Long-term social isolation stress exacerbates sex-specific neurodegeneration markers in a natural model of Alzheimer's disease

Simple item page
dc.contributor.authorOliva, Carolina A.
dc.contributor.authorLira, Matias
dc.contributor.authorJara, Claudia
dc.contributor.authorCatenaccio, Alejandra
dc.contributor.authorMariqueo, Trinidad A.
dc.contributor.authorLindsay, Carolina B.
dc.contributor.authorBozinovic, Francisco
dc.contributor.authorCavieres, Grisel
dc.contributor.authorInestrosa, Nibaldo C.
dc.contributor.authorTapia-Rojas, Cheril
dc.contributor.authorRivera, Daniela S.
dc.date.accessioned2025-01-20T17:32:43Z
dc.date.available2025-01-20T17:32:43Z
dc.date.issued2023
dc.description.abstractSocial interactions have a significant impact on health in humans and animal models. Social isolation initiates a cascade of stress-related physiological disorders and stands as a significant risk factor for a wide spectrum of morbidity and mortality. Indeed, social isolation stress (SIS) is indicative of cognitive decline and risk to neurodegenerative conditions, including Alzheimer's disease (AD). This study aimed to evaluate the impact of chronic, long-term SIS on the propensity to develop hallmarks of AD in young degus (Octodon degus), a long-lived animal model that mimics sporadic AD naturally. We examined inflammatory factors, bioenergetic status, reactive oxygen species (ROS), oxidative stress, antioxidants, abnormal proteins, tau protein, and amyloid-beta (A beta) levels in the hippocampus of female and male degus that were socially isolated from post-natal and post-weaning until adulthood. Additionally, we explored the effect of re-socialization following chronic isolation on these protein profiles. Our results showed that SIS promotes a pro-inflammatory scenario more severe in males, a response that was partially mitigated by a period of re-socialization. In addition, ATP levels, ROS, and markers of oxidative stress are severely affected in female degus, where a period of re-socialization fails to restore them as it does in males. In females, these effects might be linked to antioxidant enzymes like catalase, which experience a decline across all SIS treatments without recovery during re-socialization. Although in males, a previous enzyme in antioxidant pathway diminishes in all treatments, catalase rebounds during re-socialization. Notably, males have less mature neurons after chronic isolation, whereas phosphorylated tau and all detectable forms of A beta increased in both sexes, persisting even post re-socialization. Collectively, these findings suggest that long-term SIS may render males more susceptible to inflammatory states, while females are predisposed to oxidative states. In both scenarios, the accumulation of tau and A beta proteins increase the individual susceptibility to early-onset neurodegenerative conditions such as AD.
dc.fuente.origenWOS
dc.identifier.doi10.3389/fnagi.2023.1250342
dc.identifier.issn1663-4365
dc.identifier.urihttps://doi.org/10.3389/fnagi.2023.1250342
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/91631
dc.identifier.wosidWOS:001076374000001
dc.language.isoen
dc.revistaFrontiers in aging neuroscience
dc.rightsacceso restringido
dc.subjectOctodon degus
dc.subjectsocial isolation stress
dc.subjectAmyloid-beta protein
dc.subjecttau protein
dc.subjectinflammation
dc.subjectoxidative stress
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleLong-term social isolation stress exacerbates sex-specific neurodegeneration markers in a natural model of Alzheimer's disease
dc.typeartículo
dc.volumen15
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
Files
Collections
Artículos de revistas