The brain is a major target of sex steroids, yet relatively little is known about how these hormones shape brain function at the human cognitive neuroscience level.

Cognitive neuroscience of aging studies traditionally target participants age 65 and older. However, converging preclinical and human evidence indicates that the decline in ovarian estradiol production during the menopausal transition may play a mechanistic role in neuronal changes that occur even earlier in the aging process.

Mouse models demonstrate that reduced telomerase activity and telomere loss have widespread consequences on neurodegeneration, including restricted neurogenesis and atrophy of white matter tracts, but there is limited evidence linking TL to age-related grey and white matter deficits in humans. 

Capitalizing on a 50-year neuroimaging follow-up study of a prenatal cohort led by Jill Goldstein (Harvard Medical School), we are collaborating with the Goldstein Lab to investigate whether in utero exposures accelerate chromosomal and neural indices of aging.