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Neural and cell‐cell junction autoantibodies in megacity children: the neurodegenerative impact (835.2)
Author(s) -
CalderonGarciduenas Lilian,
Vojdani Aristo
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.835.2
Subject(s) - autoantibody , immunology , medicine , inflammation , myelin oligodendrocyte glycoprotein , neuroinflammation , immune system , occludin , neuroscience , biology , antibody , microbiology and biotechnology , tight junction , experimental autoimmune encephalomyelitis
Millions of children in the USA, Mexico and around the world are chronically exposed to concentrations of air pollutants, including fine particulate matter, above safety standards. Mexico City children exposed to high concentrations of particulate matter (PM) exhibit a breakdown of the nasal, olfactory, and brain‐blood‐barriers (BBB), along a brain gene imbalance in oxidative stress, inflammation, innate and adaptive immune responses, and the accumulation of misfolded proteins observed in the early stages of Alzheimer (AD) and Parkinson’s diseases. We measure serum autoantibodies associated with epithelial and endothelial barriers, and neural proteins in 95 Mexican children age 11.02 ±3.6 years, with exposures to megacity severe air pollution versus clean air controls. MC children had significantly increased IgG high affinity antibodies for cell‐cell junction and neural proteins including: occludin‐zonulin, actin, S‐100, myelin oligodendrocyte glycoprotein, and myelin basic protein (p<0.001). The major factor determining the impact of brain autoantibodies is the integrity of the BBB, thus, cell‐cell junction and brain autoantibodies might contribute to the white matter integrity alterations, structural/volumetric brain changes and the selective impairment in subscales tapping on attention, short term memory and learning abilities present in highly exposed children. Increasing research supports dysregulated immune responses in the pathophysiology of AD. Early neurodegeneration‐related dysregulated immune responses might indicate pathways that can be targeted for childhood interventions aiming at AD prevention. AD affects 5.2 million Americans today. By 2050, 13.8 million will be affected. Early identification of subjects at risk and effective prevention strategies are urgently needed.