Dataset Information

Age-related differences in correction behavior for unintended acceleration.

ABSTRACT: Although unintended acceleration caused by pedal misapplication is a cause of traffic accidents, fatal accidents may be avoided if drivers realize their error immediately and quickly correct how they are stepping on the pedal. This correction behavior may decline with age because the rate of fatal accidents is fairly higher for older adults than for younger adults. To investigate this possibility, the present study recruited older adults (n = 40, age range = 67-81 years) as well as younger adults (n = 40, age range = 18-32 years). In this study, they performed a pedal stepping task during which they were required to stop the simulated vehicle as quickly as possible when a red signal was presented on a monitor. During most trials, the vehicle decelerated/stopped when the brake pedal was applied in a normal manner. In a few trials, however, stepping on the brake pedal resulted in sudden acceleration of the vehicle (i.e., the occurrence of the unintended acceleration); when this occurred, the participants had to release the pedal and re-step on another pedal to decelerate/stop the vehicle as quickly as possible. We focused on the age-related differences of the reaction latencies during three time periods: from the appearance of the red signal on the screen until stepping on the pedal (Period 1), from stepping on the pedal until the release of the pedal (Period 2), and from the release of the pedal until re-stepping of another pedal (Period 3). The results showed that there was no age-related difference in the latency of Period 1, p = .771, whereas those of Periods 2 and 3 were longer for the older adults (ps < .001). The results suggest that there are age-related differences in error detection and correction abilities under unintended situations with foot pedal manipulation.

SUBMITTER: Hasegawa K

PROVIDER: S-EPMC7351190 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Age-related differences in correction behavior for unintended acceleration.

Hasegawa Kunihiro K Kimura Motohiro M Takeda Yuji Y

PloS one 20200710 7

Although unintended acceleration caused by pedal misapplication is a cause of traffic accidents, fatal accidents may be avoided if drivers realize their error immediately and quickly correct how they are stepping on the pedal. This correction behavior may decline with age because the rate of fatal accidents is fairly higher for older adults than for younger adults. To investigate this possibility, the present study recruited older adults (n = 40, age range = 67-81 years) as well as younger adult ...[more]

PMID: 32649720

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Project description:BackgroundAge-related eye diseases (AREDs) have become increasingly prevalent with the aging population, serving as the leading causes of visual impairment worldwide. Epigenetic clocks are generated based on DNA methylation (DNAm) levels and are considered one of the most promising predictors of biological age. This study aimed to investigate the bidirectional causal association between epigenetic clocks and common AREDs or glaucoma endophenotypes.MethodsInstrumental variables for epigenetic clocks, AREDs, and glaucoma endophenotypes were obtained from corresponding genome-wide association study data of European descent. Bidirectional two-sample Mendelian randomization (MR) was employed to explore the causal relationship between epigenetic clocks and AREDs or glaucoma endophenotypes. Multivariable MR (MVMR) was used to determine whether glaucoma endophenotypes mediated the association of epigenetic clocks with glaucoma. Multiple sensitivity analyses were conducted to confirm the robustness of MR estimates.ResultsThe results showed that an increased intrinsic epigenetic age acceleration (HorvathAge) was significantly associated with an increased risk of primary open-angle glaucoma (OR = 1.04, 95% CI 1.02 to 1.06, P = 6.1E-04). The epigenetic age acceleration (EEA) of HannumAge was related to a decreased risk of primary angle-closure glaucoma (OR = 0.92, 95% CI 0.86 to 0.99, P = 0.035). Reverse MR analysis showed that age-related cataract was linked to decreased HannumAge (β = -0.190 year, 95% CI -0.374 to -0.008, P = 0.041). The EEA of HannumAge (β = -0.85 μm, 95% CI -1.57 to -0.14, P = 0.019) and HorvathAge (β = -0.63 μm, 95% CI -1.18 to -0.08, P = 0.024) were associated with decreased central corneal thickness (CCT). PhenoAge was related to an increased retinal nerve fiber layer thickness (β = 0.06 μm, 95% CI 0.01 to 0.11, P = 0.027). MVMR analysis found no mediation effect of CCT in the association of HannumAge and HorvathAge with glaucoma. DNAm-based granulocyte proportions were significantly associated with presbyopia, rhegmatogenous retinal detachment, and intraocular pressure (P < 0.05). DNAm-based plasminogen activator inhibitor-1 levels were significantly related to age-related macular degeneration and intraocular pressure (P < 0.05).ConclusionThe present study revealed a causal association between epigenetic clocks and AREDs. More research is warranted to clarify the potential mechanisms of the biological aging process in AREDs.

Project description:Alzheimer's disease is characterized by the presence of amyloid-β and tau deposition in the brain, hippocampal atrophy and increased rates of hippocampal atrophy over time. Another protein, TAR DNA binding protein 43 (TDP-43) has been identified in up to 75% of cases of Alzheimer's disease. TDP-43, tau and amyloid-β have all been linked to hippocampal atrophy. TDP-43 and tau have also been linked to hippocampal atrophy in cases of primary age-related tauopathy, a pathological entity with features that strongly overlap with those of Alzheimer's disease. At present, it is unclear whether and how TDP-43 and tau are associated with early or late hippocampal atrophy in Alzheimer's disease and primary age-related tauopathy, whether either protein is also associated with faster rates of atrophy of other brain regions and whether there is evidence for protein-associated acceleration/deceleration of atrophy rates. We therefore aimed to model how these proteins, particularly TDP-43, influence non-linear trajectories of hippocampal and neocortical atrophy in Alzheimer's disease and primary age-related tauopathy. In this longitudinal retrospective study, 557 autopsied cases with Alzheimer's disease neuropathological changes with 1638 ante-mortem volumetric head MRI scans spanning 1.0-16.8 years of disease duration prior to death were analysed. TDP-43 and Braak neurofibrillary tangle pathological staging schemes were constructed, and hippocampal and neocortical (inferior temporal and middle frontal) brain volumes determined using longitudinal FreeSurfer. Bayesian bivariate-outcome hierarchical models were utilized to estimate associations between proteins and volume, early rate of atrophy and acceleration in atrophy rates across brain regions. High TDP-43 stage was associated with smaller cross-sectional brain volumes, faster rates of brain atrophy and acceleration of atrophy rates, more than a decade prior to death, with deceleration occurring closer to death. Stronger associations were observed with hippocampus compared to temporal and frontal neocortex. Conversely, low TDP-43 stage was associated with slower early rates but later acceleration. This later acceleration was associated with high Braak neurofibrillary tangle stage. Somewhat similar, but less striking, findings were observed between TDP-43 and neocortical rates. Braak stage appeared to have stronger associations with neocortex compared to TDP-43. The association between TDP-43 and brain atrophy occurred slightly later in time (∼3 years) in cases of primary age-related tauopathy compared to Alzheimer's disease. The results suggest that TDP-43 and tau have different contributions to acceleration and deceleration of brain atrophy rates over time in both Alzheimer's disease and primary age-related tauopathy.

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Age-related differences in correction behavior for unintended acceleration.

Publications

Age-related differences in correction behavior for unintended acceleration.

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