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Chronic Noise Exposure Acts Cumulatively to Exacerbate Alzheimer's Disease-Like Amyloid-β Pathology and Neuroinflammation in the Rat Hippocampus.

Cui B, Li K, Gai Z, She X, Zhang N, Xu C, Chen X, An G, Ma Q, Wang R - Sci Rep (2015)

Bottom Line: Amyloid-β (Aβ) pathology is thought to be one of the primary initiating factors in AD.This effect was accompanied by up-regulated expression of amyloid precursor protein (APP) and its cleavage enzymes, β- and γ-secretases.Furthermore, we found persistent elevations of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 expression that closely corresponded to the noise-induced increases in Aβ and neuroinflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Occupational Hygiene, Tianjin Institute of Health and Environmental Medicine, Tianjin, China.

ABSTRACT
A putative etiological association exists between noise exposure and Alzheimer's disease (AD). Amyloid-β (Aβ) pathology is thought to be one of the primary initiating factors in AD. It has been further suggested that subsequent dysregulation of Aβ may play a mechanistic role in the AD-like pathophysiology associated with noise exposure. Here, we used ELISA, immunoblotting, cytokine arrays, and RT-PCR, to examine both hippocampal Aβ pathology and neuroinflammation in rats at different time points after noise exposure. We found that chronic noise exposure significantly accelerated the progressive overproduction of Aβ, which persisted for 7 to 14 days after the cessation of exposure. This effect was accompanied by up-regulated expression of amyloid precursor protein (APP) and its cleavage enzymes, β- and γ-secretases. Cytokine analysis revealed that chronic noise exposure increased levels of tumor necrosis factor-α and the receptor for advanced glycation end products, while decreasing the expression of activin A and platelet-derived growth factor-AA. Furthermore, we found persistent elevations of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 expression that closely corresponded to the noise-induced increases in Aβ and neuroinflammation. These studies suggest that lifelong environmental noise exposure may have cumulative effects on the onset and development of AD.

No MeSH data available.


Related in: MedlinePlus

Chronic noise exposure causes persistent overexpression of GFAP in the hippocampus.(A) Comparison of GFAP mRNA expression levels at different time points in control and noise-exposed rats by quantitative real-time PCR. (B,D) Western blot analysis of GFAP and IBA1 under C (control) and N (chronic noise exposure) conditions at different time points. GAPDH was used as a loading control. The immunoreactive band density was quantified and presented as the percent change relative to control samples (C,E). Bars represent means ± S.D. *p < 0.05 and **p < 0.01, compared with respective controls by Student’s t-test (n = 6 per group).
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f4: Chronic noise exposure causes persistent overexpression of GFAP in the hippocampus.(A) Comparison of GFAP mRNA expression levels at different time points in control and noise-exposed rats by quantitative real-time PCR. (B,D) Western blot analysis of GFAP and IBA1 under C (control) and N (chronic noise exposure) conditions at different time points. GAPDH was used as a loading control. The immunoreactive band density was quantified and presented as the percent change relative to control samples (C,E). Bars represent means ± S.D. *p < 0.05 and **p < 0.01, compared with respective controls by Student’s t-test (n = 6 per group).

Mentions: Glial activation is one of the pathological hallmarks of neurodegenerative diseases including AD. IBA1 and GFAP are markers for microglia and astroglia, respectively, that can be used to detect neuroglial activation during neuroinflammation. Significant increases in GFAP mRNA expression were observed in the hippocampus at days 0, 3, 7, and 14 following noise exposure (Fig. 4A). Quantitative immunoblotting analysis also revealed that changes in GFAP protein levels were similar to those of GFAP mRNA over the course of the observation period, with the exception of GFAP expression at day 14, which decreased to the control level (Fig. 4B,C). Western blot analysis also showed a significant increase in IBA1 protein levels in the noise-exposed group at days 0, 3, 7 and 14 after exposure (Fig. 4D,E).These data suggest that chronic noise exposure may cause long-lasting neuroglial activation in the hippocampus, playing an important role in the initiation of neuroinflammation.


