BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice

Autores
López Couselo, Federico; Saba, Julieta; Friser Frederiksen, Maria; Palmieri, Mateo; Romero, Ana Clara; Bigi, Maria de Las Mercedes; Carniglia, Lila; Durand, Daniela Elizabeth; Lasaga, Mercedes Isabel; Caruso, Carla Mariana
Año de publicación
2025
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Huntington´s disease (HD) is a neurodegenerative disorder characterized by mutant huntingtin (mHTT) aggregation, striatal neuron degeneration, astrocyte dysfunction, and accompanied by oxidative stress and mitochondrial impairment. We previously demonstrated that the neurotrophin brain-derived neurotrophic factor (BDNF) exerts antioxidant and anti-inflammatoryeffects in cultured rat astrocytes. Given the critical role of astrocytes in maintaining redox homeostasis, we investigated oxidative stress in cortical and striatal astrocytes from the zQ175 knock-in mouse model of HD and examined the role of BDNF in modulatingoxidative stress in HD astrocytes. We found early and region-specific oxidative stress in mitochondrial extracts from the striatum of zQ175 HD mice and cultured striatal HD astrocytes, evidenced by elevated levels of reactive oxygen species, while cortical mitochondria remained unaffected. This was associated with reduced glutathione (GSH) levels and altered expression of key mitochondrial antioxidant proteins, including superoxide dismutase 2 (SOD2) and uncoupling protein 4 (UCP4), specifically in the striatum. Importantly, bioinformatic analyses of HD patient samples corroborated these findings. Treatment of primary HDstriatal astrocytes with BDNF (50 ng/mL) prevented oxidative stress, while cortical astrocytes showed no significant response, highlighting a region-specific protective effect. Astrocyte conditioned media (ACM) from BDNF-treated wild-type or HD astrocytes promoted the survival of mHTT expressing STHdh-Q111 striatal neuronal cells. However, depletion of mitochondria from ACM abolished this protective effect, indicating that mitochondria can be transferred from astrocytes to neurons. We confirmed the presence of mitochondria in ACM and demonstrated their uptake by STHdh-Q111 cells. Mitochondria isolated from untreated HD astrocytes were internalized but failed to enhance neuronal viability. In contrast, mitochondria derived from BDNF-treatedHD astrocytes significantly restored neuronal survival. Together, these findings reveal a selective vulnerability of the HD striatum to oxidative stress and underscore the therapeutic potential of BDNF in restoring astrocyte function, enhancing mitochondrial support, and mitigating neurodegeneration in Huntington´s disease.
Fil: López Couselo, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Saba, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Friser Frederiksen, Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Palmieri, Mateo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Romero, Ana Clara. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Bigi, Maria de Las Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Carniglia, Lila. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Durand, Daniela Elizabeth. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Lasaga, Mercedes Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Caruso, Carla Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Materia
Striatal mitochondria
BDNF
Huntington´s Disease
Astrocytes
Oxidative stress
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/291155
Acceder
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spelling BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease MiceLópez Couselo, FedericoSaba, JulietaFriser Frederiksen, MariaPalmieri, MateoRomero, Ana ClaraBigi, Maria de Las MercedesCarniglia, LilaDurand, Daniela ElizabethLasaga, Mercedes IsabelCaruso, Carla MarianaStriatal mitochondriaBDNFHuntington´s DiseaseAstrocytesOxidative stresshttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Huntington´s disease (HD) is a neurodegenerative disorder characterized by mutant huntingtin (mHTT) aggregation, striatal neuron degeneration, astrocyte dysfunction, and accompanied by oxidative stress and mitochondrial impairment. We previously demonstrated that the neurotrophin brain-derived neurotrophic factor (BDNF) exerts antioxidant and anti-inflammatoryeffects in cultured rat astrocytes. Given the critical role of astrocytes in maintaining redox homeostasis, we investigated oxidative stress in cortical and striatal astrocytes from the zQ175 knock-in mouse model of HD and examined the role of BDNF in modulatingoxidative stress in HD astrocytes. We found early and region-specific oxidative stress in mitochondrial extracts from the striatum of zQ175 HD mice and cultured striatal HD astrocytes, evidenced by elevated levels of reactive oxygen species, while cortical mitochondria remained unaffected. This was associated with reduced glutathione (GSH) levels and altered expression of key mitochondrial antioxidant proteins, including superoxide dismutase 2 (SOD2) and uncoupling protein 4 (UCP4), specifically in the striatum. Importantly, bioinformatic analyses of HD patient samples corroborated these findings. Treatment of primary HDstriatal astrocytes with BDNF (50 ng/mL) prevented oxidative stress, while cortical astrocytes showed no significant response, highlighting a region-specific protective effect. Astrocyte conditioned media (ACM) from BDNF-treated wild-type or HD astrocytes promoted the survival of mHTT expressing STHdh-Q111 striatal neuronal cells. However, depletion of mitochondria from ACM abolished this protective effect, indicating that mitochondria can be transferred from astrocytes to neurons. We confirmed the presence of mitochondria in ACM and demonstrated their uptake by STHdh-Q111 cells. Mitochondria isolated from untreated HD astrocytes were internalized but failed to enhance neuronal viability. In contrast, mitochondria derived from BDNF-treatedHD astrocytes significantly restored neuronal survival. Together, these findings reveal a selective vulnerability of the HD striatum to oxidative stress and underscore the therapeutic potential of BDNF in restoring astrocyte function, enhancing mitochondrial support, and mitigating neurodegeneration in Huntington´s disease.Fil: López Couselo, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Saba, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Friser Frederiksen, Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Palmieri, Mateo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Romero, Ana Clara. