%0 Journal Article %J J Alzheimers Dis %D 2020 %T Environmental Nanoparticles, SARS-CoV-2 Brain Involvement, and Potential Acceleration of Alzheimer's and Parkinson's Diseases in Young Urbanites Exposed to Air Pollution. %A Calderón-Garcidueñas, Lilian %A Torres-Jardón, Ricardo %A Franco-Lira, Maricela %A Kulesza, Randy %A González-Maciel, Angelica %A Reynoso-Robles, Rafael %A Brito-Aguilar, Rafael %A García-Arreola, Berenice %A Revueltas-Ficachi, Paula %A Barrera-Velázquez, Juana Adriana %A García-Alonso, Griselda %A García-Rojas, Edgar %A Mukherjee, Partha S %A Delgado-Chávez, Ricardo %K Adult %K Air Pollution %K Alzheimer Disease %K Brain Diseases %K Coronavirus Infections %K COVID-19 %K Disease Progression %K Environmental Pollutants %K Humans %K Middle Aged %K Nanoparticles %K Pandemics %K Parkinson Disease %K Pneumonia, Viral %K Suicide %K Urban Population %X

Alzheimer's and Parkinson's diseases (AD, PD) have a pediatric and young adult onset in Metropolitan Mexico City (MMC). The SARS-CoV-2 neurotropic RNA virus is triggering neurological complications and deep concern regarding acceleration of neuroinflammatory and neurodegenerative processes already in progress. This review, based on our MMC experience, will discuss two major issues: 1) why residents chronically exposed to air pollution are likely to be more susceptible to SARS-CoV-2 systemic and brain effects and 2) why young people with AD and PD already in progress will accelerate neurodegenerative processes. Secondary mental consequences of social distancing and isolation, fear, financial insecurity, violence, poor health support, and lack of understanding of the complex crisis are expected in MMC residents infected or free of SARS-CoV-2. MMC residents with pre-SARS-CoV-2 accumulation of misfolded proteins diagnostic of AD and PD and metal-rich, magnetic nanoparticles damaging key neural organelles are an ideal host for neurotropic SARS-CoV-2 RNA virus invading the body through the same portals damaged by nanoparticles: nasal olfactory epithelium, the gastrointestinal tract, and the alveolar-capillary portal. We urgently need MMC multicenter retrospective-prospective neurological and psychiatric population follow-up and intervention strategies in place in case of acceleration of neurodegenerative processes, increased risk of suicide, and mental disease worsening. Identification of vulnerable populations and continuous effort to lower air pollution ought to be critical steps.

%B J Alzheimers Dis %V 78 %P 479-503 %8 2020 %G eng %N 2 %1 https://www.ncbi.nlm.nih.gov/pubmed/32955466?dopt=Abstract %R 10.3233/JAD-200891 %0 Journal Article %J J Alzheimers Dis %D 2012 %T Neuroinflammation, hyperphosphorylated tau, diffuse amyloid plaques, and down-regulation of the cellular prion protein in air pollution exposed children and young adults. %A Calderón-Garcidueñas, Lilian %A Kavanaugh, Michael %A Block, Michelle %A D'Angiulli, Amedeo %A Delgado-Chávez, Ricardo %A Torres-Jardón, Ricardo %A González-Maciel, Angelica %A Reynoso-Robles, Rafael %A Osnaya, Norma %A Villarreal-Calderon, Rodolfo %A Guo, Ruixin %A Hua, Zhaowei %A Zhu, Hongtu %A Perry, George %A Diaz, Philippe %K Adolescent %K Adult %K Age Factors %K Air Pollution %K Child %K Child, Preschool %K Cohort Studies %K Down-Regulation %K Encephalitis %K Female %K Frontal Lobe %K Gene Regulatory Networks %K Humans %K Infant %K Male %K Mexico %K Phosphorylation %K Plaque, Amyloid %K Prions %K tau Proteins %K Young Adult %X

Air pollution exposures have been linked to neuroinflammation and neuropathology. Autopsy samples of the frontal cortex from control (n = 8) and pollution-exposed (n = 35) children and young adults were analyzed by RT-PCR (n = 43) and microarray analysis (n = 12) for gene expression changes in oxidative stress, DNA damage signaling, NFκB signaling, inflammation, and neurodegeneration pathways. The effect of apolipoprotein E (APOE) genotype on the presence of protein aggregates associated with Alzheimer's disease (AD) pathology was also explored. Exposed urbanites displayed differential (>2-fold) regulation of 134 genes. Forty percent exhibited tau hyperphosphorylation with pre-tangle material and 51% had amyloid-β (Aβ) diffuse plaques compared with 0% in controls. APOE4 carriers had greater hyperphosphorylated tau and diffuse Aβ plaques versus E3 carriers (Q = 7.82, p = 0.005). Upregulated gene network clusters included IL1, NFκB, TNF, IFN, and TLRs. A 15-fold frontal down-regulation of the prion-related protein (PrP(C)) was seen in highly exposed subjects. The down-regulation of the PrP(C) is critical given its important roles for neuroprotection, neurodegeneration, and mood disorder states. Elevation of indices of neuroinflammation and oxidative stress, down-regulation of the PrP(C) and AD-associated pathology are present in young megacity residents. The inducible regulation of gene expression suggests they are evolving different mechanisms in an attempt to cope with the constant state of inflammation and oxidative stress related to their environmental exposures. Together, these data support a role for air pollution in CNS damage and its impact upon the developing brain and the potential etiology of AD and mood disorders.

%B J Alzheimers Dis %V 28 %P 93-107 %8 2012 %G eng %N 1 %R 10.3233/JAD-2011-110722