Dr. Eischeid is a board-certified neurologist and a clinical assistant professor in the Department of Neurology, Division of Movement Disorders at Stanford University School of Medicine. He specializes in the management of a wide range of neurological conditions. His focus is on movement disorders, including Parkinson’s disease, atypical parkinsonism, Huntington’s disease, ataxia, dystonia, and tremor. He has advanced training in botulinum toxin injections for dystonia and spasticity. Dr. Eischeid also delivers expertise in deep brain stimulation programming. With each patient, his goal is to safely and effectively relieve symptoms while improving quality of life.

Dr. Eischeid has been a presenter at the Stanford Alzheimer’s Disease Research Center Neuropathology Case Conference. He also has participated in meetings of the Movement Disorders Society and American Academy of Neurology.

Scholarship activities of Dr. Eischeid include writing peer-reviewed articles on topics such as the intracellular signaling that enables microglia to increase neurogenesis. His work has appeared in BMC Neuroscience, the Journal of Immunology, PLoS One, and elsewhere.

Among his honors, Dr. Eischeid received the Resident Fincham Award, given to a graduating neurology resident who best exemplifies the qualities of dedicated patient care and the highest level of collegiality. He was also named Administrative Chief Neurology Resident, an awarded position based on leadership qualities and academic performance. As a senior resident, he earned recognition as the “Best Resident On-Call.” Dr. Eischeid is a member of the American Academy of Neurology and Movement Disorders Society. He served on the Board of Directors of the Iowa Neurological Association. In his personal time, Dr. Eischeid has provided volunteer medical services at homeless shelters.

Clinical Focus

  • Neurology

Academic Appointments

Honors & Awards

  • Resident Fincham Award, University of Iowa Hospitals and Clinics (2019)
  • Administrative Chief Neurology Resident, University of Iowa Hospitals and Clinics (2018-2019)
  • Outstanding Undergraduate Research, Nebraska Academy of Science (2010)

Boards, Advisory Committees, Professional Organizations

  • Member, Movement Disorders Society (2017 - Present)
  • Member, American Academy of Neurology (2015 - Present)
  • Member, American Medical Association (2011 - Present)

Professional Education

  • Residency: University of Iowa Hospitals and Clinics (2019) IA
  • Fellowship: Stanford University Behavioral Neurology Fellowship (2020) CA
  • Board Certification: American Board of Psychiatry and Neurology, Neurology (2019)
  • Medical Education: University of Iowa Carver College of Medicine (2015) IA


All Publications

  • Microglia induce neurogenic protein expression in primary cortical cells by stimulating PI3K/AKT intracellular signaling in vitro. Molecular biology reports Lorenzen, K., Mathy, N. W., Whiteford, E. R., Eischeid, A., Chen, J., Behrens, M., Chen, X., Shibata, A. 2021


    Emerging evidence suggests that microglia can support neurogenesis. Little is known about the mechanisms by which microglia regulate the cortical environment and stimulate cortical neurogenesis. We used an in vitro co-culture model system to investigate the hypothesis that microglia respond to soluble signals from cortical cells, particularly following mechanical injury, to alter the cortical environment and promote cortical cell proliferation, differentiation, and survival. Analyses of cortical cell proliferation, cell death, neurogenic protein expression, and intracellular signaling were performed on uninjured and injured cortical cells in co-culture with microglial cell lines. Microglia soluble cues enhanced cortical cell viability and proliferation cortical cells. Co-culture of injured cortical cells with microglia significantly reduced cell death of cortical cells. Microglial co-culture significantly increased Nestin+and alpha-internexin+cortical cells. Multiplex ELISA and RT-PCR showed decreased pro-inflammatory cytokine production by microglia co-cultured with injured cortical cells. Inhibition of AKT phosphorylation in cortical cells blocked microglial-enhanced cortical cell viability and expression of neurogenic markers in vitro. This in vitro model system allows for assessment of the effect of microglial-derived soluble signals on cortical cell viability, proliferation, and stages of differentiation during homeostasis or following mechanical injury. These data suggest that microglia cells can downregulate inflammatory cytokine production following activation by mechanical injury to enhance proliferation of new cells capable of neurogenesis via activation of AKT intracellular signaling. Increasing our understanding of the mechanisms that drive microglial-enhanced cortical neurogenesis during homeostasis and following injury in vitro will provide useful information for future primary cell and in vivo studies.

