Long-Term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain-Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid beta-42 and alpha-Synuclein in Children and. Export

@article{citeulike:2746007, abstract = {Air pollution is a serious environmental problem. We investigated whether residency in cities with high air pollution is associated with neuroinflammation/neurodegeneration in healthy children and young adults who died suddenly. We measured mRNA cyclooxygenase-2, interleukin-1beta, and CD14 in target brain regions from low (n = 12) or highly exposed residents (n = 35) aged 25.1 +/- 1.5 years. Upregulation of cyclooxygenase-2, interleukin-1beta, and CD14 in olfactory bulb, frontal cortex, substantia nigrae and vagus nerves; disruption of the blood-brain barrier; endothelial activation, oxidative stress, and inflammatory cell trafficking were seen in highly exposed subjects. Amyloid beta42 (Abeta42) immunoreactivity was observed in 58.8\% of apolipoprotein E (APOE) 3/3 < 25 y, and 100\% of the APOE 4 subjects, whereas alpha-synuclein was seen in 23.5\% of < 25 y subjects. Particulate material (PM) was seen in olfactory bulb neurons, and PM < 100 nm were observed in intraluminal erythrocytes from lung, frontal, and trigeminal ganglia capillaries. Exposure to air pollution causes neuroinflammation, an altered brain innate immune response, and accumulation of Abeta42 and alpha-synuclein starting in childhood. Exposure to air pollution should be considered a risk factor for Alzheimer's and Parkinson's diseases, and carriers of the APOE 4 allele could have a higher risk of developing Alzheimer's disease if they reside in a polluted environment.}, author = {Calder\'{o}n-Garcidue\~{n}as, Lilian and Solt, Anna C C. and Henr\'{i}quez-Rold\'{a}n, Carlos and Torres-Jard\'{o}n, Ricardo and Nuse, Bryan and Herritt, Lou and Villarreal-Calder\'{o}n, Rafael and Osnaya, Norma and Stone, Ida and Garc\'{i}a, Raquel and Brooks, Diane M M. and Gonz\'{a}lez-Maciel, Angelica and Reynoso-Robles, Rafael and Delgado-Ch\'{a}vez, Ricardo and Reed, William}, citeulike-article-id = {2746007}, citeulike-linkout-0 = {http://dx.doi.org/10.1177/0192623307313011}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/18349428}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=18349428}, doi = {10.1177/0192623307313011}, issn = {0192-6233}, journal = {Toxicologic pathology}, keywords = {barrier, blood, brain, neuroinflammation}, month = {March}, posted-at = {2008-05-02 15:37:32}, priority = {3}, title = {Long-Term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain-Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid {beta}-42 and {alpha}-Synuclein in Children and.}, url = {http://dx.doi.org/10.1177/0192623307313011}, year = {2008} }

TY - JOUR ID - citeulike:2746007 L3 - citeulike-article-id:2746007 N2 - Air pollution is a serious environmental problem. We investigated whether residency in cities with high air pollution is associated with neuroinflammation/neurodegeneration in healthy children and young adults who died suddenly. We measured mRNA cyclooxygenase-2, interleukin-1beta, and CD14 in target brain regions from low (n = 12) or highly exposed residents (n = 35) aged 25.1 +/- 1.5 years. Upregulation of cyclooxygenase-2, interleukin-1beta, and CD14 in olfactory bulb, frontal cortex, substantia nigrae and vagus nerves; disruption of the blood-brain barrier; endothelial activation, oxidative stress, and inflammatory cell trafficking were seen in highly exposed subjects. Amyloid beta42 (Abeta42) immunoreactivity was observed in 58.8% of apolipoprotein E (APOE) 3/3 < 25 y, and 100% of the APOE 4 subjects, whereas alpha-synuclein was seen in 23.5% of < 25 y subjects. Particulate material (PM) was seen in olfactory bulb neurons, and PM < 100 nm were observed in intraluminal erythrocytes from lung, frontal, and trigeminal ganglia capillaries. Exposure to air pollution causes neuroinflammation, an altered brain innate immune response, and accumulation of Abeta42 and alpha-synuclein starting in childhood. Exposure to air pollution should be considered a risk factor for Alzheimer's and Parkinson's diseases, and carriers of the APOE 4 allele could have a higher risk of developing Alzheimer's disease if they reside in a polluted environment. JF - Toxicologic pathology SN - 0192-6233 TI - Long-Term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain-Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid {beta}-42 and {alpha}-Synuclein in Children and. KW - barrier KW - blood KW - brain KW - neuroinflammation AU - Calderón-Garcidueñas, Lilian AU - Solt, Anna C AU - Henríquez-Roldán, Carlos AU - Torres-Jardón, Ricardo AU - Nuse, Bryan AU - Herritt, Lou AU - Villarreal-Calderón, Rafael AU - Osnaya, Norma AU - Stone, Ida AU - García, Raquel AU - Brooks, Diane M AU - González-Maciel, Angelica AU - Reynoso-Robles, Rafael AU - Delgado-Chávez, Ricardo AU - Reed, William PY - 2008/03/18/ UR - http://dx.doi.org/10.1177/0192623307313011 ER -