Jennifer Freeman
Purdue University, IN·Neuroscience
Exposure to chemicals early in life may leave lasting damage in the brain that shows up as disease decades later. The lab studies two such exposures: PFAS, the long-lasting "forever chemicals" found in many products, and lead (Pb).
- Fields
Neuroscience
Pharmacology
Genetics
- Topics
neurotoxicology
per- and polyfluoroalkyl substances
forever chemicals
- Grants
- 2 known grants, through Mar 2029
What they work on
- Compare the immediate effects of developmental exposure to legacy PFOA and replacement PFAS (PFBA, GenX) on dopamine neurons, using zebrafish and human iPSC-derived dopamine neurons.
- Determine whether early PFAS exposure leaves neurons more vulnerable later to known neurotoxins, measured by cell survival and synuclein aggregate buildup, and record calcium activity inside cells and across networks to find driving mechanisms.
- Explore interventions that normalize calcium balance and restore neuronal plasticity in neurons disrupted by developmental PFAS exposure.
- Test whether developmental lead exposure combined with mutation in the Alzheimer's risk gene SORL1 increases protein aggregation in human iPSC-derived cortical neurons and zebrafish.
- Define epigenetic changes that regulate NMDAR and AMPAR glutamate receptor genes, and the post-synapse structural changes behind AD-like phenotypes, using time-course sequencing and imaging.
More about the research
It focuses on how developmental exposure changes neurons and raises the risk of neurodegenerative disease. Both projects pair zebrafish, small fish whose fast-developing, transparent embryos make them a useful animal model, with human neurons grown from induced pluripotent stem cells (hiPSCs, adult cells reprogrammed into a stem-cell state).
Why it matters
Many people are exposed to PFAS and lead, and newer replacement PFAS have unknown long-term effects on the brain. Comparing their neurotoxicity could inform chemical safety decisions and regulation. Showing how early lead exposure combined with the Alzheimer's risk gene SORL1 speeds up AD-like changes may reveal molecular targets for reducing neurodegeneration risk linked to environmental exposures. Both lines of work could inform efforts to lower the risk of Parkinson's-type and Alzheimer's-type disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Lilia Iakoucheva
University of California-San Diego, CA·Neuroscience
Measure how different doses of PFAS chemicals affect the division, cell cycle and survival of human neural progenitor cells derived from induced pluripotent stem cells.
Charleen T Chu
University of Pittsburgh, PA·Neuroscience
Test whether loss of PINK1, a mitochondrial enzyme, impairs the transport of mitochondria into dendrites, using molecular genetic manipulations in Pink1-knockout mouse neurons and patient iPSC-derived cortical neurons.
Diane Re
Columbia University, NY·Neuroscience
Measure levels of potentially neurotoxic metals such as manganese, nickel, chromium and lead in aerosol from several popular e-cigarettes run under different conditions and with e-liquids that differ in flavor and nicotine content.
The school
Purdue University: 43 labs on PI Pages, $932M a year on research, 833 research doctorates a year.
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