    View details for DOI 10.1007/s11033-020-06092-0

    View details for PubMedID 33387198

  • Histone Deacetylases and NF-kappa B Signaling Coordinate Expression of CX3CL1 in Epithelial Cells in Response to Microbial Challenge by Suppressing miR-424 and miR-503 PLOS ONE Zhou, R., Gong, A., Chen, D., Miller, R. E., Eischeid, A. N., Chen, X. 2013; 8 (5): e65153


    The NF-kB pathway is key to epithelial immune defense and has been implicated in secretion of antimicrobial peptides, release of cytokines/chemokines to mobilize immune effector cells, and activation of adaptive immunity. The expression of many inflammatory genes following infection involves the remodeling of the chromatin structure. We reported here that histone deacetylases (HDACs) and NF-kB signaling coordinate expression of CX3CL1 in epithelial cells following Cryptosporidium parvum infection. Upregulation of CX3CL1 was detected in cultured human biliary epithelial cells following infection. Expression of miR-424 and miR-503 was downregulated, and was involved in the induction of CX3CL1 in infected cells. C. parvum infection suppressed transcription of the mir-424-503 gene in a NF-kB- and HDAC-dependent manner. Increased promoter recruitment of NF-kB p50 and HDACs, and decreased promoter H3 acetylation associated with the mir-424-503 gene were observed in infected cells. Upregulation of CX3CL1 in biliary epithelial cells and increased infiltration of CX3CR1(+) cells were detected during C. parvum infection in vivo. Induction of CX3CL1 and downregulation of miR-424 and miR-503 were also detected in epithelial cells in response to LPS stimulation. The above results indicate that HDACs and NF-kB signaling coordinate epithelial expression of CX3CL1 to promote mucosal antimicrobial defense through suppression of the mir-424-503 gene.

    View details for DOI 10.1371/journal.pone.0065153

    View details for Web of Science ID 000319733000122

    View details for PubMedID 23724129

    View details for PubMedCentralID PMC3665534

  • Col1A1 Production and Apoptotic Resistance in TGF-beta 1-Induced Epithelial-to-Mesenchymal Transition-Like Phenotype of 603B Cells PLOS ONE Liu, J., Eischeid, A. N., Chen, X. 2012; 7 (12): e51371


    Recent studies have suggested that proliferating cholangiocytes have an important role in the induction of fibrosis, either directly via epithelial-to-mesenchymal transition (EMT), or indirectly via activation of other liver cell types. Transforming growth factor beta 1 (TGF-β1), a critical fibrotic cytokine for hepatic fibrosis, is a potent EMT inducer. This study aimed to clarify the potential contributions of TGF-β1-induced EMT-like cholangiocyte phenotype to collagen production and cell survival of cholangiocytes in vitro. Mouse cholangiocytes (603B cells) were treated with TGF-β1 and EMT-like phenotype alterations were monitored by morphological changes and expression of EMT-associated genes. Alterations in Col1A1 gene, Col1A1-associated miR-29s, and pro-apoptotic genes were measured in TGF-β1-treated 603B cells. Snail1 knockdown was achieved using shRNA to evaluate the contribution of EMT-associated changes to Col1A1 production and cell survival. We found TGF-β1 treatment induced partial EMT-like phenotype transition in 603B cells in a Snail1-dependent manner. TGF-β1 also stimulated collagen α1(I) expression in 603B cells. However, this induction was not parallel to the EMT-like alterations and independent of Snail1 or miR-29 expression. Cells undergoing EMT-like changes showed a modest down-regulation of multiple pro-apoptotic genes and displayed resistance to TNF-α-induced apoptosis. TGF-β1-induced apoptosis resistance was attenuated in Snail1 knockdown 603B cells. TGF-β1-induced Col1A1 production seems to be independent of EMT-like transition and miR-29 expression. Nevertheless, TGF-β1-induced EMT may contribute to the increased survival capacity of cholangiocytes via modulating the expression of pro-apoptotic genes.

    View details for DOI 10.1371/journal.pone.0051371

    View details for Web of Science ID 000312064100108

    View details for PubMedID 23236489

    View details for PubMedCentralID PMC3517566

  • miR-17-5p targets the p300/CBP-associated factor and modulates androgen receptor transcriptional activity in cultured prostate cancer cells BMC CANCER Gong, A., Eischeid, A. N., Xiao, J., Zhao, J., Chen, D., Wang, Z., Young, C. F., Chen, X. 2012; 12: 492


