About

Kristen Baldwin currently serves as the Global Head of Talent Management and HR for Corporate Functions at Cencora, a Fortune 10 pharmaceutical distribution company. She has previously held the role of Chief People and Integration Officer at Selecta Biosciences and was a Senior Partner at CEO.works, a Human Capital consulting firm. Her experience includes leading HR for Bayer Pharmaceuticals Americas Regions, where she drove large-scale business transformation and culture initiatives, and serving as the Head of HR for Consumer Health North America at Bayer. Earlier in her career, Kristen worked at Otsuka Pharmaceutical Companies for seven years, supporting a large commercial leadership team and leading the transformation of Otsuka’s HR Operations function, including the implementation of Workday and SuccessFactors, as well as creating Talent Management processes and programs. She holds an MBA from Columbia Business School, is a certified Talent to Value Coach, and serves as a member of Columbia Business School’s Deming Center Advisory Board.

Research topics

• Biology
• Cell biology
• Genetics
• Neuroscience
• Computational biology

Selected publications

• Microglia-to-neuron signaling links <i>APOE4</i> and inflammation to enhanced neuronal lipid metabolism and network activity

  Proceedings of the National Academy of Sciences · 2025-09-08 · 12 citations

  articleOpen access

  Microglia regulate neuronal circuit plasticity. Disrupting their homeostatic function has detrimental effects on neuronal circuit health. Neuroinflammation contributes to the onset and progression of neurodegenerative diseases, including Alzheimer’s disease (AD), with several microglial activation genes linked to increased risk for these conditions. Inflammatory microglia alter neuronal excitability, inducing metabolic strain. Interestingly, expression of APOE4 , the strongest genetic risk factor for AD, affects both microglial activation and neuronal excitability, highlighting the interplay between lipid metabolism, inflammation, and neuronal function. It remains unclear how microglial inflammatory state is conveyed to neurons to affect circuit function and whether APOE4 expression alters this intercellular communication. Here, we use a reductionist model of human iPSC-derived microglial and neuronal monocultures to dissect how the APOE genotype in each cell type independently contributes to microglial regulation of neuronal activity during inflammation. Conditioned media (CM) from LPS-stimulated microglia increased neuronal network activity, assessed by calcium imaging, with APOE4 microglial CM driving greater neuronal activity than APOE3 CM. Both APOE3 and APOE4 neurons increase network activity in response to CM treatments, while APOE4 neurons uniquely increase presynaptic puncta in response to APOE4 microglial CM. CM-derived exosomes from LPS-stimulated microglia can mediate increases to network activity. Finally, increased network activity is accompanied by increased lipid droplet (LD) metabolism, and blocking LD metabolism abolishes network activity. These findings illuminate how microglia-to-neuron communication drives inflammation-induced changes in neuronal circuit function, demonstrate a role for neuronal LDs in network activity, and support a potential mechanism through which APOE4 increases neuronal excitability.

  PublisherOA PDFDOI

• Microglia-to-neuron signaling increases lipid droplet metabolism, enhancing neuronal network activity

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-08-03

  preprintOpen access

  Microglia regulate neuronal circuit plasticity. Disrupting their homeostatic function has detrimental effects on neuronal circuit health. Neuroinflammation contributes to the onset and progression of neurodegenerative diseases, including Alzheimers disease, with several microglial activation genes linked to increased risk for these conditions. Inflammatory microglia alter neuronal excitability, inducing metabolic strain. Interestingly, expression of APOE4, the strongest genetic risk factor for Alzheimers disease, affects both microglial activation and neuronal excitability, highlighting the interplay between lipid metabolism, inflammation, and neuronal function. It remains unclear how microglial inflammatory state is conveyed to neurons to affect circuit function and whether APOE4 expression alters this intercellular communication. Here, we use a reductionist model of human iPSC-derived microglial and neuronal monocultures to dissect how the APOE genotype in each cell-type independently contributes to microglial regulation of neuronal activity during inflammation. Conditioned media from LPS-stimulated microglia increased neuronal network activity, assessed by calcium imaging, with APOE4 microglial conditioned media driving higher neuronal firing rates than APOE3 conditioned media. Both APOE3 and APOE4 neurons increase network activity in response to conditioned media treatments, while APOE4 neurons uniquely increase presynaptic puncta with APOE4 microglial conditioned media. Conditioned media-derived exosomes from LPS-stimulated microglia can mediate increases to network activity. Lastly, increased network activity is accompanied by increased lipid droplet metabolism and blocking lipid droplet metabolism abolishes network activity. These findings illuminate how microglia-to-neuron communication drives inflammation-induced changes in neuronal circuit function, demonstrate a role for neuronal lipid droplets in network activity, and support a potential mechanism through which APOE4 increases neuronal excitability.

