Anna C. Stoll

ORCID: 0000-0001-7135-121X
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About
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Research Areas
  • Parkinson's Disease Mechanisms and Treatments
  • Botulinum Toxin and Related Neurological Disorders
  • Neurological disorders and treatments
  • Alzheimer's disease research and treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Nuclear Receptors and Signaling
  • Neurological and metabolic disorders
  • Neuroscience and Neuropharmacology Research
  • Neurogenetic and Muscular Disorders Research
  • Autophagy in Disease and Therapy
  • Congenital heart defects research
  • Nerve injury and regeneration
  • TGF-β signaling in diseases
  • Genomics and Rare Diseases
  • Epigenetics and DNA Methylation
  • RNA and protein synthesis mechanisms
  • Neurotransmitter Receptor Influence on Behavior
  • Ginkgo biloba and Cashew Applications

Michigan State University
2018-2025

University of Pennsylvania
2023

Hunter College
2019

City University of New York
2019

The Graduate Center, CUNY
2019

John Jay College of Criminal Justice
2012

Animal models that accurately recapitulate the accumulation of alpha-synuclein (α-syn) inclusions, progressive neurodegeneration nigrostriatal system and motor deficits can be useful tools for Parkinson's disease (PD) research. The preformed fibril (PFF) synucleinopathy model in rodents generally displays these PD-relevant features, however, magnitude predictability events is far from established. We therefore sought to optimize α-syn degeneration, understand time course both. Rats were...

10.1016/j.nbd.2019.104525 article EN cc-by-nc-nd Neurobiology of Disease 2019-07-02

Examination of early phases synucleinopathy when inclusions are present, but long before neurodegeneration occurs, is critical to both understanding disease progression and the development modifying therapies. The rat alpha-synuclein (α-syn) preformed fibril (PFF) model induces synchronized that recapitulates pathological features Parkinson's (PD) can be used study progression. In this model, phosphorylated α-syn (pSyn) inclusion-containing neurons reactive microglia (major...

10.1038/s41531-023-00620-y article EN cc-by npj Parkinson s Disease 2024-01-03

Parkinson's disease (PD) pathology is characterized by alpha-synuclein (α-syn) aggregates, degeneration of dopamine neurons in the substantia nigra pars compacta (SNpc), and neuroinflammation. The presence reactive glia correlates with deposition pathological α-syn early-stage PD. Thus, understanding neuroinflammatory response microglia astrocytes to synucleinopathy may identify therapeutic targets. Here we gene expression profile SNpc during early rat pre-formed fibril (PFF) model. Rats...

10.1016/j.nbd.2024.106411 article EN cc-by-nc-nd Neurobiology of Disease 2024-01-21

Animal models have significantly advanced our understanding of Parkinson's disease (PD). Alpha-synuclein (α-syn) has taken center stage due to its genetic connection familial PD and localization Lewy bodies, one pathological hallmark PD. developed on the premise elevated alpha-synuclein via germline manipulation or viral vector-mediated overexpression are used investigate pathophysiology vet novel therapeutics. While these represented a step forward compared their neurotoxicant model...

10.3389/fnins.2018.00621 article EN cc-by Frontiers in Neuroscience 2018-09-04

Abstract Parkinson’s disease (PD) is the fastest-growing neurological worldwide, with increases outpacing aging and occurring most rapidly in recently industrialized areas, suggesting a role of environmental factors. Epidemiological, post-mortem, mechanistic studies suggest that persistent organic pollutants, including organochlorine pesticide dieldrin, increase PD risk. In mice, developmental dieldrin exposure causes male-specific exacerbation neuronal susceptibility to...

10.1093/toxsci/kfad086 article EN cc-by-nc Toxicological Sciences 2023-08-22

Preclinical studies show a link between subthalamic nucleus (STN) deep brain stimulation (DBS) and neuroprotection of nigrostriatal dopamine (DA) neurons, potentially through brain-derived neurotrophic factor (BDNF) signaling. However, the question whether DBS STN can be disease-modifying in Parkinson's disease (PD) remains unanswered. In particular, impact on α-synuclein (α-syn) aggregation, inclusion-associated neuroinflammation, BDNF levels has yet to examined context synucleinopathy. To...

10.1523/jneurosci.1952-20.2020 article EN cc-by-nc-sa Journal of Neuroscience 2021-01-20

The alpha-synuclein (α-syn) preformed fibril (PFF) model of Parkinson's disease (PD) is widely used in rodents to understand the mechanisms contributing progression pathology and neurodegeneration disorder. While time course α-syn PFF rat has been well characterized, it more challenging determine reliable reproducible behavior impairments. This mainly due injections resulting a partial nigrostriatal lesion that make motor anomalies subtle difficult detect, just as patients with PD. In...

