NF-κB-regulated microRNA-574-5p underlies synaptic and cognitive impairment in response to atmospheric PM2.5 aspiration

Ku, Tingting; Li, Ben; Gao, Rui; Zhang, Yingying; Yan, Wei; Ji, Xiaotong; Li, Guangke; Sang, Nan

doi:10.1186/s12989-017-0215-3

Cited by 107 publications

(59 citation statements)

References 93 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…regions (Fonken et al, 2011), reduced synaptic function (Ku et al, 2017) in CA1 neurons (Davis et al, 2013), and decreased myelin basic protein in white matter and increased atrophy of neurites in the CA1 region (Woodward et al, 2017) have been observed. These neurotoxicological data collectively suggest that some hippocampal subfields may be more sensitive than others to the adverse PM-effects.…”

Section: Sensitivity Analysesmentioning

confidence: 92%

“…Several animal studies have demonstrated that inhaled PM 2.5 exposures affect various neural systems thought to underlie these episodic memory processes (Fonken et al, 2011;Cheng et al, 2017;Ku et al, 2017;Liu et al, 2018). Few longitudinal epidemiological studies examined the association between PM 2.5 and episodic memory (Weuve et al, 2012;Tonne et al, 2014;Wurth et al, 2018), and the majority of these studies utilized composite scores with mixed results.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Particulate matter and episodic memory decline mediated by early neuroanatomic biomarkers of Alzheimer’s disease

Younan

Petkus

Widaman

et al. 2019

Brain

140

View full text Add to dashboard Cite

Evidence suggests exposure to particulate matter with aerodynamic diameter <2.5 μm (PM2.5) may increase the risk for Alzheimer’s disease and related dementias. Whether PM2.5 alters brain structure and accelerates the preclinical neuropsychological processes remains unknown. Early decline of episodic memory is detectable in preclinical Alzheimer’s disease. Therefore, we conducted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also explored the potential mediating role of increased neuroanatomic risk of Alzheimer’s disease associated with exposure. Participants included older females (n = 998; aged 73–87) enrolled in both the Women’s Health Initiative Study of Cognitive Aging and the Women’s Health Initiative Memory Study of Magnetic Resonance Imaging, with annual (1999–2010) episodic memory assessment by the California Verbal Learning Test, including measures of immediate free recall/new learning (List A Trials 1–3; List B) and delayed free recall (short- and long-delay), and up to two brain scans (MRI-1: 2005–06; MRI-2: 2009–10). Subjects were assigned Alzheimer’s disease pattern similarity scores (a brain-MRI measured neuroanatomical risk for Alzheimer’s disease), developed by supervised machine learning and validated with data from the Alzheimer’s Disease Neuroimaging Initiative. Based on residential histories and environmental data on air monitoring and simulated atmospheric chemistry, we used a spatiotemporal model to estimate 3-year average PM2.5 exposure preceding MRI-1. In multilevel structural equation models, PM2.5 was associated with greater declines in immediate recall and new learning, but no association was found with decline in delayed-recall or composite scores. For each interquartile increment (2.81 μg/m3) of PM2.5, the annual decline rate was significantly accelerated by 19.3% [95% confidence interval (CI) = 1.9% to 36.2%] for Trials 1–3 and 14.8% (4.4% to 24.9%) for List B performance, adjusting for multiple potential confounders. Long-term PM2.5 exposure was associated with increased Alzheimer’s disease pattern similarity scores, which accounted for 22.6% (95% CI: 1% to 68.9%) and 10.7% (95% CI: 1.0% to 30.3%) of the total adverse PM2.5 effects on Trials 1–3 and List B, respectively. The observed associations remained after excluding incident cases of dementia and stroke during the follow-up, or further adjusting for small-vessel ischaemic disease volumes. Our findings illustrate the continuum of PM2.5 neurotoxicity that contributes to early decline of immediate free recall/new learning at the preclinical stage, which is mediated by progressive atrophy of grey matter indicative of increased Alzheimer’s disease risk, independent of cerebrovascular damage.

show abstract

Section: Sensitivity Analysesmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Particulate matter and episodic memory decline mediated by early neuroanatomic biomarkers of Alzheimer’s disease

Younan

Petkus

Widaman

et al. 2019

Brain

140

View full text Add to dashboard Cite

show abstract

“…1 PM2.5 can be suspended in the air for long periods of time and is believed to pose risks to health. [2][3][4][5][6] Allergic conjunctivitis (AC) is an eye inflammation condition caused by allergic reactions to substances such as pollen or mild spores. 7 It is one of the most common ocular surface diseases encountered in clinical practice and may come in either acute or chronic types.…”

mentioning

confidence: 99%

A Murine Model of Acute Allergic Conjunctivitis Induced by Continuous Exposure to Particulate Matter 2.5

Tang

Chang

Chiang

et al. 2019

Invest. Ophthalmol. Vis. Sci.