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Bigi, Maria de Las Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Carniglia, Lila. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Durand, Daniela Elizabeth. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Lasaga, Mercedes Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: Caruso, Carla Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaWiley Blackwell Publishing, Inc2025-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/291155López Couselo, Federico; Saba, Julieta; Friser Frederiksen, Maria; Palmieri, Mateo; Romero, Ana Clara; et al.; BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice; Wiley Blackwell Publishing, Inc; Journal of Neurochemistry; 169; 10; 10-2025; 1-170022-3042CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1111/jnc.70276info:eu-repo/semantics/altIdentifier/doi/10.1111/jnc.70276info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-08-25T15:47:01Zoai:ri.conicet.gov.ar:11336/291155instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982026-08-25 15:47:01.417CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice
title BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice
spellingShingle BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice
López Couselo, Federico
Striatal mitochondria
BDNF
Huntington´s Disease
Astrocytes
Oxidative stress
title_short BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice
title_full BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice
title_fullStr BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice
title_full_unstemmed BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice
title_sort BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice
dc.creator.none.fl_str_mv López Couselo, Federico
Saba, Julieta
Friser Frederiksen, Maria
Palmieri, Mateo
Romero, Ana Clara
Bigi, Maria de Las Mercedes
Carniglia, Lila
Durand, Daniela Elizabeth
Lasaga, Mercedes Isabel
Caruso, Carla Mariana
author López Couselo, Federico
author_facet López Couselo, Federico
Saba, Julieta
Friser Frederiksen, Maria
Palmieri, Mateo
Romero, Ana Clara
Bigi, Maria de Las Mercedes
Carniglia, Lila
Durand, Daniela Elizabeth
Lasaga, Mercedes Isabel
Caruso, Carla Mariana
author_role author
author2 Saba, Julieta
Friser Frederiksen, Maria
Palmieri, Mateo
Romero, Ana Clara
Bigi, Maria de Las Mercedes
Carniglia, Lila
Durand, Daniela Elizabeth
Lasaga, Mercedes Isabel
Caruso, Carla Mariana
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Striatal mitochondria
BDNF
Huntington´s Disease
Astrocytes
Oxidative stress
topic Striatal mitochondria
BDNF
Huntington´s Disease
Astrocytes
Oxidative stress
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Huntington´s disease (HD) is a neurodegenerative disorder characterized by mutant huntingtin (mHTT) aggregation, striatal neuron degeneration, astrocyte dysfunction, and accompanied by oxidative stress and mitochondrial impairment. We previously demonstrated that the neurotrophin brain-derived neurotrophic factor (BDNF) exerts antioxidant and anti-inflammatoryeffects in cultured rat astrocytes. Given the critical role of astrocytes in maintaining redox homeostasis, we investigated oxidative stress in cortical and striatal astrocytes from the zQ175 knock-in mouse model of HD and examined the role of BDNF in modulatingoxidative stress in HD astrocytes. We found early and region-specific oxidative stress in mitochondrial extracts from the striatum of zQ175 HD mice and cultured striatal HD astrocytes, evidenced by elevated levels of reactive oxygen species, while cortical mitochondria remained unaffected. This was associated with reduced glutathione (GSH) levels and altered expression of key mitochondrial antioxidant proteins, including superoxide dismutase 2 (SOD2) and uncoupling protein 4 (UCP4), specifically in the striatum. Importantly, bioinformatic analyses of HD patient samples corroborated these findings. Treatment of primary HDstriatal astrocytes with BDNF (50 ng/mL) prevented oxidative stress, while cortical astrocytes showed no significant response, highlighting a region-specific protective effect. Astrocyte conditioned media (ACM) from BDNF-treated wild-type or HD astrocytes promoted the survival of mHTT expressing STHdh-Q111 striatal neuronal cells. However, depletion of mitochondria from ACM abolished this protective effect, indicating that mitochondria can be transferred from astrocytes to neurons. We confirmed the presence of mitochondria in ACM and demonstrated their uptake by STHdh-Q111 cells. Mitochondria isolated from untreated HD astrocytes were internalized but failed to enhance neuronal viability. In contrast, mitochondria derived from BDNF-treatedHD astrocytes significantly restored neuronal survival. Together, these findings reveal a selective vulnerability of the HD striatum to oxidative stress and underscore the therapeutic potential of BDNF in restoring astrocyte function, enhancing mitochondrial support, and mitigating neurodegeneration in Huntington´s disease.
