Alzheimer’s development and progression in urban children and young adults: Nanoparticles, mitochondria, endoplasmic reticulum and cellular havoc

Lilian Calderón-Garcidueñas, Ricardo Torres-Jardón, Angélica González-Maciel, Rafael Reynoso-Robles, Rafael Brito-Aguilar, Partha S. Mukherjee

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

1 Scopus citations


Alzheimer’s disease (AD) is a fatal disease affecting millions of people across the world, including 5.8 million in the USA and a projected 14 million for 2050, and yet the issue of the early impact of air pollutants - a preventable risk factor - has been largely ignored. The development and progression of Alzheimer’s disease have been documented in children and young adults residing in Metropolitan Mexico City (MMC) exhibiting hyperphosphorylated tau and beta amyloid in 202/203 consecutive forensic autopsies in subjects ≤40y of age. Young MMC residents exhibit progressive cognitive deterioration, brainstem auditory evoked potentials abnormalities, olfaction deficits and cerebrospinal fluid changes in seemingly healthy individuals. Alzheimer’s disease defined as a biologic construct starts in childhood under conditions of sustained fine particulate air pollution (PM2.5) above the current USEPA standards and ultrafine particulate matter (UFP). Its development and progression are the result of complex interactions of genetic, nutritional, lifestyle, cardiovascular and metabolic comorbidities, cognitive reserve and cultural factors promoting and protecting exposed individuals. Evidence that Alzheimer’s disease starts in childhood is critical and means that 99.5% of the exposed population ≤ 40y can be staged for Alzheimer’s disease. Therefore, it is advisable to execute preventive measures early and control PM2.5 and UFP, particularly combustion and friction-associated nanoparticle emissions, including those from non-regulated diesel vehicles. In this Chapter, we discuss Alzheimer’s disease defined by its underlying pathologic processes and the impact of highly oxidative and ubiquitous combustion and friction-derived nanoparticles (CFDNPs). Specifically we explore their portals of entry, particle sizes, surface charge, biomolecular corona, biodistribution, mitochondrial dysfunction, endoplasmic reticulum stress, cellular toxicity, anterograde and retrograde axonal transport, and brain dysfunction associated with early and progressive damage to the neurovascular unit and key neuronal, glial and endothelial cellular organelles. The reader should be aware there is a myriad of proteins able to coat nanoparticles (NPs) and their ultimate fate depends in part on the corona composition and stability, their magnetic capabilities, the portal of entry and the target cell. Effects of PM2.5 and nanoparticles on the human brain are multifactorial, thus comparing brain effects across different populations and different air pollution profiles ought to be done with caution. CFDNPs play a major role in the early development and/or acceleration of Alzheimer’s disease. Alzheimer’s disease may be a preventable disease in the scenario of air pollution and starts in pediatric ages.

Original languageEnglish
Title of host publicationAmbient Combustion Ultrafine Particles and Health
PublisherNova Science Publishers, Inc.
Number of pages46
ISBN (Electronic)9781536190021
StatePublished - Feb 12 2021


  • Air pollution
  • And children
  • Nanoparticles


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