic-progressive disease form is more reliant on the activation of the classic complement pathway, while protecting from acute relapses. Conversely, relapsing MS appears more likely affected by the alternative pathway. Understanding the functions of the complement system in MS is critical and can lead to better, more targeted therapies in the future.

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Section: Bimentioning

confidence: 99%

Divergent complement system activation in two clinically distinct murine models of multiple sclerosis

Linzey

DiSano²,

Welsh³

et al. 2022

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…Downregulation of CD59 (75) and upregulation of the complement system have been reported in several studies involving AD mouse models and brain tissue from AD patients (76)(77)(78). However, it is still unclear if the changes in complement activity observed in AD are harmful or beneficial, as studies report both neuroprotective and neurodegenerative roles (77,(79)(80)(81)(82).…”

Section: Discussionmentioning

confidence: 99%

Music elicits different gene expression responses in the buccal cavity of age-related cognitive disorders patients and healthy controls

Gómez-Carballa,

Navarro,

El Zahraa Mallah

et al. 2024

Preprint

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Recent evidence suggests that external stimuli can shape transcriptomes (sensogenomics). Specifically, the analysis of capillary blood samples has shown that musical stimuli can modulate gene expression patterns, in healthy individuals but also in those with age-related cognitive disorders (ACD), based on. Here, we present groundbreaking evidence indicating that brief exposure to music can also impact the salivary transcriptome in both healthy donors and ACD patients. Our findings reveal that music has a more pronounced effect on patients compared to controls, inducing global gene expression changes towards upregulation in ACD patients but downregulation in controls. The most significantly dysregulated genes in ACD patients includeLGALS3(downregulated) andCXCL8(upregulated), whereas in controls,THOP1was the top significant gene (downregulated). These genes play important roles in normal brain functions and are also altered in neurodegenerative conditions. Weighted Gene Co-expression Network Analysis reveals relevant and significant modules, both positive and negative correlated with music, implicated in neurodegenerative (e.g. autophagy) and immunological processes (e.g. IL-1, MHC). This sheds light on the complex interplay between music and molecular responses in the human body. This study underscores the potential of musical stimuli to influence gene expression patterns outside of systemic circulation, paving the way for further exploration of music’s therapeutic effects.Sensogenomics Working GroupAntonio Salas Ellacuriaga – PI; Federico Martinón-Torres – PI; Laura Navarro Ramón – CoordinatorGenPoB/GenVip - Instituto de Investigación Sanitaria (IDIS) (alphabetic order)Alba Camino Mera, Albert Padín Villar, Alberto Gómez Carballa, Alejandro Pérez López, Alicia Carballal Fernández, Ana Cotovad Bellas, Ana Isabel Dacosta Urbieta, Narmeen Mallah, Ana María Pastoriza Mourelle, Ana María Senín Ferreiro, Andrés Muy Pérez, Antía Rivas Oural, Antonio Justicia Grande, Antonio Piñeiro García, Anxela Cristina Delgado García, Belén Mosquera Pérez, Blanca Díaz Esteban, Carlos Durán Suárez, Carmen Curros Novo, Carmen Gómez Vieites, Carmen Rodríguez-Tenreiro Sánchez, Celia Varela Pájaro, Claudia Navarro Gonzalo, Cristina Serén Trasorras, Cristina Talavero González, Einés Monteagudo Vilavedra, Estefanía Rey Campos, Esther Montero Campos, Fernando Álvez González, Fernando Caamaño Viñas, Francisco García Iglesias, Gloria Viz Rodríguez, Hugo Alberto Tovar Velasco, Irene Álvarez Rodríguez, Irene García Zuazola, Irene Rivero Calle, Iria Afonso Carrasco, Isabel