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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 abnormal inflammatory changes in the hippocampi of rats at different time points following noise exposure, as measured by protein array and ELISA.(A,B) Protein array format. Image representative of control (A) and noise-exposed (B) cytokine arrays in the Cy3 channel. A key to the location of spotted primary antibodies is shown in Table 2. (C) Normalized net intensity of 34 cytokines in hippocampi of control and noise-exposed rats at day 0 following noise exposure. Bars represent means ± S.D. *p < 0.05, compared with matched controls by Student’s t-test (n = 4 per group). (D-G) ELISA analysis showing the levels of cytokines following noise exposure. 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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f3: Chronic noise exposure causes abnormal inflammatory changes in the hippocampi of rats at different time points following noise exposure, as measured by protein array and ELISA.(A,B) Protein array format. Image representative of control (A) and noise-exposed (B) cytokine arrays in the Cy3 channel. A key to the location of spotted primary antibodies is shown in Table 2. (C) Normalized net intensity of 34 cytokines in hippocampi of control and noise-exposed rats at day 0 following noise exposure. Bars represent means ± S.D. *p < 0.05, compared with matched controls by Student’s t-test (n = 4 per group). (D-G) ELISA analysis showing the levels of cytokines following noise exposure. 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: To better understand the neuroinflammation induced by chronic noise exposure, we examined the hippocampi of rats for alterations in cytokines using the inflammatory cytokine antibody array, followed by ELISA analysis. A schematic of the chip format and representative image of control and noise-exposed arrays in the Cy3 channel are shown in Fig. 3A,B. When we directly analyzed hippocampal contents by antibody array analysis, two of the 34 cytokines examined (TNF-α and RAGE) were expressed more abundantly in noise-exposed rats than controls, and two (activin A and PDGF-AA) were expressed less in noise-exposed rats than in the control group (Fig. 3C).


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 abnormal inflammatory changes in the hippocampi of rats at different time points following noise exposure, as measured by protein array and ELISA.(A,B) Protein array format. Image representative of control (A) and noise-exposed (B) cytokine arrays in the Cy3 channel. A key to the location of spotted primary antibodies is shown in Table 2. (C) Normalized net intensity of 34 cytokines in hippocampi of control and noise-exposed rats at day 0 following noise exposure. Bars represent means ± S.D. *p < 0.05, compared with matched controls by Student’s t-test (n = 4 per group). (D-G) ELISA analysis showing the levels of cytokines following noise exposure. 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

f3: Chronic noise exposure causes abnormal inflammatory changes in the hippocampi of rats at different time points following noise exposure, as measured by protein array and ELISA.(A,B) Protein array format. Image representative of control (A) and noise-exposed (B) cytokine arrays in the Cy3 channel. A key to the location of spotted primary antibodies is shown in Table 2. (C) Normalized net intensity of 34 cytokines in hippocampi of control and noise-exposed rats at day 0 following noise exposure. Bars represent means ± S.D. *p < 0.05, compared with matched controls by Student’s t-test (n = 4 per group). (D-G) ELISA analysis showing the levels of cytokines following noise exposure. 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: To better understand the neuroinflammation induced by chronic noise exposure, we examined the hippocampi of rats for alterations in cytokines using the inflammatory cytokine antibody array, followed by ELISA analysis. A schematic of the chip format and representative image of control and noise-exposed arrays in the Cy3 channel are shown in Fig. 3A,B. When we directly analyzed hippocampal contents by antibody array analysis, two of the 34 cytokines examined (TNF-α and RAGE) were expressed more abundantly in noise-exposed rats than controls, and two (activin A and PDGF-AA) were expressed less in noise-exposed rats than in the control group (Fig. 3C).

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