    Androgen receptor (AR) signalling is critical to the initiation and progression of prostate cancer (PCa). Transcriptional activity of AR involves chromatin recruitment of co-activators, including the p300/CBP-associated factor (PCAF). Distinct miRNA expression profiles have been identified in PCa cells during the development and progression of the disease. Whether miRNAs regulate PCAF expression in PCa cells to regulate AR transcriptional activity is still unclear.Expression of PCAF was investigated in several PCa cell lines by qRT-PCR, Western blot, and immunocytochemistry. The effects of PCAF expression on AR-regulated transcriptional activity and cell growth in PCa cells were determined by chromatin immunoprecipitation, reporter gene construct analysis, and MTS assay. Targeting of PCAF by miR-17-5p was evaluated using the luciferase reporter assay.PCAF was upregulated in several PCa cell lines. Upregulation of PCAF promoted AR transcriptional activation and cell growth in cultured PCa cells. Expression of PCAF in PCa cells was associated with the downregulation of miR-17-5p. Targeting of the 3'-untranslated region of PCAF mRNA by miR-17-5p caused translational suppression and RNA degradation, and, consequently, modulation of AR transcriptional activity in PCa cells.PCAF is upregulated in cultured PCa cells, and upregulation of PCAF is associated with the downregulation of miR-17-5p. Targeting of PCAF by miR-17-5p modulates AR transcriptional activity and cell growth in cultured PCa cells.

    View details for DOI 10.1186/1471-2407-12-492

    View details for Web of Science ID 000312105700001

    View details for PubMedID 23095762

    View details for PubMedCentralID PMC3519561

  • miR-141 modulates androgen receptor transcriptional activity in human prostate cancer cells through targeting the small heterodimer partner protein PROSTATE Xiao, J., Gong, A., Eischeid, A. N., Chen, D., Deng, C., Young, C. F., Chen, X. 2012; 72 (14): 1514–22


    Aberrant expressions of microRNAs, including upregulation of miR-141, are closely associated with the tumorigenesis of prostate cancer (PCa). The orphan receptor small heterodimer partner (Shp) is a co-repressor to androgen receptor (AR) and represses AR-regulated transcriptional activity.Here, we investigated the correlation of Shp expression with the cellular level of miR-141 and its effects on AR transcriptional activity in non-malignant and malignant human prostate epithelial cell lines.We found that Shp was downregulated in multiple PCa cell lines. The mature form of miR-141 was upregulated in PCa cells. miR-141 could target 3'-untranslated region of Shp mRNA resulting in translational suppression and RNA degradation. Moreover, enforced expression of Shp or inhibition of miR-141 function by anti-miR-141 attenuated AR-regulated transcriptional activity in AR-responsive LNCaP cells. Phenethyl isothiocyanate, a natural constituent of many edible cruciferous vegetables, increased Shp expression, downregulated miR-141, and inhibited AR transcriptional activity in LNCaP cells.Shp is a target for miR-141 and it is downregulated in cultured human PCa cells with the involvement of upregulation of miR-141, which promotes AR transcriptional activity. Moreover, Shp and miR-141 could be targets for chemoprevention for PCa.

    View details for DOI 10.1002/pros.22501

    View details for Web of Science ID 000308091800003

    View details for PubMedID 22314666

  • miR-27b Targets KSRP to Coordinate TLR4-Mediated Epithelial Defense against Cryptosporidium parvum Infection PLOS PATHOGENS Zhou, R., Gong, A., Eischeid, A. N., Chen, X. 2012; 8 (5): e1002702


    Cryptosporidium is a protozoan parasite that infects the gastrointestinal epithelium and causes a diarrheal disease. Toll-like receptor (TLR)- and NF-κB-mediated immune responses from epithelial cells, such as production of antimicrobial peptides and generation of reactive nitrogen species, are important components of the host's defense against cryptosporidial infection. Here we report data demonstrating a role for miR-27b in the regulation of TLR4/NF-κB-mediated epithelial anti-Cryptosporidium parvum responses. We found that C. parvum infection induced nitric oxide (NO) production in host epithelial cells in a TLR4/NF-κB-dependent manner, with the involvement of the stabilization of inducible NO synthase (iNOS) mRNA. C. parvum infection of epithelial cells activated NF-κB signaling to increase transcription of the miR-27b gene. Meanwhile, downregulation of KH-type splicing regulatory protein (KSRP) was detected in epithelial cells following C. parvum infection. Importantly, miR-27b targeted the 3'-untranslated region of KSRP, resulting in translational suppression. C. parvum infection decreased KSRP expression through upregulating miR-27b. Functional manipulation of KSRP or miR-27b caused reciprocal alterations in iNOS mRNA stability in infected cells. Forced expression of KSRP and inhibition of miR-27b resulted in an increased burden of C. parvum infection. Downregulation of KSRP through upregulating miR-27b was also detected in epithelial cells following LPS stimulation. These data suggest that miR-27b targets KSRP and modulates iNOS mRNA stability following C. parvum infection, a process that may be relevant to the regulation of epithelial anti-microbial defense in general.

