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  1. Article ; Online: Seizure-induced LIN28A disrupts pattern separation via aberrant hippocampal neurogenesis.

    Choi, In-Young / Cha, Jung-Ho / Kim, Seong Yun / Hsieh, Jenny / Cho, Kyung-Ok

    JCI insight

    2024  Volume 9, Issue 1

    Abstract: Prolonged seizures can disrupt stem cell behavior in the adult hippocampus, an important brain structure for spatial memory. Here, using a mouse model of pilocarpine-induced status epilepticus (SE), we characterized spatiotemporal expression of Lin28a ... ...

    Abstract Prolonged seizures can disrupt stem cell behavior in the adult hippocampus, an important brain structure for spatial memory. Here, using a mouse model of pilocarpine-induced status epilepticus (SE), we characterized spatiotemporal expression of Lin28a mRNA and proteins after SE. Unlike Lin28a transcripts, induction of LIN28A protein after SE was detected mainly in the subgranular zone, where immunoreactivity was found in progenitors, neuroblasts, and immature and mature granule neurons. To investigate roles of LIN28A in epilepsy, we generated Nestin-Cre:Lin28aloxP/loxP (conditional KO [cKO]) and Nestin-Cre:Lin28a+/+ (WT) mice to block LIN28A upregulation in all neuronal lineages after acute seizure. Adult-generated neuron- and hippocampus-associated cognitive impairments were absent in epileptic LIN28A-cKO mice, as evaluated by pattern separation and contextual fear conditioning tests, respectively, while sham-manipulated WT and cKO animals showed comparable memory function. Moreover, numbers of hilar PROX1-expressing ectopic granule cells (EGCs), together with PROX1+/NEUN+ mature EGCs, were significantly reduced in epileptic cKO mice. Transcriptomics analysis and IHC validation at 3 days after pilocarpine administration provided potential LIN28A downstream targets such as serotonin receptor 4. Collectively, our findings indicate that LIN28A is a potentially novel target for regulation of newborn neuron-associated memory dysfunction in epilepsy by modulating seizure-induced aberrant neurogenesis.
    MeSH term(s) Animals ; Nestin/genetics ; Pilocarpine/toxicity ; Seizures/chemically induced ; Status Epilepticus/chemically induced ; Status Epilepticus/genetics ; Hippocampus ; Neurogenesis ; Epilepsy
    Chemical Substances Nestin ; Pilocarpine (01MI4Q9DI3)
    Language English
    Publishing date 2024-01-09
    Publishing country United States
    Document type Journal Article
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.175627
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Familial Alzheimer's disease-associated PSEN1 mutations affect neurodevelopment through increased Notch signaling.

    Hurley, Erin M / Mozolewski, Pawel / Dobrowolski, Radek / Hsieh, Jenny

    Stem cell reports

    2023  Volume 18, Issue 7, Page(s) 1516–1533

    Abstract: Alzheimer's disease (AD) is the most common neurodegenerative disorder, but its root cause may lie in neurodevelopment. PSEN1 mutations cause the majority of familial AD, potentially by disrupting proper Notch signaling, causing early unnoticed cellular ... ...

    Abstract Alzheimer's disease (AD) is the most common neurodegenerative disorder, but its root cause may lie in neurodevelopment. PSEN1 mutations cause the majority of familial AD, potentially by disrupting proper Notch signaling, causing early unnoticed cellular changes that affect later AD progression. While rodent models are useful for modeling later stages of AD, human induced pluripotent stem cell-derived cortical spheroids (hCSs) allow access to studying the human cortex at the cellular level over the course of development. Here, we show that the PSEN1 L435F heterozygous mutation affects hCS development, increasing size, increasing progenitors, and decreasing post-mitotic neurons as a result of increased Notch target gene expression during early hCS development. We also show altered Aβ expression and neuronal activity at later hCS stages. These results contrast previous findings, showing how individual PSEN1 mutations may differentially affect neurodevelopment and may give insight into fAD progression to provide earlier time points for more effective treatments.
    MeSH term(s) Humans ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Induced Pluripotent Stem Cells/metabolism ; Mutation ; Neurons/metabolism ; Presenilin-1/genetics ; Presenilin-1/metabolism
    Chemical Substances Amyloid beta-Peptides ; PSEN1 protein, human ; Presenilin-1
    Language English
    Publishing date 2023-06-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2720528-9
    ISSN 2213-6711 ; 2213-6711
    ISSN (online) 2213-6711
    ISSN 2213-6711
    DOI 10.1016/j.stemcr.2023.05.018
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  3. Article: Rise and Fall of the Empire: Conquering Alzheimer's Disease by Targeting Adult Neurogenesis.

