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Profil bibliographique

Anna C. Stoll

Informations fournies par OpenAlex. Research Africa ne déduit ni nationalité, ni poste, ni coordonnées personnelles.

27Publications signalées
402Citations signalées
1Affiliations récentes

Les institutions déclarées

Les domaines associés

Parkinson's Disease Mechanisms and TreatmentsBotulinum Toxin and Related Neurological DisordersAlzheimer's disease research and treatmentsNeurological disorders and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Les publications récentes

Accès ouvert 2026 article OpenAlex

Human TDP-43 expression worsens FTD-related phenotypes in progranulin-insufficient mice

Anna K. Cook, Benjamin Lin, Yumo Song, Kelsey M. Greathouse et autres

Loss-of-function progranulin ( GRN ) mutations cause frontotemporal dementia with TDP-43 pathology (FTD-TDP). Nearly all pathogenic GRN mutations cause progranulin haploinsufficiency, but it is unclear how progranulin insufficiency causes FTD-TDP. To address this question, we crossed progranulin-insufficient mice with a human TDP-43 …

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0 citations Neurobiology of Disease
Accès ouvert 2026 article OpenAlex

Interconnected roles of astrocytes and the blood–brain barrier in Parkinson’s disease: pathological evidence, mechanistic insights, and knowledge gaps

Anna C. Stoll, Ashley S. Harms

Parkinson’s disease (PD) has long been defined by α-synuclein aggregation and dopaminergic neurodegeneration, yet growing evidence indicates that non-neuronal contributors, specifically astrocytes and the blood–brain barrier (BBB), may play key roles in disease progression. Human neuropathological studies reveal BBB disruption and astrocytic …

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0 citations Frontiers in Aging Neuroscience
Accès ouvert 2026 article OpenAlex

Tau, amyloid-β and α-synuclein co-pathologies synergistically enhance neuroinflammation and hippocampal neuron loss

Jhodi M. Webster, Ya-Ting Yang, Aidan T. Miller, Asta Zane et autres

microglia, a population of activated, phagocytosing microglia, compared to single pathologies. These changes were abundant in the hippocampus and cortex, regions that showed elevated protein pathology load at 3- and 6-months post-induction and enhanced neuronal loss at 6-months post induction. Our findings …

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5 citations Neurobiology of Disease
Accès ouvert 2025 article OpenAlex

Intrastriatal injection of alpha-synuclein preformed fibrils to rats results in L-DOPA reversible sensorimotor impairments and alterations in non-motor function

Sheila M. Fleming, Edward J. Hamad, Danielle Herman, John G. Holden et autres

Introduction The alpha-synuclein ( α -syn) preformed fibril (PFF) model of Parkinson’s disease (PD) is widely used in rodents to understand the mechanisms contributing to progression of pathology and neurodegeneration in the disorder. While the time course of pathology in the α …

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2 citations Frontiers in Neuroscience
Accès ouvert 2024 preprint OpenAlex

Tau, amyloid-β and α-synuclein co-pathologies synergistically enhance neuroinflammation and neuropathology

J. Webster, Yating Yang, Aidan T. Miller, Kasandra Scholz et autres

Abstract Alzheimer’s (AD) and Parkinson disease (PD) pathology often co-occur. Amyloid-β and phosphorylated tau are found in 30-50% of idiopathic PD cases, while α-synuclein inclusions are present in 50% of AD cases. These co-pathologies are linked to increased mortality and earlier onset …

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3 citations bioRxiv (Cold Spring Harbor Laboratory)
Accès ouvert 2024 article OpenAlex

AnNoBrainer, An Automated Annotation of Mouse Brain Images using Deep Learning

Roman Peter, Petr Hrobař, Josef Navratil, Martin Vagenknecht et autres

Annotation of multiple regions of interest across the whole mouse brain is an indispensable process for quantitative evaluation of a multitude of study endpoints in neuroscience digital pathology. Prior experience and domain expert knowledge are the key aspects for image annotation quality …

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0 citations Neuroinformatics
Accès ouvert 2024 article OpenAlex

Alpha-synuclein inclusion responsive microglia are resistant to CSF1R inhibition

Anna C. Stoll, Christopher J. Kemp, Joseph R. Patterson, Michael Kubik et autres

BACKGROUND: Parkinson's disease (PD) is a neurodegenerative disorder that is characterized by the presence of proteinaceous alpha-synuclein (α-syn) inclusions (Lewy bodies), markers of neuroinflammation and the progressive loss of nigrostriatal dopamine (DA) neurons. These pathological features can be recapitulated in vivo using …

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17 citations Journal of Neuroinflammation
Accès ouvert 2024 article OpenAlex

Deficits in basal and evoked striatal dopamine release following alpha‐synuclein preformed fibril injection: An in vivo microdialysis study

Ashley Centner, Isabella Del Priore, Nicole Chambers, Sophie R. Cohen et autres

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 of PD recapitulates α-syn aggregation, progressive nigrostriatal degeneration and motor dysfunction; however, little is known about the …

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6 citations European Journal of Neuroscience
Accès ouvert 2024 article OpenAlex

Neuroinflammatory gene expression profiles of reactive glia in the substantia nigra suggest a multidimensional immune response to alpha synuclein inclusions

Anna C. Stoll, Christopher J. Kemp, Joseph R. Patterson, Jacob W. Howe et autres

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 of reactive glia correlates with deposition of pathological α-syn in early-stage PD. Thus, understanding the neuroinflammatory response …

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29 citations Neurobiology of Disease

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