Aanishaa Jhaldiyal, MS, Ph.D.

Aanishaa Jhaldiyal, MS, Ph.D.

Johns Hopkins University

H-index: 5

North America-United States

About Aanishaa Jhaldiyal, MS, Ph.D.

Aanishaa Jhaldiyal, MS, Ph.D., With an exceptional h-index of 5 and a recent h-index of 5 (since 2020), a distinguished researcher at Johns Hopkins University, specializes in the field of Neurodegeneration, Stem cells editing & differentiation, Fly Screening.

His recent articles reflect a diverse array of research interests and contributions to the field:

Enhanced mTORC1 signaling and protein synthesis in pathologic α-synuclein cellular and animal models of Parkinson’s disease

Neuronal NLRP3 is a parkin substrate that drives neurodegeneration in Parkinson’s disease

Blocking microglial activation of reactive astrocytes is neuroprotective in models of Alzheimer’s disease

Defects in mitochondrial biogenesis drive mitochondrial alterations in PARKIN-deficient human dopamine neurons

Defects in mRNA translation in LRRK2-mutant hiPSC-derived dopaminergic neurons lead to dysregulated calcium homeostasis

Aanishaa Jhaldiyal, MS, Ph.D. Information

University

Johns Hopkins University

Position

Graduate Student in Department of Physiology, Johns Hopkins School of Medicine

Citations(all)

280

Citations(since 2020)

271

Cited By

45

hIndex(all)

5

hIndex(since 2020)

5

i10Index(all)

5

i10Index(since 2020)

5

Email

University Profile Page

Johns Hopkins University

Aanishaa Jhaldiyal, MS, Ph.D. Skills & Research Interests

Neurodegeneration

Stem cells editing & differentiation

Fly Screening

Top articles of Aanishaa Jhaldiyal, MS, Ph.D.

Enhanced mTORC1 signaling and protein synthesis in pathologic α-synuclein cellular and animal models of Parkinson’s disease

Authors

Mohammed Repon Khan,Xiling Yin,Sung-Ung Kang,Jaba Mitra,Hu Wang,Taekyung Ryu,Saurav Brahmachari,Senthilkumar S Karuppagounder,Yasuyoshi Kimura,Aanishaa Jhaldiyal,Hyun Hee Kim,Hao Gu,Rong Chen,Javier Redding-Ochoa,Juan Troncoso,Chan Hyun Na,Taekjip Ha,Valina L Dawson,Ted M Dawson

Journal

Science translational medicine

Published Date

2023/11/29

Pathologic α-synuclein plays an important role in the pathogenesis of α-synucleinopathies such as Parkinson’s disease (PD). Disruption of proteostasis is thought to be central to pathologic α-synuclein toxicity; however, the molecular mechanism of this deregulation is poorly understood. Complementary proteomic approaches in cellular and animal models of PD were used to identify and characterize the pathologic α-synuclein interactome. We report that the highest biological processes that interacted with pathologic α-synuclein in mice included RNA processing and translation initiation. Regulation of catabolic processes that include autophagy were also identified. Pathologic α-synuclein was found to bind with the tuberous sclerosis protein 2 (TSC2) and to trigger the activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1), which augmented mRNA translation and protein synthesis, leading …

Neuronal NLRP3 is a parkin substrate that drives neurodegeneration in Parkinson’s disease

Authors

Nikhil Panicker,Tae-In Kam,Hu Wang,Stewart Neifert,Shih-Ching Chou,Manoj Kumar,Saurav Brahmachari,Aanishaa Jhaldiyal,Jared T Hinkle,Fatih Akkentli,Xiaobo Mao,Enquan Xu,Senthilkumar S Karuppagounder,Eric T Hsu,Sung-Ung Kang,Olga Pletnikova,Juan Troncoso,Valina L Dawson,Ted M Dawson

Journal

Neuron

Published Date

2022/8/3

Parkinson's disease (PD) is mediated, in part, by intraneuronal accumulation of α-synuclein aggregates andsubsequent death of dopamine (DA) neurons in the substantia nigra pars compacta (SNpc). Microglial hyperactivation of the NOD-like receptor protein 3 (NLRP3) inflammasome has been well-documented in various neurodegenerative diseases, including PD. We show here that loss of parkin activity in mouse and human DA neurons results in spontaneous neuronal NLRP3 inflammasome assembly, leading to DA neuron death. Parkin normally inhibits inflammasome priming by ubiquitinating and targeting NLRP3 for proteasomal degradation. Loss of parkin activity also contributes to the assembly of an active NLRP3 inflammasome complex via mitochondrial-derived reactive oxygen species (mitoROS) generation through the accumulation of another parkin ubiquitination substrate, ZNF746/PARIS. Inhibition …

Blocking microglial activation of reactive astrocytes is neuroprotective in models of Alzheimer’s disease

Authors

Jong-Sung Park,Tae-In Kam,Saebom Lee,Hyejin Park,Yumin Oh,Seung-Hwan Kwon,Jae-Jin Song,Donghoon Kim,Hyunhee Kim,Aanishaa Jhaldiyal,Dong Hee Na,Kang Choon Lee,Eun Ji Park,Martin G Pomper,Olga Pletnikova,Juan C Troncoso,Han Seok Ko,Valina L Dawson,Ted M Dawson,Seulki Lee

