This was in the news, so I tracked it down. More evidence that PM2.5 pollution and E4s don't mix well. Another reason to work towards cleaner air. Maybe we should be cooperating with local clean air boards or other efforts to lower PM2.5 pollution.
It seems to be a real, and significant risk to E4s.Hallmarks of Alzheimer disease are evolving relentlessly in Metropolitan
Mexico City infants, children and young adults. APOE4 carriers have higher
suicide risk and higher odds of reaching NFT stage V at ≤40 years of agehttps://doi.org/10.1016/j.envres.2018.03.023
Exposures to fine particulate matter (PM2.5) and ozone (O3) above USEPA standards are associated with
Alzheimer's disease (AD) risk. Metropolitan Mexico City (MMC) residents have life time exposures to PM2.5 and
O3 above USEPA standards. We investigated AD intra and extracellular protein aggregates and ultrastructural
neurovascular pathology in 203 MMC residents age 25.36 ± 9.23 y. Immunohistochemical methods were used
to identify AT8 hyperphosphorilated tau (Htau) and 4G8 (amyloid β 17-24). Primary outcomes: staging of Htau
and amyloid, per decade and cumulative PM2.5 (CPM2.5) above standard. Apolipoprotein E allele 4 (APOE4), age
and cause of death were secondary outcomes.
Subcortical pretangle stage b was identified in an 11month old baby. Cortical tau pre-tangles, neurofibrillary
tangles (NFT) Stages I-II, amyloid phases 1–2, Htau in substantia nigrae, auditory, oculomotor, trigeminal and
autonomic systems were identified by the 2nd decade. Progression to NFT stages III-V was present in 24.8% of
30–40 y old subjects. APOE4 carriers have 4.92 times higher suicide odds (p=0.0006), and 23.6 times higher
odds of NFT V (p < 0.0001) v APOE4 non-carriers having similar CPM2.5 exposure and age. Age (p=0.0062)
and CPM2.5 (p=0.0178) were significant for developing NFT V. Combustion-derived nanoparticles were associated
with early and progressive damage to the neurovascular unit. Alzheimer's disease starting in the
brainstem of young children and affecting 99.5% of young urbanites is a serious health crisis. Air pollution
control should be prioritised. Childhood relentless Htau makes a fundamental target for neuroprotective interventions
and the first two decades are critical. We recommend the concept of preclinical AD be revised and
emphasize the need to define paediatric environmental, nutritional, metabolic and genetic risk factor interactions
of paramount importance to prevent AD. AD evolving from childhood is threating the wellbeing of our
children and future generations.
Concerned, but hopeful. Introverted, but will talk about science.