Judi Juvancic-Heltzel

Serum brain-derived neurotrophic factor is associated with cognitive function in healthy older adults.

Cognitive decline is common in older adults, even in the absence of significant medical or neurological conditions. Recent work implicates serum levels of brain-derived neurotrophic factor in age-related cognitive decline, though no study has directly examined this possibility. A total of 35 older adults without neurological history underwent fasting blood draw and completed a brief neuropsychological test battery during a single session. After adjusting for demographic and medical confounds, higher serum brain-derived neurotrophic factor levels were associated with better performance on the Mini-Mental State Examination (r = .36) and short form of the Boston Naming Test (r = .39). These findings extend work from Alzheimer disease and vascular dementia samples and indicate that higher brain-derived neurotrophic factor levels are associated with better neuropsychological function in healthy older adults. The exact mechanisms for this relationship are unknown and require further examination.

Serum leptin levels are associated with cognitive function in older adults

Recent work suggests that leptin, a circulating adipokinine hormone, might contribute to age-related cognitive decline. The present study investigated the relationship between serum leptin levels and cognitive function in older adults. Thirty-five older adults (73.69+/-6.62 years of age) without significant neurologic or psychiatric history completed a fasting blood draw and a brief neuropsychological test battery. Partial correlations adjusting for demographic and medical conditions showed that higher leptin levels were associated with poorer performance on Trail Making Test B (r = .46, p = .01). These findings indicate that serum leptin levels are negatively associated with speeded executive function in older adults without significant neurological or psychiatric conditions. The mechanisms for this relationship are unknown and require further examination. Such studies may provide key insight into the mechanisms of age-related cognitive decline and identify possible interventions.

The Influence of Ethnicity on Thermoregulation After Acute Cold Exposure

Abstract Objective.—It is well established that a combination of factors, including ethnicity, may influence an individuals response to cold stress. Previous work from our laboratory has demonstrated that when faced with a cold challenge, there is a similar response in heat production between Caucasian (CAU) and African American (AA) individuals that is accompanied by a differential response in core temperature. The objective of this study was to evaluate the influence of ethnicity (CAU vs AA) on the thermoregulatory response after acute cold exposure (ACE-REC, 25°C air). Methods.—Five AA males (20.8 ± 0.5 years) and 10 CAU males (25.6±4.9 years) underwent pre-experimental testing to determine Vo2max (AA = 37.2 ± 0.1 mL·kg−1·min−1, CAU = 44.3 ± 8.7 mL·kg−1·min−1) and body composition (AA = 14.6 ± 5.4%, CAU = 19.2 ± 5.0%). Participants underwent acute cold exposure that consisted of 120 minutes of exposure to 10°C air (ACE) followed by 120 minutes of recovery in 25°C air (ACE-REC). Rectal temperature (Tre) was measured via a rectal thermistor. Mean skin temperature (Tsk) was assessed with thermistors. Oxygen consumption (Vo2) was assessed via indirect open circuit spirometry. Rectal temperature and Tsk were measured continuously, and if Tre ≤ 35°C, testing was terminated. Results.—Analysis of variance for ACE-REC revealed a significant main effect for Tsk across time (P < .001), Tre across time (P < .001), and Vo2 across time (P < .001). In addition, a significant time × ethnicity interaction was revealed for Tre (P = .008), Tsk (P = .042), and Vo2 (P = .019) during ACE-REC. Conclusions.—Based on these data, there is a differential response between CAU and AA across time for Vo2, Tre, and Tsk ACE-REC.

Aβ40 is associated with cognitive function, body fat and physical fitness in healthy older adults

Abstract Primary objectives: Body composition and obesity-related lifestyle factors are associated with increased risk for Alzheimers disease (AD). Amyloid beta (Aβ) is a peptide integral in the pathogenesis of AD. Aβ has been shown to be related to body fat and exercise in younger adults; however, no study to date has examined the possible relationship among Aβ, body composition and fitness indices in older adults. Methods and procedures: Thirty-five older adults without significant neurological or psychiatric history, underwent fasting blood draw and completed cognitive testing and body composition and physical fitness assessments. Results: Partial correlations showed Aβ levels were inversely related to cognitive function, body fat and physical fitness measures. Conclusions: Findings indicate Aβ is associated with cognitive function, body fat and physical fitness in neurologically healthy older adults. Further work is needed to clarify possible mechanisms, particularly longitudinal studies.

Increased S100beta is associated with reduced cognitive function in healthy older adults.

Objectives: Vascular pathology is associated with reduced performance on neuropsychological tests, particularly in older adults. A likely explanation involves a disruption in the blood brain barrier (BBB). Work from clinical samples show alterations in BBB function is associated with cognitive dysfunction on testing, though no study has examined this possibility in healthy older adults. Materials and Methods: 35 older adults, without significant neurological or psychiatric history, underwent fasting blood draw and neuropsychological testing. Serum levels of S100β were quantified to provide a measure of BBB function. Results: Partial correlations showed S100β levels were inversely related to performance in multiple cognitive domains, including memory (r = 0.43, p = 0.02), psychomotor speed and visual attention (r = 0.37, p = 0.05), and working memory (r = –0.48, p = 0.008). Conclusions: Findings indicate that increased S100β levels are associated with poorer cognitive function in neurologically healthy older adults, implicating BBB function in age-related cognitive decline. Further work is needed to clarify possible mechanisms, particularly longitudinal studies that involve neuroimaging.

LIGHT TO MODERATE ALCOHOL CONSUMPTION IS ASSOCIATED WITH S100β AND AMYLOID BETA LEVELS IN HEALTHY OLDER ADULTS

Heavy alcohol consumption has been associated with several adverse neurocognitive outcomes in older adults, though little is known about lower consumption levels. No study has investigated the associations between S100β and amyloid beta (Aβ) serum levels (biomarkers that provide evidence of neurological pathology) and light to moderate alcohol consumption in healthy older adults without neurological conditions. Thirty-five healthy older adults underwent neuropsychological testing and fasting blood draw with subsequent serum S100β and Aβ 1–40 level quantification. Increased S100β levels were associated with increased frequency of alcohol consumption and increased total monthly consumption of alcohol. Increased Aβ levels were associated with increased quantity of alcohol consumption. Further work investigating possible mechanisms is needed, particularly longitudinal studies and studies employing neuroimaging.

Troponin and S100β are associated with depression in healthy older adults

Objectives: Depression has a significant impact on the functioning of older adults and often precedes cognitive decline or dementia. The current study examines the association between biomarkers related to neurocognitive outcome and depression in this population. Method: Thirty-five older adults without significant neurological or psychiatric history underwent fasting blood draw and psychological testing. Self-reported measures of current and history of depression and assays for brain-derived neurotrophic factor, S100-beta, amyloid beta, and troponin were analyzed. Results: Troponin levels were found to be inversely related to current depression (r = −0.35, p = 0.03), while individuals who reported having a past history of depression had significantly higher levels of S100β than those who did not report this (t (33) = −2.08, p < 0.05). Conclusion: The current study shows some support for the association of neurocognitive biomarkers to depression, though the mechanisms for these relationships are unclear and warrant further investigation.