Journal

Acta neuropathologica communications

Published Date

2021/4/26

Alzheimer’s disease (AD) is the most common cause of age-related dementia. Increasing evidence suggests that neuroinflammation mediated by microglia and astrocytes contributes to disease progression and severity in AD and other neurodegenerative disorders. During AD progression, resident microglia undergo proinflammatory activation, resulting in an increased capacity to convert resting astrocytes to reactive astrocytes. Therefore, microglia are a major therapeutic target for AD and blocking microglia-astrocyte activation could limit neurodegeneration in AD. Here we report that NLY01, an engineered exedin-4, glucagon-like peptide-1 receptor (GLP-1R) agonist, selectively blocks β-amyloid (Aβ)-induced activation of microglia through GLP-1R activation and inhibits the formation of reactive astrocytes as well as preserves neurons in AD models. In two transgenic AD mouse models (5xFAD and 3xTg-AD …

Defects in mitochondrial biogenesis drive mitochondrial alterations in PARKIN-deficient human dopamine neurons

Authors

Manoj Kumar,Jesús Acevedo-Cintrón,Aanishaa Jhaldiyal,Hu Wang,Shaida A Andrabi,Stephen Eacker,Senthilkumar S Karuppagounder,Saurav Brahmachari,Rong Chen,Hyesoo Kim,Han Seok Ko,Valina L Dawson,Ted M Dawson

Journal

Stem Cell Reports

Published Date

2020/9/8

Mutations and loss of activity in PARKIN, an E3 ubiquitin ligase, play a role in the pathogenesis of Parkinson's disease (PD). PARKIN regulates many aspects of mitochondrial quality control including mitochondrial autophagy (mitophagy) and mitochondrial biogenesis. Defects in mitophagy have been hypothesized to play a predominant role in the loss of dopamine (DA) neurons in PD. Here, we show that although there are defects in mitophagy in human DA neurons lacking PARKIN, the mitochondrial deficits are primarily due to defects in mitochondrial biogenesis that are driven by the upregulation of PARIS and the subsequent downregulation of PGC-1α. CRISPR/Cas9 knockdown of PARIS completely restores the mitochondrial biogenesis defects and mitochondrial function without affecting the deficits in mitophagy. These results highlight the importance mitochondrial biogenesis versus mitophagy in the …

Defects in mRNA translation in LRRK2-mutant hiPSC-derived dopaminergic neurons lead to dysregulated calcium homeostasis

Authors

Jungwoo Wren Kim,Xiling Yin,Aanishaa Jhaldiyal,Mohammed Repon Khan,Ian Martin,Zhong Xie,Tamara Perez-Rosello,Manoj Kumar,Leire Abalde-Atristain,Jinchong Xu,Li Chen,Stephen M Eacker,D James Surmeier,Nicholas T Ingolia,Ted M Dawson,Valina L Dawson

Journal

Cell stem cell

Published Date

2020/10/1

The G2019S mutation in leucine-rich repeat kinase 2 (LRRK2) is a common cause of familial Parkinson's disease (PD). This mutation results in dopaminergic neurodegeneration via dysregulated protein translation, although how alterations in protein synthesis contribute to neurodegeneration in human neurons is not known. Here we define the translational landscape in LRRK2-mutant dopaminergic neurons derived from human induced pluripotent stem cells (hiPSCs) via ribosome profiling. We found that mRNAs that have complex secondary structure in the 5′ untranslated region (UTR) are translated more efficiently in G2019S LRRK2 neurons. This leads to the enhanced translation of multiple genes involved in Ca2+ regulation and to increased Ca2+ influx and elevated intracellular Ca2+ levels, a major contributor to PD pathogenesis. This study reveals a link between dysregulated translation control and Ca2 …

See List of Professors in Aanishaa Jhaldiyal, MS, Ph.D. University(Johns Hopkins University)

Aanishaa Jhaldiyal, MS, Ph.D. FAQs

What is Aanishaa Jhaldiyal, MS, Ph.D.'s h-index at Johns Hopkins University?

The h-index of Aanishaa Jhaldiyal, MS, Ph.D. has been 5 since 2020 and 5 in total.

What are Aanishaa Jhaldiyal, MS, Ph.D.'s top articles?

The articles with the titles of

Enhanced mTORC1 signaling and protein synthesis in pathologic α-synuclein cellular and animal models of Parkinson’s disease

Neuronal NLRP3 is a parkin substrate that drives neurodegeneration in Parkinson’s disease

Blocking microglial activation of reactive astrocytes is neuroprotective in models of Alzheimer’s disease

Defects in mitochondrial biogenesis drive mitochondrial alterations in PARKIN-deficient human dopamine neurons

Defects in mRNA translation in LRRK2-mutant hiPSC-derived dopaminergic neurons lead to dysregulated calcium homeostasis

are the top articles of Aanishaa Jhaldiyal, MS, Ph.D. at Johns Hopkins University.

What are Aanishaa Jhaldiyal, MS, Ph.D.'s research interests?

The research interests of Aanishaa Jhaldiyal, MS, Ph.D. are: Neurodegeneration, Stem cells editing & differentiation, Fly Screening

What is Aanishaa Jhaldiyal, MS, Ph.D.'s total number of citations?

Aanishaa Jhaldiyal, MS, Ph.D. has 280 citations in total.

What are the co-authors of Aanishaa Jhaldiyal, MS, Ph.D.?

The co-authors of Aanishaa Jhaldiyal, MS, Ph.D. are Valina L. Dawson, Tae-In Kam, Manoj Kumar, Nikhil Panicker.

    Co-Authors

    H-index: 158
    Valina L. Dawson

    Valina L. Dawson

    Johns Hopkins University

    H-index: 26
    Tae-In Kam

    Tae-In Kam

    Johns Hopkins University

    H-index: 18
    Manoj Kumar

    Manoj Kumar

    Johns Hopkins University

    H-index: 17
    Nikhil Panicker

    Nikhil Panicker

    Johns Hopkins University

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