Post-Laramide, Eocene epeirogeny in central Colorado—The result of a mantle drip?

The Southern Rocky Mountains first rose during the Laramide Orogeny (ca. 75–45 Ma), but today's mountains and adjacent Great Plains owe their current height to later epeirogenic surface uplift. When and why epeirogeny affected the region are controversial. Sedimentation histories in two central Colorado basins, the South Park–High Park and Denver basins, shifted at 56–54 Ma from an orogenic to an epeirogenic pattern, suggesting central Colorado experienced epeirogeny at that time. To interrogate that hypothesis, we analyzed thermal histories for seven samples from central Colorado's Arkansas Hills and High Park using thermochronometers with closure temperatures below ~180 °C, enabling us to track sample exhumation from ~5–7 km depth. Three samples are from the Cretaceous Whitehorn pluton, and four are Precambrian granitoids. All zircon and titanite (U-Th)/He dates (ZHe and THe) and one apatite fission-track (AFT) date are similar to the 67 Ma pluton emplacement age. Whitehorn dates using the lower-temperature apatite (U-Th)/He (AHe) thermochronometer are 55–41 Ma. These data require two exhumation episodes, one ca. 67–60 Ma, the second beginning at 54–46 Ma. The pluton reached the surface by 37 Ma, based on the age of volcanic tuff filling a pluton-cutting paleovalley. The Precambrian samples do not further refine this thermal history owing to the comparatively higher He closure temperature of their more radiation-damaged apatite. Laramide crustal shortening caused 67–60 Ma exhumation. Arkansas Hills shortening ended before 67 Ma, so shortening could not have caused the exhumation event that began 54–46 Ma; thermochronology supports the Eocene epeirogeny hypothesis. Epeirogeny affected >2.0 × 104 km2, from the Sawatch Range to the Denver Basin. We attribute epeirogeny to an Eocene mantle drip that likely triggered subsequent drips, causing younger exhumation events in adjacent areas

Cenozoic Exhumation Across the High Plains of Southeastern Colorado from (U-Th)/He Thermochronology

Colorado’s High Plains stand at anomalously high elevations (~1300–2100 m) for their continental interior setting, but when and why this region became elevated is poorly understood. The Cenozoic history of the High Plains is also likely linked with that of the Rocky Mountains, where the timing and cause(s) of uplift are similarly debated. We present apatite (U-Th)/He (AHe) data for 10 samples from Tertiary intrusives along a ~200 km west-to-east transect across the High Plains of southeastern Colorado to constrain the timing of exhumation and to gain insight into when and why regional elevation gain occurred. Mean sample AHe dates for the ~24–22 Ma East Spanish Peak pluton and associated radial dikes from the westernmost High Plains are 18.8 ± 1.4 to 14.1 ± 1.7 Ma, recording substantial postemplacement erosion. AHe results for the mafic to ultramafic Apishapa Dikes (oldest ~37 Ma, youngest ~14 Ma) located ~20–40 km farther north and east on the High Plains range from 12.0 ± 1.4 to 6.2 ± 1.9 Ma, documenting continued exhumation on the western High Plains during the ~12–5 Ma deposition of the Ogallala Formation farther east and suggesting that the western limit of Ogallala deposition was east of the Apishapa Dikes. In far southeastern Colorado, the Two Buttes lamprophyre was emplaced at 36.8 ± 0.4 Ma and yields a Late Oligocene AHe date of 27.1 ± 4 Ma. Here, the Ogallala Formation unconformably overlies Two Buttes, indicating that the regional ~12 Ma age for the base of the Ogallala is a minimum age for the exposure of the pluton at the surface. The AHe data presented here document that kilometer-scale erosion affected all of the southeastern Colorado High Plains in Oligo-Miocene time. While exhumation can have multiple possible causes, we favor contemporaneous surface uplift capable of elevating the region to modern heights

Cenozoic Exhumation Across the High Plains of Southeastern Colorado from (U-Th)/He Thermochronology

Colorado&rsquo;s High Plains stand at anomalously high elevations (~1300&ndash;2100 m) for their continental interior setting, but when and why this region became elevated is poorly understood. The Cenozoic history of the High Plains is also likely linked with that of the Rocky Mountains, where the timing and cause(s) of uplift are similarly debated. We present apatite (U-Th)/He (AHe) data for 10 samples from Tertiary intrusives along a ~200 km west-to-east transect across the High Plains of southeastern Colorado to constrain the timing of exhumation and to gain insight into when and why regional elevation gain occurred. Mean sample AHe dates for the ~24&ndash;22 Ma East Spanish Peak pluton and associated radial dikes from the westernmost High Plains are 18.8 &plusmn; 1.4 to 14.1 &plusmn; 1.7 Ma, recording substantial postemplacement erosion. AHe results for the mafic to ultramafic Apishapa Dikes (oldest ~37 Ma, youngest ~14 Ma) located ~20&ndash;40 km farther north and east on the High Plains range from 12.0 &plusmn; 1.4 to 6.2 &plusmn; 1.9 Ma, documenting continued exhumation on the western High Plains during the ~12&ndash;5 Ma deposition of the Ogallala Formation farther east and suggesting that the western limit of Ogallala deposition was east of the Apishapa Dikes. In far southeastern Colorado, the Two Buttes lamprophyre was emplaced at 36.8 &plusmn; 0.4 Ma and yields a Late Oligocene AHe date of 27.1 &plusmn; 4 Ma. Here, the Ogallala Formation unconformably overlies Two Buttes, indicating that the regional ~12 Ma age for the base of the Ogallala is a minimum age for the exposure of the pluton at the surface. The AHe data presented here document that kilometer-scale erosion affected all of the southeastern Colorado High Plains in Oligo-Miocene time. While exhumation can have multiple possible causes, we favor contemporaneous surface uplift capable of elevating the region to modern heights. &nbsp;</p

