Archana Ashok

ORCID: 0009-0003-0175-6993
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Neuroscience and Neuropharmacology Research
  • Mitochondrial Function and Pathology
  • RNA regulation and disease
  • TiO2 Photocatalysis and Solar Cells
  • RNA Research and Splicing
  • Advanced Photocatalysis Techniques
  • RNA and protein synthesis mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Optical Coatings and Gratings
  • Nitric Oxide and Endothelin Effects
  • Perovskite Materials and Applications
  • Conducting polymers and applications
  • Electric Vehicles and Infrastructure
  • Cellular transport and secretion
  • Sphingolipid Metabolism and Signaling
  • Gas Sensing Nanomaterials and Sensors
  • Nuclear Receptors and Signaling
  • Adipose Tissue and Metabolism
  • Smart Grid Energy Management
  • Pluripotent Stem Cells Research
  • 3D Printing in Biomedical Research
  • Neuroscience and Neural Engineering
  • Memory and Neural Mechanisms
  • Cytokine Signaling Pathways and Interactions

Columbia University Irving Medical Center
2017-2024

Karunya University
2024

Columbia University
2018-2023

Institute on Aging
2023

Intel (United States)
2023

KTH Royal Institute of Technology
2020

The ε4 allele of apolipoprotein E (APOE) is the dominant genetic risk factor for late-onset Alzheimer's disease (AD). However, reason APOE4 associated with increased AD remains a source debate. Neuronal hyperactivity an early phenotype in both mouse models and human AD, which may play direct role pathogenesis disease. Here, we have identified APOE4-associated brains aged APOE mice using four complimentary techniques-fMRI, vitro electrophysiology, vivo metabolomics-with most prominent...

10.1038/s41467-017-01444-0 article EN cc-by Nature Communications 2017-11-07

Possession of the ε4 allele apolipoprotein E (APOE) is major genetic risk factor for late-onset Alzheimer's disease (AD). Although numerous hypotheses have been proposed, precise cause this increased AD not yet known. In order to gain a more comprehensive understanding APOE4's role in AD, we performed RNA-sequencing on an AD-vulnerable vs. AD-resistant brain region from aged APOE targeted replacement mice. This transcriptomics analysis revealed significant enrichment genes involved...

10.3389/fnins.2017.00702 article EN cc-by Frontiers in Neuroscience 2017-12-12

Abstract During the early stages of Alzheimer’s disease (AD) in both mouse models and human patients, soluble forms Amyloid-β 1–42 oligomers (Aβ42o) trigger loss excitatory synapses (synaptotoxicity) cortical hippocampal pyramidal neurons (PNs) prior to formation insoluble amyloid plaques. In a transgenic AD model, we observed spatially restricted structural remodeling mitochondria apical tufts CA1 PNs dendrites corresponding dendritic domain where earliest synaptic is detected vivo. We also...

10.1038/s41467-022-32130-5 article EN cc-by Nature Communications 2022-08-01

Apolipoprotein E ε4 (APOE4) is the primary genetic risk factor for late-onset form of Alzheimer's disease (AD). Although reason this association not completely understood, researchers have uncovered numerous effects APOE4 expression on AD-relevant brain processes, including amyloid beta (Aβ) accumulation, lipid metabolism, endosomal-lysosomal trafficking, and bioenergetics. In study, we aimed to determine effect allelic dosage regional composition in aged mice, as well cultured neurons. We...

10.1038/s41398-022-01881-6 article EN cc-by Translational Psychiatry 2022-03-29

The ε4 allele of apolipoprotein E (APOE) is the dominant genetic risk factor for late-onset Alzheimer's disease (AD). However, reason association between APOE4 and AD remains unclear. While much research has focused on ability apoE4 protein to increase aggregation decrease clearance Aβ, there also an abundance data showing that negatively impacts many additional processes in brain, including bioenergetics. In order gain a more comprehensive understanding APOE4's role pathogenesis, we...

10.1038/s41598-020-61142-8 article EN cc-by Scientific Reports 2020-03-09

Microgrids are small-scale electricity networks that integrate distributed generation with consumers and, potentially, storage devices. There is growing interest in these systems, as they can offer solutions for electrification of remote areas, deployment renewable energy resources, and decarbonization supply. However, the potential benefits microgrids terms climate change mitigation have not yet been thoroughly assessed. In this study, Life Cycle Assessment was performed to determine impact...

