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Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE176506 | GEO | 2025/06/04

REPOSITORIES: GEO

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Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease II

Project description:Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease. 72 post-mortem perfused brain tissue samples from male and female mice (5xFAD and C57BL/6) with and without sepsis, 25 days post CLP infection.

2025-06-04 | GSE176505 | GEO

Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease I

Project description:Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease. 40 post-mortem perfused brain tissue samples from both male and female mice (5xFAD and C57BL/6) with and without sepsis, 5 days post CLP infection.

2025-06-04 | GSE176504 | GEO

Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease

Project description:Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease

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Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease I

Project description:Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease I

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Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease II

Project description:Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease II

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Salidroside reduces neuropathology in Alzheimer’s disease models by targeting NRF2/SIRT3 pathway

Project description:Background Neurite dystrophy is a pathologic hallmark of Alzheimer’s disease (AD). However, drug discovery targeting neurite protection in AD remains largely unexplored. Methods Aβ-induced neurite and mitochondrial damage assays were used to evaluate Aβ toxicity and the neuroprotective efficacy of a natural compound salidroside (SAL). The 5×FAD transgenic mouse model of AD was used to study the neuroprotective function of SAL. To verify the direct target of SAL, we used surface plasmon resonance and cellular thermal shift assays to analyze the drug-protein interaction. Results SAL ameliorates Aβ-mediated neurite damage in cell culture. We further reveal that SAL represses mitochondrial damage in neurites by promoting mitophagy and maintaining mitochondrial homeostasis, dependent on an NAD-dependent deacetylase SIRT3. In AD mice, SAL protects neurite morphology, mitigates Aβ pathology, and improves cognitive function, which are all SIRT3-dependent. Notably, SAL directly binds to transcription factor NRF2, inhibits its degradation by blocking its interaction with KEAP1 ubiquitin ligase, and then advances NRF2-mediated SIRT3 transcription. Conclusions Overall, we demonstrate that SAL, a potential anti-aging drug candidate, attenuates AD pathology by targeting NRF2/SIRT3 pathway for mitochondrial and neurite protection. Drug discovery strategies focusing on SAL may thus provide promising therapeutics for AD. Supplementary Information The online version contains supplementary material available at 10.1186/s13578-022-00918-z.

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Project description:This SuperSeries is composed of the SubSeries listed below.

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Methylomic signatures of tau and beta amyloid in transgenic mouse models of Alzheimer’s disease neuropathology [RRBS]

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Synergistic effects of long-term antioxidant diet and behavioral enrichment on beta-amyloid load and non-amyloidogenic processing in aged canines.

Project description:A long-term intervention (2.69 years) with an antioxidant diet, behavioral enrichment, or the combined treatment preserved and improved cognitive function in aged canines. Although each intervention alone provided cognitive benefits, the combination treatment was additive. We evaluate the hypothesis that antioxidants, enrichment, or the combination intervention reduces age-related beta-amyloid (Abeta) neuropathology, as one mechanism mediating observed functional improvements. Measures assessed were Abeta neuropathology in plaques, biochemically extractable Abeta(40) and Abeta(42) species, soluble oligomeric forms of Abeta, and various proteins in the beta-amyloid precursor protein (APP) processing pathway. The strongest and most consistent effects on Abeta pathology were observed in animals receiving the combined antioxidant and enrichment treatment. Specifically, Abeta plaque load was significantly decreased in several brain regions, soluble Abeta(42) was decreased selectively in the frontal cortex, and a trend for lower Abeta oligomer levels was found in the parietal cortex. Reductions in Abeta may be related to shifted APP processing toward the non-amyloidogenic pathway, because alpha-secretase enzymatic activity was increased in the absence of changes in beta-secretase activity. Although enrichment alone had no significant effects on Abeta, reduced Abeta load and plaque maturation occurred in animals receiving antioxidants as a component of treatment. Abeta measures did not correlate with cognitive performance on any of the six tasks assessed, suggesting that modulation of Abeta alone may be a relatively minor mechanism mediating cognitive benefits of the interventions. Overall, the data indicate that multidomain treatments may be a valuable intervention strategy to reduce neuropathology and improve cognitive function in humans.

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Transcriptional Signatures of Tau and Amyloid Neuropathology.

Project description:Alzheimer's disease (AD) is associated with the intracellular aggregation of hyperphosphorylated tau and the accumulation of β-amyloid in the neocortex. We use transgenic mice harboring human tau (rTg4510) and amyloid precursor protein (J20) mutations to investigate transcriptional changes associated with the progression of tau and amyloid pathology. rTg4510 mice are characterized by widespread transcriptional differences in the entorhinal cortex with changes paralleling neuropathological burden across multiple brain regions. Differentially expressed transcripts overlap with genes identified in genetic studies of familial and sporadic AD. Systems-level analyses identify discrete co-expression networks associated with the progressive accumulation of tau that are enriched for genes and pathways previously implicated in AD pathology and overlap with co-expression networks identified in human AD cortex. Our data provide further evidence for an immune-response component in the accumulation of tau and reveal molecular pathways associated with the progression of AD neuropathology.

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