Physical activity, physical function, and incident dementia in elderly men: The Honolulu-Asia Aging Study

Background. Although evidence is accumulating for a protective effect of late life physical activity on the risk of dementia, the findings are inconsistent, especially in men. We examined the association of late life physical activity and the modifying effect of physical function with future risk of dementia in a well-characterized cohort of elderly men participating in the Honolulu-Asia Aging Study (HAAS). Methods. Physical activity by self-report and performance-based physical function was assessed in 2263 men aged 71-92 years without dementia at the baseline examination of the HAAS in 1991-1993. Follow-up for incident dementia occurred at repeat examinations conducted in 1994-1996 and 1997-1999. Analyses were based on Cox proportional hazards models with adjustment for potential confounders, including age, baseline cognitive function, education, and apolipoprotein E genotype. Results. There were 173 incident cases of dementia with a mean follow-up of 6.1 years. Although the incidence of dementia tended to decline with increasing physical activity and function, there was a significant interaction between the latter two factors on dementia risk (p = .022). For men with low physical function, high levels of physical activity were associated with half the risk of dementia versus men who were the least active (hazard ratio [HR], 0.50; 95% confidence interval [CI], 0.28-0.89), with a moderate level of physical activity also providing a protective effect (HR, 0.57; 95% CI, 0.32-0.99). Risk of dementia and Alzheimer's disease declined significantly with increasing physical activity. Findings persisted after age and risk factor adjustment. Similar associations were absent in men with moderate and high physical function. Conclusions. In elderly men with poor physical function, increasing general physical activity may potentially confer a protective effect or delay the onset for dementia. Copyright 2008 by The Gerontological Society of America

Midlife milk consumption and substantia nigra neuron density at death

ObjectiveTo examine the relationship between midlife milk intake and Parkinson disease (PD) incidence through associations with substantia nigra (SN) neuron density and organochlorine pesticide exposure in decedent brains from the Honolulu-Asia Aging Study.MethodsMilk intake data were collected from 1965 to 1968 in 449 men aged 45-68 years with postmortem examinations from 1992 to 2004. Neuron density (count/mm(2)) was measured in quadrants from a transverse section of the SN. Additional measures included brain residues of heptachlor epoxide, an organochlorine pesticide found at excessively high levels in the milk supply in Hawaii in the early 1980s.ResultsNeuron density was lowest in nonsmoking decedents who consumed high amounts of milk (&gt;16 oz/d). After removing cases of PD and dementia with Lewy bodies, adjusted neuron density in all but the dorsomedial quadrant was 41.5% lower for milk intake &gt;16 oz/d vs intake that was less (95% confidence interval 22.7%-55.7%, p &lt; 0.001). Among those who drank the most milk, residues of heptachlor epoxide were found in 9 of 10 brains as compared to 63.4% (26/41) for those who consumed no milk (p = 0.017). For those who were ever smokers, an association between milk intake and neuron density was absent.ConclusionsMilk intake is associated with SN neuron loss in decedent brains unaffected by PD. Whether contamination of milk with organochlorine pesticides has a role in SN neurodegeneration warrants further study

Midlife milk consumption and substantia nigra neuron density at death

OBJECTIVE: To examine the relationship between midlife milk intake and Parkinson disease (PD) incidence through associations with substantia nigra (SN) neuron density and organochlorine pesticide exposure in decedent brains from the Honolulu-Asia Aging Study. METHODS: Milk intake data were collected from 1965 to 1968 in 449 men aged 45–68 years with postmortem examinations from 1992 to 2004. Neuron density (count/mm(2)) was measured in quadrants from a transverse section of the SN. Additional measures included brain residues of heptachlor epoxide, an organochlorine pesticide found at excessively high levels in the milk supply in Hawaii in the early 1980s. RESULTS: Neuron density was lowest in nonsmoking decedents who consumed high amounts of milk (>16 oz/d). After removing cases of PD and dementia with Lewy bodies, adjusted neuron density in all but the dorsomedial quadrant was 41.5% lower for milk intake >16 oz/d vs intake that was less (95% confidence interval 22.7%–55.7%, p < 0.001). Among those who drank the most milk, residues of heptachlor epoxide were found in 9 of 10 brains as compared to 63.4% (26/41) for those who consumed no milk (p = 0.017). For those who were ever smokers, an association between milk intake and neuron density was absent. CONCLUSIONS: Milk intake is associated with SN neuron loss in decedent brains unaffected by PD. Whether contamination of milk with organochlorine pesticides has a role in SN neurodegeneration warrants further study

Excessive daytime sleepiness and topographic expansion of Lewy pathology.

