Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats

Liu, Jie; Yang, Chen; Yang, Jing; Song, Xiaojie; Han, Wei; Xie, Mingdan; Cheng, Li; Xie, Lingling; Chen, Hengsheng; Jiang, Li

doi:10.1002/brb3.1453

Cited by 45 publications

(11 citation statements)

References 52 publications

(61 reference statements)

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“…In this study, with chronic exposure to low-dose PM 2.5 , there was no signi cant difference in spatial learning function, but memory easily decayed after exposure, as shown by the Morris water maze test. Previous similar animal studies with prominent memory insult might be dose-dependent [63,64]. Relatively low-dosage exposure, similar to the experimental design of the ambient atmosphere environment in this study, only induced minimal cognitive or behavioral changes.…”

Section: Discussionsupporting

confidence: 62%

White Matter Pathology in Alzheimer’s Transgenic Mice With Chronic Exposure to Low-Level Ambient Fine Particulate Matter

Chen

Lee

Zheng

et al. 2021

Preprint

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Background: Air pollution, especially fine particulate matter (PM), can cause brain damage, cognitive decline, and an increased risk of neurodegenerative disease, especially Alzheimer’s disease (AD). Typical pathological findings of amyloid and tau protein accumulation have been detected in the brain after exposure in animal studies. However, these observations were based on high levels of PM exposure, which were far from the WHO guidelines and those present in our environment. In addition, white matter involvement by air pollution has been less reported. Thus, this experiment was designed to simulate the true human world and to discuss the possible white matter pathology caused by air pollution. Results: 6-month-old female 3xTg-AD mice were divided into exposure and control groups and housed in the Taipei Air Pollutant Exposure System (TAPES) for 5 months. The mice were subjected to the Morris water maze test after exposure and were then sacrificed with brain dissection for further analyses. The mean mass concentration of PM2.5 during the exposure period was 13.85 μg/m3. After exposure, there was no difference in spatial learning function between the two groups, but there was significant decay of memory in the exposure group. Significantly decreased total brain volume and more neuronal death in the cerebral and entorhinal cortex and demyelination of the corpus callosum were noted by histopathological staining after exposure. However, there was no difference in the accumulation of amyloid or tau on immunohistochemistry staining. For the protein analysis, amyloid was detected at significantly higher levels in the cerebral cortex, with lower expression of myelin basic protein in the white matter. A diffuse tensor image study also revealed insults in multiple white matter tracts, including the optic tract. Conclusions: In conclusion, this pilot study showed that even chronic exposure to low PM2.5 concentrations still caused brain damage, such as gross brain atrophy, cortical neuron damage, and multiple white matter tract damage. Typical amyloid cascade pathology did not appear prominently in the vulnerable brain region after exposure. These findings imply that multiple pathogenic pathways induce brain injury by air pollution, and the optic nerve is another direct invasion route in addition to olfactory nerve.

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Section: Discussionsupporting

confidence: 62%

White Matter Pathology in Alzheimer’s Transgenic Mice With Chronic Exposure to Low-Level Ambient Fine Particulate Matter

Chen

Lee

Zheng

et al. 2021

Preprint

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“…Chronic exposure of PM 2.5 also has shown to increase the risk of disturbed emotional expression and related affective behaviors [34–36]. Previous studies have shown that long-term exposure of PM 2.5 caused significant increase in anxiety-related behavior measured by EPM [37,38]. Although our EPM data (Fig.…”

Section: Discussionmentioning

confidence: 62%

Subchronic exposure to ambient PM_2.5impairs novelty recognition and spatial memory

