- Research papers on prediabetes discuss the condition of elevated blood sugar but the blood sugar is not high enough for it to be diagnosed as type 2 diabeties.
The association between long-term exposure to ambient air pollution and PD/AD has not been explored in large-scale epidemiologic studies, with the exception of three studies that examined the relationship between airborne metal exposures and PD and showed evidence suggestive of the harmful effects of manganese (; ) and mercury (). Moreover, although there is some evidence that air pollution may be involved in the initiation of neurodegeneration (, ), we propose that it might also be involved in disease progression, potentially by worsening intermediate processes such as oxidative stress, systemic inflammation, and neuroinflammation, and by accelerating, through these pathways, the occurrence of first hospital admission. , for instance, reported that both acute and chronic systemic inflammation are associated with an increase in cognitive decline among early AD patients.
Data analysis. Health models. We ran separate models for each outcome of interest, that is, PD, AD, and dementia, using the first available, either primary or secondary, hospitalization for these conditions. We fit time-varying Cox proportional hazards models separately for each city. City-wide annual PM2.5 concentrations were included as the time-varying exposure of interest, as well as a term for calendar year (linear). We employed the counting process extension of the model by to create multiple observations per subject, with each observation representing a single person-year of follow-up.
As a nation, our fear of losing our minds and memories outstrips our fear of any other terminal illness, according to a 2012 survey by the Marist Institute for Public Opinion.
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For comparability with other long-term PM2.5 studies (e.g., ) we also present our results per 5-μg/m3 increase (). We found no evidence of a non-linear relationship, as all observed associations by quartiles increased monotonically (results not shown).
We fit city-specific models to avoid confounding by factors that varied across cities. By also adjusting for calendar year, we estimated whether year-to-year variations in PM2.5 concentrations around their long-term city-specific trends were related to year-to-year variations in cause-specific admissions in each city. With this approach, we eliminated all confounding by covariates that varied across cities because this was a city-specific analysis, and by covariates whose long-term trends coincided with trends in PM2.5 within cities because those trends were removed. We assumed that year-to-year differences in PM2.5 concentrations around their city-specific trends were driven by year-to-year variations in the percent of time the city was downwind from more- or less-polluted areas and year-to-year variations in wind speed and inversions. Long-term changes in other exposures, such as changes in smoking rates and socioeconomic status, should be captured in the long-term trends, for which we adjusted. We think it is implausible that, for example, year-to-year variations in smoking rates around the long-term trend within a given city were correlated with year-to-year fluctuations in pollution concentrations driven by back trajectories or other such phenomena. Assuming this statement is true, our exposure variations were random with respect to other risk factors for admissions, and hence, our models should provide an unbiased estimate of the effects of PM2.5.
Further evidence of patients’ deficiencies in storage (i.e., consolidation) is provided by their severe impairments on recognition as well as on recall tasks and by their very limited improvement in acquisition over repeated learning trials. The numerous observations that Alzheimer’s patients tend to recall only the most recently presented stimuli (i.e., heightened recency effects) support the notion that these patients have great difficulty in transferring information from short- to long-term storage.
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Memory impairments, even in patients in the early stages of the disease, are apparent on clinical and experimental memory tasks that require the learning and retention of either verbal or nonverbal information over a series of trials. This severe anterograde amnesia appears to primarily result from a failure in consolidation that is mediated by damage to the hippocampus and entorhinal cortex, and neurotransmitter changes in the cholinergic system. This inability of Alzheimer’s patients to transform to-be-remembered information into a form suitable for long-term retention cannot be circumvented by effortful or elaborative processing at the time of acquisition. This contrasts with normal elderly, who have been shown to benefit from engaging in elaborative or semantic processing of information during the study phase of free recall tasks.
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