PMID- 31299618 OWN - NLM STAT- MEDLINE DCOM- 20200415 LR - 20200415 IS - 1096-0953 (Electronic) IS - 0013-9351 (Linking) VI - 176 DP - 2019 Sep TI - Combustion and friction-derived nanoparticles and industrial-sourced nanoparticles: The culprit of Alzheimer and Parkinson's diseases. PG - 108574 LID - S0013-9351(19)30371-8 [pii] LID - 10.1016/j.envres.2019.108574 [doi] AB - Redox-active, strongly magnetic, combustion and friction-derived nanoparticles (CFDNPs) are abundant in particulate matter air pollution. Urban children and young adults with Alzheimer disease Continuum have higher numbers of brain CFDNPs versus clean air controls. CFDNPs surface charge, dynamic magnetic susceptibility, iron content and redox activity contribute to ROS generation, neurovascular unit (NVU), mitochondria, and endoplasmic reticulum (ER) damage, and are catalysts for protein misfolding, aggregation and fibrillation. CFDNPs respond to external magnetic fields and are involved in cell damage by agglomeration/clustering, magnetic rotation and/or hyperthermia. This review focus in the interaction of CFDNPs, nanomedicine and industrial NPs with biological systems and the impact of portals of entry, particle sizes, surface charge, biomolecular corona, biodistribution, mitochondrial dysfunction, cellular toxicity, anterograde and retrograde axonal transport, brain dysfunction and pathology. NPs toxicity information come from researchers synthetizing particles and improving their performance for drug delivery, drug targeting, magnetic resonance imaging and heat mediators for cancer therapy. Critical information includes how these NPs overcome all barriers, the NPs protein corona changes as they cross the NVU and the complexity of NPs interaction with soluble proteins and key organelles. Oxidative, ER and mitochondrial stress, and a faulty complex protein quality control are at the core of Alzheimer and Parkinson's diseases and NPs mechanisms of action and toxicity are strong candidates for early development and progression of both fatal diseases. Nanoparticle exposure regardless of sources carries a high risk for the developing brain homeostasis and ought to be included in the AD and PD research framework. CI - Copyright (c) 2019 Elsevier Inc. All rights reserved. FAU - Calderon-Garciduenas, Lilian AU - Calderon-Garciduenas L AD - The University of Montana, Missoula, MT, 59812, USA; Universidad Del Valle de Mexico, 04850, Mexico City, Mexico. Electronic address: lilian.calderon-garciduenas@umontana.edu. FAU - Reynoso-Robles, Rafael AU - Reynoso-Robles R AD - Instituto Nacional de Pediatria, 04530, Mexico. FAU - Gonzalez-Maciel, Angelica AU - Gonzalez-Maciel A AD - Instituto Nacional de Pediatria, 04530, Mexico. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20190705 PL - Netherlands TA - Environ Res JT - Environmental research JID - 0147621 SB - IM MH - Alzheimer Disease/*epidemiology MH - Environmental Exposure/*statistics & numerical data MH - Friction MH - Humans MH - *Nanoparticles MH - Parkinson Disease/*epidemiology MH - Tissue Distribution OTO - NOTNLM OT - Agglomeration OT - Air pollution OT - Alpha-synuclein OT - Alzheimer disease continuum in children and young adults OT - Brain magnetite/maghemite OT - Combustion and friction derived nanoparticles OT - Endothelial damage OT - External magnetic fields OT - Fibrillation OT - Misfolded proteins OT - Mitochondrial and endoplasmic reticulum stress OT - Nanoparticles OT - Neurovascular unit OT - Oxidative stress OT - Parkinson OT - Transition metals EDAT- 2019/07/13 06:00 MHDA- 2020/04/16 06:00 CRDT- 2019/07/13 06:00 PHST- 2019/05/08 00:00 [received] PHST- 2019/06/11 00:00 [revised] PHST- 2019/07/02 00:00 [accepted] PHST- 2019/07/13 06:00 [pubmed] PHST- 2020/04/16 06:00 [medline] PHST- 2019/07/13 06:00 [entrez] AID - S0013-9351(19)30371-8 [pii] AID - 10.1016/j.envres.2019.108574 [doi] PST - ppublish SO - Environ Res. 2019 Sep;176:108574. doi: 10.1016/j.envres.2019.108574. Epub 2019 Jul 5.