ObjectiveWhile excessive daytime sleepiness (EDS) can predate the clinical diagnosis of Parkinson disease (PD), associations with underlying PD pathogenesis are unknown. Our objective is to determine if EDS is related to brain Lewy pathology (LP), a marker of PD pathogenesis, using clinical assessments of EDS with postmortem follow-up.MethodsIdentification of LP was based on staining for α-synuclein in multiple brain regions in a sample of 211 men. Data on EDS were collected at clinical examinations from 1991 to 1999 when participants were aged 72-97 years.ResultsAlthough EDS was more common in the presence vs absence of LP (p = 0.034), the association became stronger in neocortical regions. When LP was limited to the olfactory bulb, brainstem, and basal forebrain (Braak stages 1-4), frequency of EDS was 10% (4/40) vs 17.5% (20/114) in decedents without LP (p = 0.258). In contrast, compared to the absence of LP, EDS frequency doubled (36.7% [11/30], p = 0.023) when LP reached the anterior cingulate gyrus, insula mesocortex, and midfrontal, midtemporal, and inferior parietal neocortex (Braak stage 5). With further infiltration into the primary motor and sensory neocortices (Braak stage 6), EDS frequency increased threefold (51.9% [14/27], p &lt; 0.001). Findings were similar across sleep-related features and persisted after adjustment for age and other covariates, including the removal of PD and dementia with Lewy bodies.ConclusionsThe association between EDS and PD includes relationships with extensive topographic LP expansion. The neocortex could be especially vulnerable to adverse relationships between sleep disorders and aggregation of misfolded α-synuclein and LP formation

Association of brain heptachlor epoxide and other organochlorine compounds with lewy pathology

BackgroundOrganochlorine pesticides are associated with an increased risk of Parkinson's disease. A preliminary analysis from the Honolulu-Asia Aging Study suggested that heptachlor epoxide, a metabolite from an organochlorine pesticide extensively used in Hawaii, may be especially important. This was a cross sectional analysis to evaluate the association of heptachlor epoxide and other organochlorine compounds with Lewy pathology in an expanded survey of brain organochlorine residues from the longitudinal Honolulu-Asia Aging Study.MethodsOrganochlorines were measured in frozen occipital or temporal lobes in 705 brains using gas chromatography with mass spectrometry. Lewy pathology was identified using hematoxylin and eosin- and α-synuclein immunochemistry-stained sections from multiple brain regions.ResultsThe prevalence of Lewy pathology was nearly doubled in the presence versus the absence of heptachlor epoxide (30.1% versus 16.3%, P &lt; 0.001). Although associations with other compounds were weaker, hexachlorobenzene (P = 0.003) and α-chlordane (P = 0.007) were also related to Lewy pathology. Most of the latter associations, however, were a result of confounding from heptachlor epoxide. Neither compound was significantly related to Lewy pathology after adjustment for heptachlor epoxide. In contrast, the association of heptachlor epoxide with Lewy pathology remained significant after adjustments for hexachlorobenzene (P = 0.013) or α-chlordane (P = 0.005). Findings were unchanged after removal of cases of PD and adjustment for age and other characteristics.ConclusionsOrganochlorine pesticides are associated with the presence of Lewy pathology in the brain, even after exclusion of PD cases. Although most of the association is through heptachlor epoxide, the role of other organochlorine compounds is in need of clarification. © 2018 International Parkinson and Movement Disorder Society

Brain organochlorines and Lewy pathology: The Honolulu‐Asia aging study

Although organochlorines have been reported more frequently in Parkinson's disease (PD) brains than in controls, the association with brain Lewy pathology is unknown. Honolulu-Asia Aging Study (HAAS) participants, exposed to organochlorines from a variety of sources during midlife, represent a population well suited to determining the relationship of brain organochlorines with Lewy pathology in decedents from the longitudinal HAAS. The study design included the measurement of 21 organochlorine levels in frozen occipital lobe samples from HAAS decedents. Alpha-synuclein immunostaining performed on 225 brains was used to identify Lewy bodies and Lewy neurites. With the potential for spurious associations to appear between Lewy pathology and 17 organochlorine compounds found in at least 1 brain, initial assessments identified heptachlor epoxide isomer b, methoxychlor, and benzene hexachloride b as being most important. The prevalence of Lewy pathology was 75% (6 of 8) among brains with any 2 of the 3 compounds, 48.8% (79 of 162) among those with 1, and 32.7% (18 of 55) for those with neither (P = .007 test for trend). Although findings persisted after removing cases with PD and dementia with Lewy bodies and after adjustment for age at death, body mass index, pack-years of cigarette smoking, and coffee intake (P = .013), the results were insignificant when correcting for multiple testing. Although consistent with earlier accounts of an association between organochlorines and clinical PD, associations with Lewy pathology warrant further study