10.1016/j.apenergy.2020.114981 article EN cc-by Applied Energy 2020-04-20

It is essential to generate isolated populations of human neuronal subtypes in order understand cell-type-specific roles brain function and susceptibility disease pathology. Here we describe a protocol for in-parallel generation cortical glutamatergic (excitatory) GABAergic (inhibitory) neurons from pluripotent stem cells (hPSCs) by using the neurogenic transcription factors Ngn2 combination Ascl1 Dlx2, respectively. In contrast majority neural transdifferentiation protocols that use...

10.1002/cpz1.141 article EN Current Protocols 2021-06-01

ZCCHC17 is a putative master regulator of synaptic gene dysfunction in Alzheimer's disease (AD), and protein declines early AD brain tissue, before significant gliosis or neuronal loss. Here, we investigate the function its role pathogenesis using data from human autopsy tissue (consisting males females) female cell lines. Co-immunoprecipitation (co-IP) followed by mass spectrometry analysis iPSC-derived neurons reveals that ZCCHC17's binding partners are enriched for RNA-splicing proteins....

10.1523/jneurosci.2324-22.2023 article EN cc-by-nc-sa Journal of Neuroscience 2023-11-22

Understanding how high-risk individuals are protected from Alzheimer's disease (AD) may illuminate potential therapeutic targets. A previously identified non-coding SNP in SH3RF3/POSH2 significantly delayed onset a Caribbean Hispanic cohort carrying the PSEN1

10.1101/2024.06.23.600281 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-06-28

Abstract During the early stages of Alzheimer’s disease (AD) in both mouse models and human patients, soluble forms Amyloid-β1-42 oligomers (Aβ42o) trigger loss excitatory synapses (synaptotoxicity) cortical hippocampal pyramidal neurons (PNs) prior to formation insoluble Aβ plaques. We observed a spatially restricted structural remodeling mitochondria apical tufts CA1 PNs dendrites hAPP SWE,IND transgenic AD model (J20), corresponding dendritic domain receiving presynaptic inputs from...

10.1101/637199 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2019-05-14

Computational study of optical coupling efficiencies selected passive alignment options has done. Passive placement fiber array in V-grooves, and high-precision pick & place aligners have immense potential applicable for high-volume manufacturing with the benefits advancement low-tolerance fabrication SiPIC, micro-optic parts, array. The tight 1dB- 3dB-loss tolerances lateral direction V-groove focusing lens can be improved by using beam collimation approach. Combined packaging micro optics...

10.1117/12.2653403 article EN 2023-01-24

Abstract ZCCHC17 is a putative master regulator of synaptic gene dysfunction in Alzheimer’s Disease (AD), and protein declines early AD brain tissue, before significant gliosis or neuronal loss. Here, we investigate the function its role pathogenesis. Co-immunoprecipitation followed by mass spectrometry analysis human iPSC-derived neurons reveals that ZCCHC17’s binding partners are enriched for RNA splicing proteins. knockdown results widespread changes significantly overlap with found genes...

10.1101/2023.03.21.533654 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-03-21

The ε4 allele of apolipoprotein E (APOE) is the dominant genetic risk factor for late-onset Alzheimer's disease (AD). However, why APOE4 variant associated with increased AD remains a source debate. We investigated phenotype an mouse model in absence overt pathology using three complementary techniques. First, we used fMRI to map brain metabolism hippocampal formation young and old APOE3 vs. mice. Next, performed vitro vivo electrophysiology on hippicampal slices from aged Finally,...

10.1016/j.jalz.2017.07.070 article EN Alzheimer s & Dementia 2017-07-01

ABSTRACT The ε4 allele of apolipoprotein E ( APOE ) is the dominant genetic risk factor for late-onset Alzheimer’s disease (AD). However, reason association between APOE4 and AD remains unclear. While much research has focused on ability apoE4 protein to increase aggregation decrease clearance Aβ, there also an abundance data showing that negatively impacts many additional processes in brain, including bioenergetics. In order gain a more comprehensive understanding ’s role pathogenesis, we...

10.1101/482422 preprint EN cc-by-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-11-29
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