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Temporal impact of sepsis on Alzheimer's disease pathology and neuroinflammation

ABSTRACT: Epidemiological evidence has reported an associative link between sepsis survivorship and increased risk of dementia, particularly Alzheimer's disease (AD). Paradoxically, population studies show females are less susceptible to sepsis but more vulnerable to post-sepsis dementia, including Alzheimer's disease (AD). Here, we examined the temporal impacts of sepsis on AD pathology using an AD-model (TgCRND8) and wild-type mice, assessing outcomes at 7 days and 3 months post-sepsis. Following 7-days recovery, all male and female post-septic mice showed robust systemic immune activation. At this time, the female AD-model mice accumulated higher hippocampal amyloid-beta (Aβ) and upregulated AD-type transcriptomic signature. On the other hand, male AD-model mice showed no Aβ changes. Notably, wild-type post-septic males, but not females, displayed robust astrocytosis, with little change in microglial proliferation. By 3 months post-sepsis, microgliosis was specifically elevated in wild-type females, indicating a prolonged central immune response. At this time, both male and female AD-model mice showed exacerbated Aβ and anxiety. Gene network analysis revealed a stronger female immune response, while the male response was linked to estrogen receptor (ESR) signaling, with increased ERα protein observed in the brains of post-septic AD males. Together, our data highlights a sex-dimorphic temporal response in post-sepsis neuroinflammation, with ESR signaling playing a key role in males, while Aβ burden is affected similarly in both males and females.

ORGANISM(S): Mus musculus

PROVIDER: GSE292277 | GEO | 2025/05/31

REPOSITORIES: GEO

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Project description:Globally invasive Aedes aegypti mosquitoes disseminate numerous arboviruses that impact human health. One promising method to control Ae. aegypti populations is transinfection with the intracellular bacterium Wolbachia pipientis, a symbiont that naturally infects ~40-52% of insects but is normally absent from Ae. aegypti. Transinfection of Ae. aegypti with the wMel Wolbachia strain induces cytoplasmic incompatibility (CI), allowing infected individuals to rapidly invade native populations. Further, wMel Wolbachia-infected females display refractoriness to medically relevant arboviruses. Thus, wMel Wolbachia-infected Ae. aegypti are being released in several areas to replace native populations, thereby suppressing disease transmission by this species. Wolbachia is reported to have minimal effects on Ae. aegypti fertility, but its influence on other reproductive processes is unknown. Female insects undergo several post-mating physiological and behavioral changes required for optimal fertility. Post-mating responses (PMRs) in female insects are typically elicited by receipt of male seminal fluid proteins (SFPs) transferred with sperm during mating, but can be modified by other factors, such as adult age, nutritional status, and microbiome composition. To assess how Wolbachia infection influences Ae. aegypti female PMRs, we collected wMel Wolbachia-infected Ae. aegypti from the field in Medellín, Colombia and introduced the bacterium into our laboratory strain. We found that Wolbachia influences female fecundity, fertility, and re-mating incidence. Further, we observed that Wolbachia significantly extends longevity of virgin females. Changes in female PMRs are not due to defects in sperm transfer by infected males, or sperm storage by infected females. Using proteomic methods to examine the seminal proteome of infected males, we found that Wolbachia infection has a moderate effect on SFP composition. However, we identified 125 Wolbachia proteins that are paternally transferred to females by infected males. Surprisingly, the CI factor proteins (Cifs), were not detected in the ejaculates of Wolbachia-infected males. Our findings indicate that Wolbachia infection of Ae. aegypti alters female post-mating responses, potentially influencing control programs that utilize Wolbachia-infected individuals.

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Temporal impact of sepsis on Alzheimer's disease pathology and neuroinflammation

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