Chronic Noise Exposure Acts Cumulatively to Exacerbate Alzheimer's Disease-Like Amyloid-β Pathology and Neuroinflammation in the Rat Hippocampus.

Cui B, Li K, Gai Z, She X, Zhang N, Xu C, Chen X, An G, Ma Q, Wang R - Sci Rep (2015)

Chronic noise exposure causes persistent overexpression of GFAP in the hippocampus.(A) Comparison of GFAP mRNA expression levels at different time points in control and noise-exposed rats by quantitative real-time PCR. (B,D) Western blot analysis of GFAP and IBA1 under C (control) and N (chronic noise exposure) conditions at different time points. GAPDH was used as a loading control. The immunoreactive band density was quantified and presented as the percent change relative to control samples (C,E). Bars represent means ± S.D. *p < 0.05 and **p < 0.01, compared with respective controls by Student’s t-test (n = 6 per group).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4528219&req=5

f4: Chronic noise exposure causes persistent overexpression of GFAP in the hippocampus.(A) Comparison of GFAP mRNA expression levels at different time points in control and noise-exposed rats by quantitative real-time PCR. (B,D) Western blot analysis of GFAP and IBA1 under C (control) and N (chronic noise exposure) conditions at different time points. GAPDH was used as a loading control. The immunoreactive band density was quantified and presented as the percent change relative to control samples (C,E). Bars represent means ± S.D. *p < 0.05 and **p < 0.01, compared with respective controls by Student’s t-test (n = 6 per group).
Mentions: Glial activation is one of the pathological hallmarks of neurodegenerative diseases including AD. IBA1 and GFAP are markers for microglia and astroglia, respectively, that can be used to detect neuroglial activation during neuroinflammation. Significant increases in GFAP mRNA expression were observed in the hippocampus at days 0, 3, 7, and 14 following noise exposure (Fig. 4A). Quantitative immunoblotting analysis also revealed that changes in GFAP protein levels were similar to those of GFAP mRNA over the course of the observation period, with the exception of GFAP expression at day 14, which decreased to the control level (Fig. 4B,C). Western blot analysis also showed a significant increase in IBA1 protein levels in the noise-exposed group at days 0, 3, 7 and 14 after exposure (Fig. 4D,E).These data suggest that chronic noise exposure may cause long-lasting neuroglial activation in the hippocampus, playing an important role in the initiation of neuroinflammation.

Bottom Line: Amyloid-β (Aβ) pathology is thought to be one of the primary initiating factors in AD.This effect was accompanied by up-regulated expression of amyloid precursor protein (APP) and its cleavage enzymes, β- and γ-secretases.Furthermore, we found persistent elevations of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 expression that closely corresponded to the noise-induced increases in Aβ and neuroinflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Occupational Hygiene, Tianjin Institute of Health and Environmental Medicine, Tianjin, China.

ABSTRACT
A putative etiological association exists between noise exposure and Alzheimer's disease (AD). Amyloid-β (Aβ) pathology is thought to be one of the primary initiating factors in AD. It has been further suggested that subsequent dysregulation of Aβ may play a mechanistic role in the AD-like pathophysiology associated with noise exposure. Here, we used ELISA, immunoblotting, cytokine arrays, and RT-PCR, to examine both hippocampal Aβ pathology and neuroinflammation in rats at different time points after noise exposure. We found that chronic noise exposure significantly accelerated the progressive overproduction of Aβ, which persisted for 7 to 14 days after the cessation of exposure. This effect was accompanied by up-regulated expression of amyloid precursor protein (APP) and its cleavage enzymes, β- and γ-secretases. Cytokine analysis revealed that chronic noise exposure increased levels of tumor necrosis factor-α and the receptor for advanced glycation end products, while decreasing the expression of activin A and platelet-derived growth factor-AA. Furthermore, we found persistent elevations of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 expression that closely corresponded to the noise-induced increases in Aβ and neuroinflammation. These studies suggest that lifelong environmental noise exposure may have cumulative effects on the onset and development of AD.

No MeSH data available.


Related in: MedlinePlus