  PublisherOA PDFDOI

• Alpha-synuclein abundance and localization are regulated by the RNA-binding protein PUMILIO1

  Cell Reports · 2025-08-01 · 6 citations

  articleOpen access

  The protein α-synuclein, encoded by SNCA, accumulates in Parkinson's disease (PD) and other synucleinopathies for reasons that remain unclear. Here, we investigated whether SNCA is regulated in vivo by the RNA-binding protein PUM1. We establish that PUM1 binds to SNCA's 3' UTR in mouse and human cells. In induced neurons from patients with SNCA locus triplication, PUM1 mRNA levels are lower than in healthy controls, but increasing PUM1 normalizes both SNCA mRNA and α-synuclein protein levels, largely by suppressing the long 3' UTR SNCA isoform. In microfluidic chamber experiments, silencing PUM1 causes a redistribution of SNCA between the soma and axons. We also show that the previously described miR-7 regulation of SNCA mRNA requires PUM1. Lastly, we report finding several individuals with PD in clinical databases bearing variants in PUM1 that affect its RNA-binding ability. Understanding how RNA-binding proteins regulate α-synuclein could lead to viable new therapies for synucleinopathies.

  PublisherDOI

• Functional sensory circuits built from neurons of two species

  Cell · 2024-04-01 · 15 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Building functional circuits in multispecies brains

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-04-15 · 1 citations

  preprintOpen accessSenior authorCorresponding

  Abstract The genome is the ultimate architect of the brain. Its evolutionary variations build the neural circuits that endow each species with its innate senses and behaviors. A central question for neuroscience and translational medicine is whether neural circuits from two species can be made to function in an intact brain. Here, we establish genetic tools and use blastocyst complementation to selectively build and test interspecies neural circuits in rat-mouse brains. Despite ∼10-20 million years of evolution and prominent differences in brain size and cellular composition, rat pluripotent stem cells injected into mouse blastocysts widely populate and persist in the mouse brain. Unexpectedly, the mouse niche reprograms the birthdates of cortical and hippocampal rat neurons, where they also form synaptically active rat-mouse circuits. By genetically disabling host olfactory circuitry, we show that rat neurons restore synaptic information flow from the nose to the cortex. Rat neurons can also rescue a primal olfactory behavior (food-seeking), though less than mouse controls. By enabling a mouse to sense the world with rat neurons, we highlight the power of interspecies neural blastocyst complementation to uncover mechanisms of neural circuit development and evolution, and to inform efforts to rescue neural circuits affected by injury or disease.

  PublisherOA PDFDOI

• Rates of contributory de novo mutation in high and low-risk autism families

  Communications Biology · 2021-09-01 · 51 citations

  articleOpen access

  Autism arises in high and low-risk families. De novo mutation contributes to autism incidence in low-risk families as there is a higher incidence in the affected of the simplex families than in their unaffected siblings. But the extent of contribution in low-risk families cannot be determined solely from simplex families as they are a mixture of low and high-risk. The rate of de novo mutation in nearly pure populations of high-risk families, the multiplex families, has not previously been rigorously determined. Moreover, rates of de novo mutation have been underestimated from studies based on low resolution microarrays and whole exome sequencing. Here we report on findings from whole genome sequence (WGS) of both simplex families from the Simons Simplex Collection (SSC) and multiplex families from the Autism Genetic Resource Exchange (AGRE). After removing the multiplex samples with excessive cell-line genetic drift, we find that the contribution of de novo mutation in multiplex is significantly smaller than the contribution in simplex. We use WGS to provide high resolution CNV profiles and to analyze more than coding regions, and revise upward the rate in simplex autism due to an excess of de novo events targeting introns. Based on this study, we now estimate that de novo events contribute to 52-67% of cases of autism arising from low risk families, and 30-39% of cases of all autism.