    View details for DOI 10.1371/journal.ppat.1002702

    View details for Web of Science ID 000305322900035

    View details for PubMedID 22615562

    View details for PubMedCentralID PMC3355088

  • Downregulation of PCAF by miR-181a/b Provides Feedback Regulation to TNF-alpha-Induced Transcription of Proinflammatory Genes in Liver Epithelial Cells JOURNAL OF IMMUNOLOGY Zhao, J., Gong, A., Zhou, R., Liu, J., Eischeid, A. N., Chen, X. 2012; 188 (3): 1266–74


    Aberrant cellular responses to proinflammatory cytokines, such as TNF-α, are pathogenic features in most chronic inflammatory diseases. A variety of extracellular and intracellular feedback pathways has evolved to prevent an inappropriate cellular reaction to these proinflammatory cytokines. In this study, we report that TNF-α treatment of human and mouse cholangiocytes and hepatocytes downregulated expression of p300/CBP-associated factor (PCAF), a coactivator and an acetyltransferase that promotes histone acetylation and gene transcription. Of these upregulated microRNAs in TNF-α-treated cells, miR-181a/b (miR-181a and miR-181b) suppressed translation of PCAF mRNA. Functional manipulation of miR-181a/b caused reciprocal alterations in PCAF protein expression in cultured cholangiocytes and hepatocytes. Inhibition of miR-181a/b function with anti-miRs blocked TNF-α-induced suppression of PCAF expression. Promoter recruitment of PCAF was shown to be associated with TNF-α-induced transcription of inflammatory genes. Intriguingly, pretreatment of cells with TNF-α inhibited transcription of inflammatory genes in response to subsequent TNF-α stimulation. Overexpression of PCAF or inhibition of miR-181a/b function with anti-miRs attenuated the inhibitory effects of TNF-α pretreatment on epithelial inflammatory response to subsequent TNF-α stimulation. Downregulation of PCAF and the inhibitory effects of TNF-α pretreatment on liver epithelial inflammatory response were further confirmed in a mouse model of TNF-α i.p. injection. These data suggest that PCAF is a target for miR-181a/b, and downregulation of PCAF by TNF-α provides negative feedback regulation to inflammatory reactions in liver epithelial cells, a process that may be relevant to the epigenetic fine-tuning of epithelial inflammatory processes in general.

    View details for DOI 10.4049/jimmunol.1101976

    View details for Web of Science ID 000299690200041

    View details for PubMedID 22219331

    View details for PubMedCentralID PMC3262895

  • MicroRNA-98 and let-7 Confer Cholangiocyte Expression of Cytokine-Inducible Src Homology 2-Containing Protein in Response to Microbial Challenge JOURNAL OF IMMUNOLOGY Hu, G., Zhou, R., Liu, J., Gong, A., Eischeid, A. N., Dittman, J. W., Chen, X. 2009; 183 (3): 1617–24


    Posttranscriptional gene regulation by microRNAs (miRNAs) has been implicated in the fine-tuning of TLR-mediated inflammatory response. The cytokine-inducible Src homology 2-containing protein (CIS), one member of the suppressors of cytokine signaling family of proteins, is an important negative regulator for inflammatory cytokine signaling. Using in vitro models using normal human biliary epithelial cells (cholangiocytes), we demonstrated that LPS stimulation or infection with the parasitic protozoan Cryptosporidium parvum induced expression of CIS protein without a change in CIS mRNA levels by activating the TLR signaling pathway. Of those miRNAs expressed in cholangiocytes, we found that targeting of the 3'-untranslated region of CIS by microRNA-98 (miR-98) or let-7 resulted in translational repression, but not CIS mRNA degradation. LPS stimulation or C. parvum infection decreased cholangiocyte expression of miR-98 and let-7. Down-regulation of miR-98 and let-7 relieved miRNA-mediated translational suppression of CIS and contributed to LPS- and C. parvum-stimulated CIS protein expression. Moreover, gain-of-function (by overexpression of CIS) and loss-of-function (by siRNA interference) studies revealed that CIS could enhance IkappaBalpha degradation and regulate NF-kappaB activation in cholangiocytes in response to LPS stimulation or C. parvum infection. Our data suggest that miR-98 and let-7 confer cholangiocyte expression of CIS in response to microbial challenge, a process that may be relevant to the regulation of TLR-mediated epithelial innate immune response.

    View details for DOI 10.4049/jimmunol.0804362

    View details for Web of Science ID 000268519500017

    View details for PubMedID 19592657

    View details for PubMedCentralID PMC2906382

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