    Varma, Parul / Hsieh, Jenny

    Epilepsy currents

    2019  Volume 19, Issue 6, Page(s) 411–413

    Abstract: Box: see text]. ...

    Abstract [Box: see text].
    Language English
    Publishing date 2019-09-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2270080-8
    ISSN 1535-7597
    ISSN 1535-7597
    DOI 10.1177/1535759719874813
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  4. Article: Human Brain Organoid Models of Developmental Epilepsies.

    Nieto-Estévez, Vanesa / Hsieh, Jenny

    Epilepsy currents

    2020  Volume 20, Issue 5, Page(s) 282–290

    Abstract: Epilepsy is a common neurological disorder characterized by recurrent and unprovoked seizures due to neuronal hyperactivity. A large proportion of epilepsy cases begin during childhood. Causes of epilepsy include stroke, infections, brain injury, genetic ...

    Abstract Epilepsy is a common neurological disorder characterized by recurrent and unprovoked seizures due to neuronal hyperactivity. A large proportion of epilepsy cases begin during childhood. Causes of epilepsy include stroke, infections, brain injury, genetic factors, or other factors that alter brain structure and development, but in up to 50% of cases the cause is unknown. Approximately 35% of patients have refractory seizures that do not respond to medication. Animal models and in vitro cultures have contributed to our understanding of epilepsy, but there is a clear need for better models to explore the human brain in normal and pathological conditions. Human pluripotent stem cell (PSC) technologies opened the door for new models for analyzing brain development and disease, especially conditions with a genetic component. Initially, PSCs were differentiated into 2-dimensional cultures of a homogenous population of neural cells, such as glutamatergic excitatory or γ-aminobutyric acidergic inhibitory neurons, as well as glial cells. Nevertheless, these cultures lacked the structure and complexity of a human brain. In the last decade, PSC technology has advanced to the next level through the development of 3-dimensional culture, called organoids. These organoids recapitulate features of the human brain that are missing in animal models, enabling a deeper study of the human brain. In this review, we will summarize the current status of organoid research and its application to epilepsy.
    Language English
    Publishing date 2020-09-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2270080-8
    ISSN 1535-7597
    ISSN 1535-7597
    DOI 10.1177/1535759720949254
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  5. Article ; Online: Gestational buprenorphine exposure disrupts dopamine neuron activity and related behaviors in adulthood.

    Elam, Hannah B / Donegan, Jennifer J / Hsieh, Jenny / Lodge, Daniel J

    eNeuro

    2022  

    Abstract: Opioid misuse among pregnant women is rapidly increasing in the United States. The number of maternal opioid-related diagnoses increased by 131% in the last ten years, resulting in an increased number of infants exposed to ... ...

    Abstract Opioid misuse among pregnant women is rapidly increasing in the United States. The number of maternal opioid-related diagnoses increased by 131% in the last ten years, resulting in an increased number of infants exposed to opioids
    Language English
    Publishing date 2022-07-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2800598-3
    ISSN 2373-2822 ; 2373-2822
    ISSN (online) 2373-2822
    ISSN 2373-2822
    DOI 10.1523/ENEURO.0499-21.2022
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  6. Article: An emerging entity after pandemic: Post-coronavirus disease 2019 syndrome and associated medical complications.

    Hsieh, Jenny Yi Chen / Chin, Tan Tze

    SAGE open medicine

    2021  Volume 9, Page(s) 20503121211023631

    Abstract: The coronavirus disease 2019 is a devastating illness that has infected millions of people since the beginning of year 2020, through its multi-systemic manifestations that range widely in severity. Because current knowledge on the types and severities of ...

    Abstract The coronavirus disease 2019 is a devastating illness that has infected millions of people since the beginning of year 2020, through its multi-systemic manifestations that range widely in severity. Because current knowledge on the types and severities of medical illnesses encountered by patients who recovered from coronavirus disease 2019 is limited, it remains unknown whether these illnesses are direct sequelae of coronavirus disease 2019 infection or unrelated coincidences. In this article, we summarize the evidence currently available on post-coronavirus disease 2019 medical complications and propose directions for studying the long-term complications of coronavirus disease 2019 in the future.
    Language English
    Publishing date 2021-06-10
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2735399-0
    ISSN 2050-3121
    ISSN 2050-3121
    DOI 10.1177/20503121211023631
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  7. Article: Dual effects of

    Nieto-Estevez, Vanesa / Varma, Parul / Mirsadeghi, Sara / Caballero, Jimena / Gamero-Alameda, Sergio / Hosseini, Ali / Goswami, Sonal / Silvosa, Marc J / Thodeson, Drew M / Lybrand, Zane R / Giugliano, Michele / Navara, Christopher / Hsieh, Jenny

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Mutations ... ...