View full text Add to dashboard Cite

PURPOSE. Several pieces of epidemiologic evidence have indicated PM2.5 (particulate matter with a diameter of 2.5 lm or less) as a causing factor of allergic conjunctivitis, but without experimental elucidation of mechanism. In the present study, PM2.5 in solution was directly applied to the mouse ocular surface to elucidate whether PM2.5 might cause allergic conjunctivitis, and its underlying mechanisms were analyzed. METHODS. ICR mice were challenged for 18 consecutive days with eye drops containing PM2.5 at 3.2, 6.4, and 12.8 mg/mL in 0.9% NaCl saline, along with the controls prepared in parallel without PM2.5 and another control group treated with both PM2.5 at 12.8 mg/mL and artificial tears. On day 19, the whole eyes and meibomian glands were harvested for histopathological analyses and assessment of clinical scoring, tear volume, tear breakup time, and tear ferning. Furthermore, goblet cells by periodic acid Schiff stain and infiltrated eosinophils by Giemsa stain were quantified and compared among study groups. RESULTS. Clinical scoring showed more eyelid edema, tearing, and scratching behaviors, with longer tear breakup time under the influence of increased PM2.5 concentrations. Tear ferning assay showed less tear crystal formation and decreased crystal branches after exposure to PM2.5. In addition, higher goblet cell density in the upper palpebral conjunctiva and extensive eosinophil infiltration in the entire conjunctiva and in the meibomian glands were induced by PM2.5. CONCLUSIONS. These results demonstrate that PM2.5 can induce symptoms similar to clinical allergic conjunctivitis and that the murine acute allergic conjunctivitis model can be induced by direct exposure to PM2.5.

show abstract

“…For one thing, microglia could protect neuron cells by engulfing alien substances, clearing cell fragments, Aβ deposition and etc. For another, microglia related inflammatory responses could contribute to the increasing of Aβ deposition, neuron damage and even AD risk [22,23].…”

Section: Introductionmentioning

confidence: 99%

PM2.5 can Promote the Alzheimer's Disease-like Changes through Microglia Related Mechanism in Mice

Wang

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: PM2.5, the main particulate air pollutant, poses serious hazard to human health. Alzheimer's disease (AD) is a major neurodegenerative disease characterized by amyloid plaques and neurofibrillary tangles. Recent studies reported that PM could promote AD-like pathologies in human brain. However, the mechanism of PM2.5-induced AD-like changes is still unclear and more investigations are needed for further understanding.Methods: In this study, we established experimental model of long-term PM2.5 exposure with young/old wildtype C57BL/6 and APP/PS transgenic mice. Behavior assessments were monitored after four weeks of exposure. The changes of blood cells were detected by Complete Blood Count and splenic macrophages were detected by flow cytometry. Immunohistochemical staining was used to observe the damage of PM2.5 on neurons, the deposition of Aβ and the changes of microglia. RNA-seq was used to analyze the whole genome changes of hippocampus after PM2.5 exposure. In addition, microglia related genes were analyzed via Real-time PCR. Results: After mice were exposed to PM2.5 for a month, some AD-like behavioral changes, such as learning and memory impairment were detected especially in old and transgenic mice. The histopathological changes, such as β-amyloid (Aβ) deposition, morphological changes of microglia, as well as great impairments of hippocampus neurons but not cortex neurons were observed. The analyze of whole-genome expression in the hippocampus suggested long term PM2.5 exposure changed the expression of genes related with AD process (mouse behavior and microglia differentiation). Furthermore, the mRNA level, which related to microglia, of CD86, CD22, IL-1β was upregulated and CD206, TREM2, TGF-β2 was downregulated. Conclusions: Aged population were more susceptible to long-term PM2.5 exposure and PM2.5 could promote AD-like phenotype through microglia related mechanism.

show abstract

NF-κB-regulated microRNA-574-5p underlies synaptic and cognitive impairment in response to atmospheric PM2.5 aspiration

Cited by 107 publications

References 93 publications

Particulate matter and episodic memory decline mediated by early neuroanatomic biomarkers of Alzheimer’s disease

Particulate matter and episodic memory decline mediated by early neuroanatomic biomarkers of Alzheimer’s disease

A Murine Model of Acute Allergic Conjunctivitis Induced by Continuous Exposure to Particulate Matter 2.5

PM2.5 can Promote the Alzheimer's Disease-like Changes through Microglia Related Mechanism in Mice

Contact Info

Product

Resources

About