Ph.D., York University
Postdoc, Washington University
Research in my lab uses neuroimaging and behavioral methods to study age-related changes in neurocognitive pathways. We are also actively involved in the development of neuroimaging biomarkers of Alzheimer’s disease (AD) and cerebrovascular disease (CVD). This work is made possible through our affiliation with UK’s Sanders-Brown Center on Aging (SBCoA), one of the nation’s leading centers on aging. Much of our research relies on the dedicated research volunteers who are followed longitudinally at the SBCoA. Our neuroimaging approach is multimodal in nature, making use of functional techniques, such as fMRI and ASL, and structural methods such as volumetric measurement, white matter hyperintensity assessment and white matter microstructural measurement. Combining data from these different imaging modalities may help reflect the distributed set of structural and functional systems supporting cognition and how they change as a result of healthy aging compared to dementia.
Our work related to dementia is primarily focused on preclinical stages of AD. One aim in this line of work is to attempt to understand brain changes that may precede cognitive declines in the development of AD. For example, we are attempting to understand neural correlates of genetic and familial risk factors in preclinical AD. More recently, we have become interested in understanding how certain lifestyle variables (e.g., exercise, cognitive stimulation) may slow cognitive decline and brain aging. Growing data shows that certain factors appear improve the brain’s ability to cope with age-related neurodegenerative changes, mitigating its effects on cognition. A greater understanding about these potential cognitive reserve variables, and their neural bases, may help promote healthier lifestyles in aging and improve the sensitivity of early dementia diagnosis. In our previous work in this area, we have found that older adults who are aerobically fit appear to have stronger brain connectivity than their aerobically unfit peers. We have also found evidence from both functional and structural brain imaging suggesting that lifelong bilingualism may contribute to cognitive reserve in aging.
Zhu Z, Johnson NF,Kim C, Gold BT (2015). Reduced frontal cortex efficiency is associated with lower white matter integrity in aging. Cerebral Cortex 25, 138-146.
Gold BT, Zhu Z, Brown CA, Andersen AH, LaDu MJ, Tai L, Jicha GA, Kryscio RJ, Estus S, Nelson PT, Scheff SW, Abner E, Schmitt FA, Van Eldik LJ, & Smith CD (2014). White matter integrity is associated with CSF markers of AD in normal adults. Neurobiology of Aging 35, 2263-2271.
Gold BT, Kim C, Johnson NF, Kryscio RJ, & Smith CD (2013). Lifelong bilingualism maintains neural efficiency for cognitive control in aging. The Journal of Neuroscience 33: 387-396.
Gold BT, Johnson NF, Powell DK, Smith CD (2012). White matter integrity and vulnerability to Alzheimer's disease: Preliminary findings and future directions. BBA – Molecular Basis of Disease 1822: 416-422.
Johnson NF, Kim C, Clasey J, Bailey A, & Gold BT (2012). Cardiorespiratory Fitness is Positively Correlated with Cerebral White Matter Integrity in Healthy Seniors. Neuroimage 59:1514-1523.
Kim C, Johnson NF, Cilles SE, & Gold BT (2011). Common and distinct mechanisms of cognitive flexibility in prefrontal cortex. The Journal of Neuroscience 31: 4771-4779.
Gold BT, Powell DK, Xuan L, Jicha GA, & Smith CD (2010). Age-related slowing of task switching is associated with decreased integrity of frontoparietal white matter. Neurobiology of Aging 31: 512-522.
Martin SB, Smith CD,Collins HR, Schmitt FA, & Gold BT (2010). Evidence that volume of anterior medial temporal lobe is reduced in seniors destined for mild cognitive impairment. Neurobiology of Aging 31: 1099-1106.
Gold BT,Jiang Y, Jicha GA, & Smith CD (2010). Functional response in ventral temporal cortex differentiates mild cognitive impairment from normal aging. Human Brain Mapping 31: 1249-1259.