    Abstract Mutations in
    Language English
    Publishing date 2024-01-25
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.25.577271
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  8. Article ; Online: An emerging entity after pandemic

    Jenny Yi Chen Hsieh / Tan Tze Chin

    SAGE Open Medicine, Vol

    Post-coronavirus disease 2019 syndrome and associated medical complications

    2021  Volume 9

    Abstract: The coronavirus disease 2019 is a devastating illness that has infected millions of people since the beginning of year 2020, through its multi-systemic manifestations that range widely in severity. Because current knowledge on the types and severities of ...

    Abstract The coronavirus disease 2019 is a devastating illness that has infected millions of people since the beginning of year 2020, through its multi-systemic manifestations that range widely in severity. Because current knowledge on the types and severities of medical illnesses encountered by patients who recovered from coronavirus disease 2019 is limited, it remains unknown whether these illnesses are direct sequelae of coronavirus disease 2019 infection or unrelated coincidences. In this article, we summarize the evidence currently available on post-coronavirus disease 2019 medical complications and propose directions for studying the long-term complications of coronavirus disease 2019 in the future.
    Keywords Medicine (General) ; R5-920
    Language English
    Publishing date 2021-06-01T00:00:00Z
    Publisher SAGE Publishing
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article: One-Hit Wonders and 2-Hit Tubers: A Second-Hit to TSC2 Causes Tuber-Like Cells in Spheroids.

    Goswami, Sonal / Hsieh, Jenny

    Epilepsy currents

    2019  Volume 19, Issue 1, Page(s) 49–50

    Abstract: Genetically Engineered Human Cortical Spheroid Models of Tuberous Sclerosis Blair JD, Hockemeyer D, Bateup HS. Nat Med. 2018;24(10):1568-1578. doi:10.1038/s41591-018-0139-y. Epub 2018 Aug 20. PubMed PMID: 30127391; PubMed Central PMCID: PMC6261470. ... ...

    Abstract Genetically Engineered Human Cortical Spheroid Models of Tuberous Sclerosis Blair JD, Hockemeyer D, Bateup HS. Nat Med. 2018;24(10):1568-1578. doi:10.1038/s41591-018-0139-y. Epub 2018 Aug 20. PubMed PMID: 30127391; PubMed Central PMCID: PMC6261470. Tuberous sclerosis complex (TSC) is a multisystem developmental disorder caused by mutations in the TSC1 or TSC2 genes, whose protein products are negative regulators of mechanistic target of rapamycin complex 1 signaling. Hallmark pathologies of TSC are cortical tubers-regions of dysmorphic, disorganized neurons, and glia in the cortex that are linked to epileptogenesis. To determine the developmental origin of tuber cells, we established human cellular models of TSC by CRISPR-Cas9-mediated gene editing of TSC1 or TSC2 in human pluripotent stem cells (hPSCs). Using heterozygous TSC2 hPSCs with a conditional mutation in the functional allele, we show that mosaic biallelic inactivation during neural progenitor expansion is necessary for the formation of dysplastic cells and increased glia production in 3-dimensional cortical spheroids. Our findings provide support for the second-hit model of cortical tuber formation and suggest that variable developmental timing of somatic mutations could contribute to the heterogeneity in the neurological presentation of TSC.
    Language English
    Publishing date 2019-01-31
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2270080-8
    ISSN 1535-7597
    ISSN 1535-7597
    DOI 10.1177/1535759718822036
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  10. Article: You Have Brains in Your Head, You Have Organoids in Your Dish, You Can Steer Yourself in any Direction You Wish.

    Thodeson, Drew M / Hsieh, Jenny

    Epilepsy currents

    2017  Volume 17, Issue 5, Page(s) 311–313

    Language English
    Publishing date 2017-07-27
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2270080-8
    ISSN 1535-7597
    ISSN 1535-7597
    DOI 10.5698/1535-7597.17.5.311
    Database MEDical Literature Analysis and Retrieval System OnLINE

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