Age-Related Hearing Loss, Cognitive Performance, and Metabolic Risk in Healthy Adults: A Seven-Year Longitudinal Study.

Objectives: Sensorineural hearing loss (presbycusis) affects up to half of the adults, is associated with cognitive decline. Whether this association reflects the cause, the consequence, or parallel processes driven by other factors remains unclear. Both presbycusis and cognition are linked to elevated metabolic risk, which in turn raises with age.

Changes in cerebral arterial pulsatility and hippocampal volume: a transcranial doppler ultrasonography study.

The physiological mechanisms of age-related cognitive decline remain unclear, in no small part due to the lack of longitudinal studies. Extant longitudinal studies focused on gross neuroanatomy and diffusion properties of the brain. We present herein a longitudinal analysis of changes in arterial pulsatility - a proxy for arterial stiffness - in two major cerebral arteries, middle cerebral and vertebral.

Lost Dynamics and the Dynamics of Loss: Longitudinal Compression of Brain Signal Variability is Coupled with Declines in Functional Integration and Cognitive Performance.

Reduced moment-to-moment blood oxygen level-dependent (BOLD) signal variability has been consistently linked to advanced age and poorer cognitive performance, showing potential as a functional marker of brain aging. To date, however, this promise has rested exclusively on cross-sectional comparisons. In a sample of 74 healthy adults, we provide the first longitudinal evidence linking individual differences in BOLD variability, age, and performance across multiple cognitive domains over an average period of 2.

Metabolic risk affects fluid intelligence changes in healthy adults.

Metabolic syndrome affects persons of all ages and has been associated with cognitive decline. In a sample of 221 healthy adults (18.57 to 85.

Regional brain shrinkage and change in cognitive performance over two years: The bidirectional influences of the brain and cognitive reserve factors.

We examined relationships between regional brain shrinkage and changes in cognitive performance, while taking into account the influence of chronological age, vascular risk, Apolipoprotein E variant and socioeconomic status. Regional brain volumes and cognitive performance were assessed in 167 healthy adults (age 19-79 at baseline), 90 of whom returned for the follow-up after two years. Brain volumes were measured in six regions of interest (ROIs): lateral prefrontal cortex (LPFC), prefrontal white matter (PFw), hippocampus (Hc), parahippocampal gyrus (PhG), cerebellar hemispheres (CbH), and primary visual cortex (VC), and cognitive performance was evaluated in three domains: episodic memory (EM), fluid intelligence (Gf), and vocabulary (V).

Volume of the hippocampal subfields in healthy adults: differential associations with age and a pro-inflammatory genetic variant.

The hippocampus is one of the most age-sensitive brain regions, yet the mechanisms of hippocampal shrinkage remain unclear. Recent studies suggest that hippocampal subfields are differentially vulnerable to aging and differentially sensitive to vascular risk. Promoters of inflammation are frequently proposed as major contributors to brain aging and vascular disease but their effects on hippocampal subfields are unknown.

Path Complexity in Virtual Water Maze Navigation: Differential Associations with Age, Sex, and Regional Brain Volume.

Studies of human navigation in virtual maze environments have consistently linked advanced age with greater distance traveled between the start and the goal and longer duration of the search. Observations of search path geometry suggest that routes taken by older adults may be unnecessarily complex and that excessive path complexity may be an indicator of cognitive difficulties experienced by older navigators. In a sample of healthy adults, we quantify search path complexity in a virtual Morris water maze with a novel method based on fractal dimensionality.

Volume of white matter hyperintensities in healthy adults: contribution of age, vascular risk factors, and inflammation-related genetic variants.

Aging is associated with appearance of white matter hyperintensities (WMH) on MRI scans. Vascular risk and inflammation, which increase with age, may contribute to white matter deterioration and proliferation of WMH. We investigated whether circulating biomarkers and genetic variants associated with elevated vascular risk and inflammation are associated with WMH volume in healthy adults (144 volunteers, 44-77 years of age).

Effects of age, genes, and pulse pressure on executive functions in healthy adults.

Executive functions (EF) evidence significant age-related declines, but the mechanisms underpinning those changes are unclear. In this study, we focus on two potential sources of variation: a physiological indicator of vascular health, and genetic variants related to vascular functions. In a sample of healthy adults (n=158, ages 18-81), we examine the effects of age, pulse pressure, and two polymorphisms (comt val158met and ace insertion/deletion) on working memory and cognitive flexibility.

Aging, vascular risk, and cognition: blood glucose, pulse pressure, and cognitive performance in healthy adults.

Advanced age is associated with decline in many areas of cognition as well as increased frequency of vascular disease. Well-described risk factors for vascular disease, such as diabetes and arterial hypertension, have been linked to cognitive deficits beyond those associated with aging. To examine whether vascular health indices such as fasting blood glucose levels and arterial pulse pressure can predict subtle deficits in age-sensitive abilities, the authors studied 104 healthy adults (ages 18 to 78) without diagnoses of diabetes or hypertension.

Brain-derived neurotrophic factor Val66Met and blood glucose: a synergistic effect on memory.

Age-related declines in episodic memory performance are frequently reported, but their mechanisms remain poorly understood. Although several genetic variants and vascular risk factors have been linked to mnemonic performance in general and age differences therein, it is unknown whether and how they modify age-related memory declines. To address that question, we investigated the effect of Brain-Derived Neurotrophic Factor (BDNF) Val66Met polymorphism that affects secretion of BDNF, and fasting blood glucose level (a vascular risk factor) on episodic memory in a sample of healthy volunteers (age 19-77).