10.3389/fnins.2025.1556447 article EN cc-by Frontiers in Neuroscience 2025-04-01

Abstract Background Positron emission tomography (PET) imaging in early Parkinson's disease (PD) subjects reveals that increased dopamine (DA) turnover and reduced transporter (DAT) density precede decreases DA synthesis storage. The rat α‐synuclein preformed fibril (α‐syn PFF) model provides a platform to investigate dynamics during multiple stages of α‐syn inclusion‐triggered nigrostriatal degeneration. Objectives We investigated aspects vivo dopaminergic deficits longitudinally...

10.1002/mds.29051 article EN cc-by-nc-nd Movement Disorders 2022-05-07

Abstract Parkinson's disease (PD) is characterized by the accumulation of misfolded alpha‐synuclein (α‐syn) protein, forming intraneuronal Lewy body (LB) inclusions. The α‐syn preformed fibril (PFF) model PD recapitulates aggregation, progressive nigrostriatal degeneration and motor dysfunction; however, little known about time course PFF‐induced alterations in basal evoked dopamine (DA). In vivo microdialysis well suited for identifying small changes neurotransmitter levels over extended...

10.1111/ejn.16275 article EN cc-by-nc-nd European Journal of Neuroscience 2024-02-14

Abstract Background Parkinson’s disease (PD) is a neurodegenerative disorder that characterized by the presence of proteinaceous alpha-synuclein (α-syn) inclusions (Lewy bodies), markers neuroinflammation and progressive loss nigrostriatal dopamine (DA) neurons. These pathological features can be recapitulated in vivo using α-syn preformed fibril (PFF) model synucleinopathy. We have previously determined microglia proximal to PFF-induced nigral increase soma size, upregulate...

10.1186/s12974-024-03108-5 article EN cc-by Journal of Neuroinflammation 2024-04-25

β2-adrenoreceptor (β2AR) agonists have been associated with a decreased risk of developing Parkinson's disease (PD) and are hypothesized to decrease expression both alpha-synuclein mRNA (Snca) protein (α-syn). Effects β2AR agonist clenbuterol on the levels Snca α-syn were evaluated in vivo (rats mice) rat primary cortical neurons by two independent laboratories. A modest substantia nigra was observed after single acute dose rats, however, this not maintained multiple doses. In contrast,...

10.1038/s41531-022-00322-x article EN cc-by npj Parkinson s Disease 2022-05-24

Abstract Background: Parkinson’s disease (PD) is a neurodegenerative disorder that characterized by the presence of proteinaceous alpha-synuclein (α-syn) inclusions (Lewy bodies), markers neuroinflammation and progressive loss nigrostriatal dopamine (DA) neurons. These pathological features can be recapitulated in vivo using α-syn preformed fibril (PFF) model synucleinopathy. We have previously described time course microglial major-histocompatibility complex-II (MHC-II) expression...

10.21203/rs.3.rs-2890683/v1 preprint EN cc-by Research Square (Research Square) 2023-05-04

<b>Abstract ID 91058</b> <b>Poster Board 567</b> Mutations in the <i>GNAO1</i> gene, which encodes abundant brain G-protein Gα<sub>o</sub>, result neurologic disorders characterized by developmental delay, epilepsy, and movement abnormalities. There are over 50 mutant alleles associated with disorders; R209H mutation results dystonia, choreoathetosis, delay without seizures. has been success controlling these motor symptoms deep stimulation some medications, but there is a clear need for...

10.1124/jpet.567.910580 article EN Journal of Pharmacology and Experimental Therapeutics 2024-05-13

Abstract Parkinson’s disease (PD) is the most common movement disorder and one of fastest-growing neurological diseases worldwide. This increase outpaces rate aging rapid in recently industrialized areas, suggesting role environmental factors. Consistent with this, epidemiological studies show an association between exposure to persistent organic pollutants increased risk PD. When combined post-mortem analysis mechanistic studies, a for specific compounds, including organochlorine pesticide...

10.1101/2023.06.21.545967 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-06-24

Abstract Examination of early phases synucleinopathy when inclusions are present, but long before neurodegeneration occurs, is critical to both understanding disease progression and the development modifying therapies. The rat alpha-synuclein (α-syn) preformed fibril (PFF) model induces synchronized that recapitulates pathological features Parkinson’s (PD) can be used study progression. In this model, phosphorylated α-syn (pSyn) inclusion-containing neurons reactive microglia (major...

10.21203/rs.3.rs-3253289/v1 preprint EN cc-by Research Square (Research Square) 2023-08-18

Mn‐containing dithiocarbamates, such as maneb (MB) and mancozeb (MZ), have been known to increase the toxicity of neurotoxin MPTP on dopaminergic neurons leading cell death Parkinson‐like symptoms. Dopamine transporter (DAT), a key protein in MPTP's toxicity, transports active metabolite (MPP + ) into neurons; increasing surface expression DAT increases uptake MPTP. Alpha‐synuclein (both wt A30P &amp; A53T mutants) associated with Parkinson's, are thought regulate trafficking by interacting...

10.1096/fasebj.26.1_supplement.lb228 article EN The FASEB Journal 2012-04-01
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