Kim,

Das,

Sillé

et al. 2023

Preprint

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Air pollution remains a great challenge for public health, with the detrimental effects of air pollution on cardiovascular, rhinosinusitis, and pulmonary health increasingly well understood. Recent epidemiological associations point to the adverse effects of air pollution on cognitive decline and neurodegenerative diseases. Mouse models of subchronic exposure to PM2.5(ambient air particulate matter < 2.5 µm) provide an opportunity to demonstrate the causality of target diseases. Here, we subchronically exposed mice to concentrated ambient PM2.5for 7 weeks (5 days/week; 8h/day) and assessed its effect on behavior using standard tests measuring cognition or anxiety-like behaviors. Average daily PM2.5concentration was 200 µg/m3in the PM2.5group and 10 µg/m3in the filtered air group. The novel object recognition (NOR) test was used to assess the effect of PM2.5exposure on recognition memory. The increase in exploration time for a novel object versus a familiarized object was lower for PM2.5-exposed mice (42% increase) compared to the filtered air (FA) control group (110% increase). In addition, the calculated discrimination index for novel object recognition was significantly higher in FA mice (67 %) compared to PM2.5exposed mice (57.3%). The object location test (OLT) was used to examine the effect of PM2.5exposure on spatial memory. In contrast to the FA-exposed control mice, the PM2.5exposed mice exhibited no significant increase in their exploration time between novel location versus familiarized location indicating their deficit in spatial memory. Furthermore, the discrimination index for novel location was significantly higher in FA mice (62.6%) compared to PM2.5exposed mice (51%). Overall, our results demonstrate that subchronic exposure to higher levels of PM2.5in mice causes impairment of novelty recognition and spatial memory.

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“…Interestingly, chloroquine administration significantly decreased the number of degenerative and necrotic neurons and attenuated the absence of Nissl bodies when compared with the vehicle-treated HI group. A classic indicator of neural regeneration, GAP43, was detected by the western blot at 7 days after the H/I injury. The western blot analysis of GAP43 is shown in Figure B.…”

Section: Resultsmentioning

confidence: 99%

Chloroquine Protects Hypoxia/Ischemia-Induced Neonatal Brain Injury in Rats by Mitigating Blood–Brain Barrier Disruption

Fang

Liu

Zhang

et al. 2023

ACS Chem. Neurosci.

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Neonatal hypoxic-ischemic (H/I) brain damage (HIBD) is a devastating condition for which there are presently no effective therapeutic strategies against its severe neurological deficits in neonates and young children. Traditionally, H/I induces the compromise of the blood–brain barrier (BBB), which causes neuronal cell death, eventually resulting in brain secondary injury. In addition to neonatal HIBD, chloroquine (CQ) has been proved to exert a protective effect on BBB disruption in several brain injury models. The main purpose of this research was to study whether CQ protects the BBB from H/I insult and confers beneficial neuroprotection in the neonatal Rice–Vannucci rat model. Herein, we reported that CQ administration significantly reduced brain damage and improved behavioral dysplasia after H/I injury. Moreover, we demonstrated the protective effects of CQ on BBB integrity, evidenced by ameliorating brain edema and Evans blue extravasation, inhibiting the degeneration of the tight junction and adherens junction proteins, and improving pericyte survival in neonatal rats after HIBD. These findings indicated that CQ administration protected the BBB against H/I injury, thereby ameliorating brain damage and promoting neurofunctional recovery. Collectively, our data demonstrated that CQ played a crucial role in BBB integrity after neonatal H/I injury, which sheds light on the development of therapeutic agents to treat HIBD.

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Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats

Cited by 45 publications

References 52 publications

White Matter Pathology in Alzheimer’s Transgenic Mice With Chronic Exposure to Low-Level Ambient Fine Particulate Matter

White Matter Pathology in Alzheimer’s Transgenic Mice With Chronic Exposure to Low-Level Ambient Fine Particulate Matter

Subchronic exposure to ambient PM_2.5impairs novelty recognition and spatial memory

Chloroquine Protects Hypoxia/Ischemia-Induced Neonatal Brain Injury in Rats by Mitigating Blood–Brain Barrier Disruption

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Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats

Cited by 45 publications

References 52 publications

White Matter Pathology in Alzheimer’s Transgenic Mice With Chronic Exposure to Low-Level Ambient Fine Particulate Matter

White Matter Pathology in Alzheimer’s Transgenic Mice With Chronic Exposure to Low-Level Ambient Fine Particulate Matter

Subchronic exposure to ambient PM2.5impairs novelty recognition and spatial memory

Chloroquine Protects Hypoxia/Ischemia-Induced Neonatal Brain Injury in Rats by Mitigating Blood–Brain Barrier Disruption

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Subchronic exposure to ambient PM_2.5impairs novelty recognition and spatial memory