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Determining the biological associates of acute cold pressor post-encoding stress effects on human memory: The role of salivary interleukin-1?.

ABSTRACT: Stress generally hurts many aspects of memory, but an interesting finding to emerge from the stress and memory literature is that stress that occurs shortly after learning (i.e., post-encoding stress) usually benefits memory. Although this effect is well established, the biological mechanisms underpinning this effect are not-especially in humans. We addressed this gap in the present study by collecting saliva samples from 80 participants who were randomized to a post-encoding stress (i.e., cold pressor for 3?min) or control task (i.e., warm water for 3?min) and 48?h later completed a recognition memory task. Saliva was collected both prior to and 15?min after the offset of (18?min after the onset of) the stress/control manipulation. Drawing on animal and human work, we examined how five stress-responsive biomarkers-cortisol, salivary ?-amylase, progesterone, estradiol, and the proinflammatory cytokine interleukin (IL)-1?, all assessed in saliva-related to the effects of stress on memory. We found that stress enhanced recollection of negative images and that these effects were selectively related to salivary IL-1?. Moreover, we found that the beneficial effects of stress on memory were statistically mediated by salivary IL-1?. We found no robust associations-either linear or quadratic-between memory and any other biomarker, nor did we find significant interactions between biomarkers in predicting memory. These results suggest that immune system activity indexed by salivary IL-1? may play an important role in contributing to post-encoding stress effects on human memory.

SUBMITTER: Shields GS

PROVIDER: S-EPMC6754786 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Determining the biological associates of acute cold pressor post-encoding stress effects on human memory: The role of salivary interleukin-1β.

Shields Grant S GS Dunn Tiffany M TM Trainor Brian C BC Yonelinas Andrew P AP

Brain, behavior, and immunity 20190607

Stress generally hurts many aspects of memory, but an interesting finding to emerge from the stress and memory literature is that stress that occurs shortly after learning (i.e., post-encoding stress) usually benefits memory. Although this effect is well established, the biological mechanisms underpinning this effect are not-especially in humans. We addressed this gap in the present study by collecting saliva samples from 80 participants who were randomized to a post-encoding stress (i.e., cold ...[more]

PMID: 31176727

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Project description:BackgroundThe lack of effective treatments for Alzheimer's disease (AD) reflects an incomplete understanding of disease mechanisms. Alterations in proteins involved in mitochondrial dynamics, an essential process for mitochondrial integrity and function, have been reported in AD brains. Impaired mitochondrial dynamics causes mitochondrial dysfunction and has been associated with cognitive impairment in AD. Here, we investigated a possible link between pro-inflammatory interleukin-1 (IL-1), mitochondrial dysfunction, and cognitive impairment in AD models.MethodsWe exposed primary hippocampal cell cultures to amyloid-β oligomers (AβOs) and carried out AβO infusions into the lateral cerebral ventricle of cynomolgus macaques to assess the impact of AβOs on proteins that regulate mitochondrial dynamics. Where indicated, primary cultures were pre-treated with mitochondrial division inhibitor 1 (mdivi-1), or with anakinra, a recombinant interleukin-1 receptor (IL-1R) antagonist used in the treatment of rheumatoid arthritis. Cognitive impairment was investigated in C57BL/6 mice that received an intracerebroventricular (i.c.v.) infusion of AβOs in the presence or absence of mdivi-1. To assess the role of interleukin-1 beta (IL-1β) in AβO-induced alterations in mitochondrial proteins and memory impairment, interleukin receptor-1 knockout (Il1r1-/-) mice received an i.c.v. infusion of AβOs.ResultsWe report that anakinra prevented AβO-induced alteration in mitochondrial dynamics proteins in primary hippocampal cultures. Altered levels of proteins involved in mitochondrial fusion and fission were observed in the brains of cynomolgus macaques that received i.c.v. infusions of AβOs. The mitochondrial fission inhibitor, mdivi-1, alleviated synapse loss and cognitive impairment induced by AβOs in mice. In addition, AβOs failed to cause alterations in expression of mitochondrial dynamics proteins or memory impairment in Il1r1-/- mice.ConclusionThese findings indicate that IL-1β mediates the impact of AβOs on proteins involved in mitochondrial dynamics and that strategies aimed to prevent pathological alterations in those proteins may counteract synapse loss and cognitive impairment in AD.

Dataset Information

Determining the biological associates of acute cold pressor post-encoding stress effects on human memory: The role of salivary interleukin-1?.

Publications

Determining the biological associates of acute cold pressor post-encoding stress effects on human memory: The role of salivary interleukin-1β.

Similar Datasets

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