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Amy E. Pinkham

Possible papers associated with this exact author name in Arrow. This page groups case-insensitive exact name matches and is not a full identity disambiguation profile.

2 papers
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2

YNICL Journal 2018 Journal Article

Hippocampal metabolites in asthma and their implications for cognitive function

  • Juliet L. Kroll
  • Ashton M. Steele
  • Amy E. Pinkham
  • Changho Choi
  • David A. Khan
  • Sheenal V. Patel
  • Justin R. Chen
  • Sina Aslan

Emerging research indicates that individuals with asthma have an increased risk of cognitive impairment, yet the associations of asthma with neural correlates of memory remain relatively unknown. The hippocampus is the predominant neural structure involved in memory, and alterations in the hippocampal metabolic profile are observed in individuals with mild cognitive impairment. We therefore hypothesized that individuals with asthma may have altered hippocampal metabolites compared to healthy controls. Structural magnetic resonance imaging (sMRI) and proton magnetic resonance spectroscopy (1H-MRS) were used to compare hippocampal volume and metabolites of otherwise healthy adults with and without asthma (N = 40), and to study the association of these measures with cognitive function and asthma-related variables. Participants underwent 3-Tesla sMRI and 1H-MRS, with the volume of interest placed in the left hippocampus to measure levels of N-acetylaspartate (NAA), glutamate (Glu), creatine (Cr), and myo-inositol (MI), as indicators of neuronal viability, cellular activity, cellular energy reserve, as well as glial activation. Individuals with asthma had lower hippocampal NAA compared to healthy controls. For all participants, poorer cognitive function was associated with reduced NAA and Glu. For individuals with asthma, poorer cognitive function was associated with reduced disease control. Additionally, short-acting rescue bronchodilator use was associated with significantly lower NAA, and Glu, whereas inhaled corticosteroid use was related to significantly higher Cr and in tendency higher NAA and Glu. All findings controlled for left hippocampal volume, which was not different between groups. These findings highlight that asthma and/or its treatment may affect hippocampal chemistry. It is possible that the observed reductions in hippocampal metabolites in younger individuals with asthma may precede cognitive and hippocampal structural deficits observed in older individuals with asthma.

YNIMG Journal 2014 Journal Article

Age-related increase of resting metabolic rate in the human brain

  • Shin-Lei Peng
  • Julie A. Dumas
  • Denise C. Park
  • Peiying Liu
  • Francesca M. Filbey
  • Carrie J. McAdams
  • Amy E. Pinkham
  • Bryon Adinoff

With age, many aspects of the brain structure undergo a pronounced decline, yet individuals generally function well until advanced old age. There appear to be several compensatory mechanisms in brain aging, but their precise nature is not well characterized. Here we provide evidence that the brain of older adults expends more energy when compared to younger adults, as manifested by an age-related increase (P=0. 03) in cerebral metabolic rate of oxygen (CMRO2) (N=118, men=56, ages 18 to 74). We further showed that, before the mean menopausal age of 51years old, female and male groups have similar rates of CMRO2 increase (P=0. 015) and there was no interaction between age and sex effects (P=0. 85). However, when using data from the entire age range, women have a slower rate of CMRO2 change when compared to men (P<0. 001 for age×sex interaction term). Thus, menopause and estrogen level may have played a role in this sex difference. Our data also revealed a possible circadian rhythm of CMRO2 in that brain metabolic rate is greater at noon than in the morning (P=0. 02). This study reveals a potential neurobiological mechanism for age-related compensation in brain function and also suggests a sex-difference in its temporal pattern.