  PublisherOA PDFDOI

• Genomic integrity of human induced pluripotent stem cells across nine studies in the NHLBI NextGen program

  Stem Cell Research · 2020-05-05 · 12 citations

  articleOpen access

  Human induced pluripotent stem cell (hiPSC) lines have previously been generated through the NHLBI sponsored NextGen program at nine individual study sites. Here, we examined the structural integrity of 506 hiPSC lines as determined by copy number variations (CNVs). We observed that 149 hiPSC lines acquired 258 CNVs relative to donor DNA. We identified six recurrent regions of CNVs on chromosomes 1, 2, 3, 16 and 20 that overlapped with cancer associated genes. Furthermore, the genes mapping to regions of acquired CNVs show an enrichment in cancer related biological processes (IL6 production) and signaling cascades (JNK cascade & NFκB cascade). The genomic region of instability on chr20 (chr20q11.2) includes transcriptomic signatures for cancer associated genes such as ID1, BCL2L1, TPX2, PDRG1 and HCK. Of these HCK shows statistically significant differential expression between carrier and non-carrier hiPSC lines. Overall, while a low level of genomic instability was observed in the NextGen generated hiPSC lines, the observation of structural instability in regions with known cancer associated genes substantiates the importance of systematic evaluation of genetic variations in hiPSCs before using them as disease/research models.

  PublisherDOI

• Mechanical activation of noncoding-RNA-mediated regulation of disease-associated phenotypes in human cardiomyocytes

  Nature Biomedical Engineering · 2019-01-28 · 41 citations

  articleOpen access
  PublisherOA PDFDOI

• Diverse reprogramming codes for neuronal identity

  Nature · 2018-05-01 · 113 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Transcriptional profiling of isogenic Friedreich ataxia induced pluripotent stem cell-derived neurons

  bioRxiv (Cold Spring Harbor Laboratory) · 2018-10-30

  preprintOpen access

  Abstract Friedreich ataxia (FRDA) is a rare childhood neurodegenerative disorder with no effective treatment. FRDA is caused by transcriptional silencing of the FXN gene and consequent loss of the essential mitochondrial protein frataxin. Based on the knowledge that a GAA•TTC repeat expansion in the first intron of FXN leads to heterochromatin formation and gene silencing, we have shown that members of the 2-aminobenzamide family of histone deacetylase inhibitors (HDACi) reproducibly increase FXN mRNA levels in induced pluripotent stem cell (iPSC)-derived FRDA neuronal cells and in peripheral blood mononuclear cells from patients treated with the drug in a phase I clinical trial. How the reduced expression of frataxin leads to neurological and other systemic symptoms in FRDA patients remains unclear. Similarly to other triplet repeat disorders, it is not known why only specific cells types are affected in the disease, primarily the large sensory neurons of the dorsal root ganglia and cardiomyocytes. The combination of iPSC technology and genome editing techniques offers the unique possibility of addressing these questions in a relevant cell model of the disease, without the confounding effect of different genetic backgrounds. We derived a set of isogenic iPSC lines that differ only in the length of the GAA•TTC repeats, using “scarless” gene-editing methods (helper-dependent adenovirus-mediated homologous recombination). To uncover the gene expression signature due to GAA•TTC repeat expansion in FRDA neuronal cells and the effect of HDACi on these changes, we performed transcriptomic analysis of iPSC-derived central nervous system (CNS) and isogenic sensory neurons by RNA sequencing. We find that multiple cellular pathways are commonly affected by the loss of frataxin in CNS and peripheral nervous system neurons and these changes are partially restored by HDACi treatment.

  PublisherOA PDFDOI

Recent grants

• NIH Grant U01HL107436

  NIH · $7.7M · 2017

• Defining a transcriptional periodic table of the human brain using reprogramming

  NIH · $7.2M · 2020–2023

• NIH Grant R01DC012592

  NIH · $2.3M · 2018

• Genome-wide investigation of somatic mutation in the developing and aging brain

  NIH · $3.4M · 2014–2021

Frequent coauthors

• Mark M. Davis

  Howard Hughes Medical Institute

  28 shared

• Philip A. Reay

  Stanford University

  25 shared

• Andrew G. Farr

  University of Washington

  25 shared

• Lawren C. Wu

  PCR Oncology

  25 shared

• Benjamin T. Throesch

  Scripps Research Institute

  17 shared

• Kiely N. James

  University of California, San Diego

  15 shared

• Alberto R. Rodriguez

  Scripps Research Institute

  14 shared

• Sergey Kupriyanov

  National Research Tomsk State University

  14 shared

Awards & honors

• Columbia SPS CUNY Fellowship
• Columbia HBCU Fellowship Program
• Deming Center Advisory Board