Category Archives: 2.5

PM 2.5 nearly doubles the risk of dementia in older women

Breathing an atmosphere contaminated with particulate matter (PM) diameter is <2.5μm nearly doubles the risk of dementia in older women(Translational Psychiatry).   Fossil fuel combustion by-products are a major source of  PM2.5 which we recognize as “smog. ”  Automobile exhaust emissions are a major source of the air pollution city dwellers inhale and account for 25% of ambient PM2.5..

The researchers focused on the effects of breathing in the tiny particles found in air pollution. They concluded that women who are exposed to levels of particulate matter exceeding federal standards were more likely to develop dementia. Fine particulate matter comes from a range of sources, including burning of fossil fuels.

Exposure to particulate matter (PM) in the ambient air and its interactions with APOE alleles may contribute to the acceleration of brain aging and the pathogenesis of Alzheimer’s disease (AD). Neurodegenerative effects of particulate air pollutants were examined in a US-wide cohort of older women from the Women’s Health Initiative Memory Study (WHIMS) and in experimental mouse models. Residing in places with fine PM exceeding EPA standards increased the risks for global cognitive decline and all-cause dementia respectively by 81 and 92%, with stronger adverse effects in APOE ε4/4 carriers. Female EFAD transgenic mice (5xFAD+/−/human APOE ε3 or ε4+/+) with 225 h exposure to urban nanosized PM (nPM) over 15 weeks showed increased cerebral β-amyloid by thioflavin S for fibrillary amyloid and by immunocytochemistry for Aβ deposits, both exacerbated by APOE ε4. Moreover, nPM exposure increased Aβ oligomers, caused selective atrophy of hippocampal CA1 neurites, and decreased the glutamate GluR1 subunit. Wildtype C57BL/6 female mice also showed nPM-induced CA1 atrophy and GluR1 decrease. In vitro nPM exposure of neuroblastoma cells (N2a-APP/swe) increased the pro-amyloidogenic processing of the amyloid precursor protein (APP). We suggest that airborne PM exposure promotes pathological brain aging in older women, with potentially a greater impact in ε4 carriers. The underlying mechanisms may involve increased cerebral Aβ production and selective changes in hippocampal CA1 neurons and glutamate receptor subunits. Top of page Introduction Environmental influences on Alzheimer’s disease (AD) and related dementias (ADRD) are poorly documented.1 Apolipoprotein E (APOE) ε4 and other loci identified by large GWAS account for less than 50% of heritable AD risk.2 Thus, attention is drawn to environmental risk factors, including common neurotoxins and their interactions with APOE and other genes.2, 3