Kartik S. Pradeepan

ORCID: 0000-0003-0979-7928
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About
Contact & Profiles
Research Areas
  • Neural dynamics and brain function
  • Neuroscience and Neural Engineering
  • Genetics and Neurodevelopmental Disorders
  • Autism Spectrum Disorder Research
  • Neural Networks and Applications
  • Neuroscience and Neuropharmacology Research
  • stochastic dynamics and bifurcation
  • Energy Harvesting in Wireless Networks
  • Advanced Memory and Neural Computing
  • Memory and Neural Mechanisms
  • EEG and Brain-Computer Interfaces
  • Pluripotent Stem Cells Research

Western University
2019-2025

Robarts Clinical Trials
2023-2024

Mutations in MECP2 predominantly cause Rett syndrome (RTT) and can be modelled vitro using human stem cell-derived neurons. RTT patients have signs of cortical hyperexcitability, such as seizures. Human null excitatory neurons smaller soma size reduced synaptic connectivity but are also hyperexcitable due to higher input resistance. Paradoxically, networks show a decrease the frequency network bursts consistent with hypoconnectivity phenotype. Here, we examine this issue. We reanalyzed...

10.1016/j.bpsgos.2024.100290 article EN cc-by-nc-nd Biological Psychiatry Global Open Science 2024-01-25

Abstract Rett syndrome (RTT) is a severe neurodevelopmental disorder primarily caused by heterozygous loss-of-function mutations in the X-linked gene MECP2 that global transcriptional regulator. Mutations methyl-CpG binding domain (MBD) of disrupt its interaction with methylated DNA. Here, we investigate effect novel L124W missense mutation MBD an atypical RTT patient preserved speech comparison to null mutations. protein had limited ability heterochromatic chromocenters due decreased...

10.1038/s41398-022-02216-1 article EN cc-by Translational Psychiatry 2022-10-18

ABSTRACT Variants in the gene encoding postsynaptic scaffolding protein SHANK2 are associated with several neurodevelopmental disorders, including autism spectrum disorder. Here, we used vitro multielectrode arrays and pharmacological manipulations to characterize how functional connectivity network-level firing properties were altered cultures of human iPSC-derived neurons. Using two isogenic pairs cell lines, showed that hyperconnectivity phenotype was recapitulated at network level....

10.1101/2024.07.30.605451 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-07-30

Abstract Recordings of cortical neurons isolated from brain slices and dissociated their networks, display intrinsic spike frequency adaptation (I-SFA) to a constant current input. Interestingly, extracellular recordings in behaving subjects also show extrinsic-SFA (E-SFA) response sustained visual stimulation. Because are networks slice recordings, it is challenging infer how I-SFA contributes E-SFA interconnected brains during behavior. To investigate this, we recorded responses macaque...

10.1101/2024.09.03.610998 preprint EN cc-by-nc bioRxiv (Cold Spring Harbor Laboratory) 2024-09-05

ABSTRACT Rett syndrome (RTT) is a severe neurodevelopmental disorder primarily caused by heterozygous loss-of-function mutations in the X-linked gene MECP2 that global transcriptional regulator. Mutations methyl-CpG binding domain (MBD) of disrupt its interaction with methylated DNA. Here, we investigate effect L124W missense mutation MBD an atypical RTT patient comparison to null mutations. protein had limited ability heterochromatic chromocenters due decreased dynamics. We isolated two...

10.1101/2020.07.12.189621 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2020-07-12

ABSTRACT Rett syndrome (RTT) patients show abnormal developmental trajectories including loss of language and repetitive hand movements but also have signs cortical hyperexcitability such as seizures. RTT is predominantly caused by mutations in MECP2 can be modelled vitro using human stem cell-derived neurons. null excitatory neurons are smaller soma size reduced synaptic connectivity hyperexcitable, due to higher input resistance, which increases the chance evoke action potentials with a...

10.1101/2023.09.12.557388 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-09-13

10.29173/hsi17 article EN Health Science Inquiry 2019-06-01
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