Ferreirós Vidal, Isabel Lista García, Isabel Rego Lijo, Iván Prieto Gómez, Iván Quintana Cepedal, Jacobo Pardo Seco, Jesús Eirís Puñal, José Gómez Rial, José Manuel Fernández García, José María Martinón Martínez, Julia Cela Mosquera, Julia García Currás, Julián Montoto Louzao, Lara Martínez Martínez, Laura Navarro Marrón, Lidia Piñeiro Rodríguez, Lorenzo Redondo Collazo, Lúa Castelo Martínez, Lucía Company Arciniegas, Luis Crego Rodríguez, Luisa García Vicente, Manuel Vázquez Donsión, María Dolores Martínez García, María Elena Gamborino Caramés, María Elena Sobrino Fernández, María José Currás Tuala, María Martínez Leis, María Soledad Vilas Iglesias, María Sol Rodriguez Calvo, María Teresa Autran García, Marina Casas Pérez, Marta Aldonza Torres, Marta Bouzón Alejandro, Marta Lendoiro Fuentes, Miriam Ben García, Miriam Cebey López, Montserrat López Franco, Nour El Zahraa Mallah, Narmeen Mallah, Natalia García Sánchez, Natalia Vieito Perez, Patricia Regueiro Casuso, Ricardo Suárez Camacho, Rita García Fernández, Rita Varela Estévez, Rosaura Picáns Leis, Ruth Barral Arca, Sandra Carnota Antonio, Sandra Viz Lasheras, Sara Pischedda, Sara Rey Vázquez, Sonia Marcos Alonso, Sonia Serén Fernández, Susana Rey García, Vanesa Álvarez Iglesias, Victoria Redondo Cervantes, Vanesa Álvarez Iglesias, Wiktor Dominik Nowak, Xabier Bello Paderne, Xabier Mazaira LópezNursing volunteers (alphabetic order)Alejandra Fernández Méndez, Ana Isabel Abadín Campaña, Ana María León Caamaño, Ana María Buide Illobre, Ángeles Mera Cores, Carmen Nieves Vastro, Carolina Suarez Crego, Concepción Rey Iglesias, Cristina Candal Regueira, Dolores Barreiro Puente, Elvira Rodríguez Rodríguez, Eugenia González Budiño, Eva Rey Álvarez, Fernando Rodríguez Gerpe, Gemma Albela Silva, Isabel Castro Pérez, Isabel Domínguez Ríos, José Ángel Fernández de la Iglesia, José Cruces Vázquez, José Luis Cambeiro Quintela, José Ramón Magariños Iglesias, Julia Rey Brandariz, Julio Abel Fernández López, Luisa García Vicente, Manuel González Lito, Manuel González Lijó, Manuela Pérez Rivas, Margarita Turnes Paredes, María Aurora Méndez López, María Begoña Tomé Arufe, María Campos Torres, María del Carmen Baloira Nogueira, María del Carmen García juan, María Esther Moricosa García, María Luz Chao Jarel, María Martínez Leis, María Mercedes Jiménez Santos, María Salomé Buide Illobre, María Victoria López Pereira, Mercedes Jorge González, Mercedes Isolina Rodríguez Rodríguez, Miren Payo Puente, Natalia Carter Domínguez, Olga María Reyes González, Pilar Mera Rodríguez, Purificación Sebio Brandariz, Salomé Quintáns lago, Yolanda Rodríguez Taboada, María Pereira Grau.Other volunteers (alphabetic order)Alba Arias Gómez, Alejandro Moreno Díaz, Ana Arca Marán, Astro González Guirado, Brais García Iglesias, Carlos Sánchez Rubín, Carmen Otero de Andrés, Clara Pérez Errazquin Barrera, Claudia Rey Posse, Cristina Rojas García, Eduardo Xavier Giménez Bargiela, Elena Gloria Morales García, Fabio Izquierdo García Escribano, Gabriel Guisande García, Jaime López Martín, Lara Pais Ramiro, Lucía Rico Montero, Luís Estévez Martínez, Manuel Estévez Casal, María Aránzazu Palomino Caño, María Rubio Valdés, Marisol Nogales Benítez, Miryam Tilve Pérez, Nuria Villar Muiños, Pablo Del Cerro Rodríguez, Pablo Pozuelo Martínez Cardeñoso, Salma Ouahabi El Ouahabi, Santiago Vázquez Calvache

show abstract

C1q induces a program of gene expression in amyloid beta injured neurons necessary for neuron survival

Cited by 2 publications

References 0 publications

Divergent complement system activation in two clinically distinct murine models of multiple sclerosis

Divergent complement system activation in two clinically distinct murine models of multiple sclerosis

Music elicits different gene expression responses in the buccal cavity of age-related cognitive disorders patients and healthy controls

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