Fil: López Couselo, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Saba, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Friser Frederiksen, Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Palmieri, Mateo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Romero, Ana Clara. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Bigi, Maria de Las Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Carniglia, Lila. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Durand, Daniela Elizabeth. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Lasaga, Mercedes Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: Caruso, Carla Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
description Huntington´s disease (HD) is a neurodegenerative disorder characterized by mutant huntingtin (mHTT) aggregation, striatal neuron degeneration, astrocyte dysfunction, and accompanied by oxidative stress and mitochondrial impairment. We previously demonstrated that the neurotrophin brain-derived neurotrophic factor (BDNF) exerts antioxidant and anti-inflammatoryeffects in cultured rat astrocytes. Given the critical role of astrocytes in maintaining redox homeostasis, we investigated oxidative stress in cortical and striatal astrocytes from the zQ175 knock-in mouse model of HD and examined the role of BDNF in modulatingoxidative stress in HD astrocytes. We found early and region-specific oxidative stress in mitochondrial extracts from the striatum of zQ175 HD mice and cultured striatal HD astrocytes, evidenced by elevated levels of reactive oxygen species, while cortical mitochondria remained unaffected. This was associated with reduced glutathione (GSH) levels and altered expression of key mitochondrial antioxidant proteins, including superoxide dismutase 2 (SOD2) and uncoupling protein 4 (UCP4), specifically in the striatum. Importantly, bioinformatic analyses of HD patient samples corroborated these findings. Treatment of primary HDstriatal astrocytes with BDNF (50 ng/mL) prevented oxidative stress, while cortical astrocytes showed no significant response, highlighting a region-specific protective effect. Astrocyte conditioned media (ACM) from BDNF-treated wild-type or HD astrocytes promoted the survival of mHTT expressing STHdh-Q111 striatal neuronal cells. However, depletion of mitochondria from ACM abolished this protective effect, indicating that mitochondria can be transferred from astrocytes to neurons. We confirmed the presence of mitochondria in ACM and demonstrated their uptake by STHdh-Q111 cells. Mitochondria isolated from untreated HD astrocytes were internalized but failed to enhance neuronal viability. In contrast, mitochondria derived from BDNF-treatedHD astrocytes significantly restored neuronal survival. Together, these findings reveal a selective vulnerability of the HD striatum to oxidative stress and underscore the therapeutic potential of BDNF in restoring astrocyte function, enhancing mitochondrial support, and mitigating neurodegeneration in Huntington´s disease.
publishDate 2025
dc.date.none.fl_str_mv 2025-10
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info:ar-repo/semantics/articulo
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status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/291155
López Couselo, Federico; Saba, Julieta; Friser Frederiksen, Maria; Palmieri, Mateo; Romero, Ana Clara; et al.; BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice; Wiley Blackwell Publishing, Inc; Journal of Neurochemistry; 169; 10; 10-2025; 1-17
0022-3042
CONICET Digital
CONICET
url http://hdl.handle.net/11336/291155
identifier_str_mv López Couselo, Federico; Saba, Julieta; Friser Frederiksen, Maria; Palmieri, Mateo; Romero, Ana Clara; et al.; BDNF Mitigates Early Oxidative Stress and Promotes Release of Neuroprotective Mitochondria From Striatal Astrocytes of zQ175 Huntington's Disease Mice; Wiley Blackwell Publishing, Inc; Journal of Neurochemistry; 169; 10; 10-2025; 1-17
0022-3042
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
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repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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