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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 leads to a persistent increase of Aβ in the hippocampus.(A) Western blot analysis of Aβ in the hippocampus under C (control) and N (chronic noise exposure) conditions. GAPDH was used as a loading control. (B) Quantification of immunoreactive band density measured in Panel A. Data are presented as the percent change relative to control samples. (C,D) Quantification of Aβ 1–40 and Aβ 1–42 levels by ELISA at different time points following noise exposure. Levels of Aβ 1–40 and Aβ 1–42 are shown as means ± standard deviation. *p < 0.05 and **p < 0.01, compared with respective controls by Student’s t-test (n = 6 per group).
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f1: Chronic noise exposure leads to a persistent increase of Aβ in the hippocampus.(A) Western blot analysis of Aβ in the hippocampus under C (control) and N (chronic noise exposure) conditions. GAPDH was used as a loading control. (B) Quantification of immunoreactive band density measured in Panel A. Data are presented as the percent change relative to control samples. (C,D) Quantification of Aβ 1–40 and Aβ 1–42 levels by ELISA at different time points following noise exposure. Levels of Aβ 1–40 and Aβ 1–42 are shown as means ± standard deviation. *p < 0.05 and **p < 0.01, compared with respective controls by Student’s t-test (n = 6 per group).

Mentions: In order to evaluate the effect of chronic noise exposure on the production of Aβ, we performed immunoblotting and ELISA assays to determine the relative levels of Aβ, Aβ1-40, and Aβ1-42 in hippocampus tissue. The expression of Aβ was significantly increased after 4 weeks of exposure to noise, with an increasing trend that persisted up to 7 days after the cessation of exposure (Fig. 1A,B). The amount of Aβ1-40 in the hippocampus was 1.7-fold higher than the amount in control rats at day 0 and decreased to 1.2-fold of this level at the end of observation period (Fig. 1C). Assessment of the Aβ1-42 content revealed a similar trend in the hippocampus after noise exposure (Fig. 1D).


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 leads to a persistent increase of Aβ in the hippocampus.(A) Western blot analysis of Aβ in the hippocampus under C (control) and N (chronic noise exposure) conditions. GAPDH was used as a loading control. (B) Quantification of immunoreactive band density measured in Panel A. Data are presented as the percent change relative to control samples. (C,D) Quantification of Aβ 1–40 and Aβ 1–42 levels by ELISA at different time points following noise exposure. Levels of Aβ 1–40 and Aβ 1–42 are shown as means ± standard deviation. *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

f1: Chronic noise exposure leads to a persistent increase of Aβ in the hippocampus.(A) Western blot analysis of Aβ in the hippocampus under C (control) and N (chronic noise exposure) conditions. GAPDH was used as a loading control. (B) Quantification of immunoreactive band density measured in Panel A. Data are presented as the percent change relative to control samples. (C,D) Quantification of Aβ 1–40 and Aβ 1–42 levels by ELISA at different time points following noise exposure. Levels of Aβ 1–40 and Aβ 1–42 are shown as means ± standard deviation. *p < 0.05 and **p < 0.01, compared with respective controls by Student’s t-test (n = 6 per group).
Mentions: In order to evaluate the effect of chronic noise exposure on the production of Aβ, we performed immunoblotting and ELISA assays to determine the relative levels of Aβ, Aβ1-40, and Aβ1-42 in hippocampus tissue. The expression of Aβ was significantly increased after 4 weeks of exposure to noise, with an increasing trend that persisted up to 7 days after the cessation of exposure (Fig. 1A,B). The amount of Aβ1-40 in the hippocampus was 1.7-fold higher than the amount in control rats at day 0 and decreased to 1.2-fold of this level at the end of observation period (Fig. 1C). Assessment of the Aβ1-42 content revealed a similar trend in the hippocampus after noise exposure (Fig. 1D).

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