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  1. Article: A Precision Medicine Approach to Dementia Care: Syndrome, Etiology, and Copathology.

    Fischer, D Luke / Seeley, William W

    Practical neurology (Fort Washington, Pa.)

    2023  Volume 2023, Page(s) 17–22

    Abstract: Recognizing multiple neuropathological entities in people with dementia improves understanding of diagnosis, prognosis, and expected outcomes from therapies. Care for the individual with dementia includes the evaluation and management of diseases ... ...

    Abstract Recognizing multiple neuropathological entities in people with dementia improves understanding of diagnosis, prognosis, and expected outcomes from therapies. Care for the individual with dementia includes the evaluation and management of diseases associated with the aged brain, most commonly neurodegeneration and vascular brain injury (VBI). Terminology has evolved to keep pace with diagnostic, prognostic, and therapeutic advances, and autopsy studies have shown that multiple comorbid neuropathological entities are the rule, not the exception, especially in older individuals. With the advent of disease-modifying therapies, delivering dementia care requires an encompassing framework that allows clinicians to consider all of an individual's underlying diseases and their contributions to symptom burden. A diagnostic approach, common co-occurring pathologies, and implications for current and future clinical care are reviewed.
    Language English
    Publishing date 2023-08-03
    Publishing country United States
    Document type Journal Article
    ISSN 1540-1367
    ISSN 1540-1367
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  2. Article ; Online: The Salience Network: A Neural System for Perceiving and Responding to Homeostatic Demands.

    Seeley, William W

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2019  Volume 39, Issue 50, Page(s) 9878–9882

    Abstract: The term "salience network" refers to a suite of brain regions whose cortical hubs are the anterior cingulate and ventral anterior insular (i.e., frontoinsular) cortices. This network, which also includes nodes in the amygdala, hypothalamus, ventral ... ...

    Abstract The term "salience network" refers to a suite of brain regions whose cortical hubs are the anterior cingulate and ventral anterior insular (i.e., frontoinsular) cortices. This network, which also includes nodes in the amygdala, hypothalamus, ventral striatum, thalamus, and specific brainstem nuclei, coactivates in response to diverse experimental tasks and conditions, suggesting a domain-general function. In the 12 years since its initial description, the salience network has been extensively studied, using diverse methods, concepts, and mammalian species, including healthy and diseased humans across the lifespan. Despite this large and growing body of research, the essential functions of the salience network remain uncertain. In this paper, which makes no attempt to comprehensively review this literature, I describe the circumstances surrounding the initial discovery, conceptualization, and naming of the salience network, highlighting aspects that may be unfamiliar to many readers. I then discuss some of the key advances provided by subsequent research and conclude by posing a few of the questions that remain to be explored.
    MeSH term(s) Animals ; Brain/physiology ; Cerebral Cortex/physiology ; Homeostasis/physiology ; Humans ; Nerve Net/physiology ; Neural Pathways/physiology
    Language English
    Publishing date 2019-11-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.1138-17.2019
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  3. Article ; Online: Behavioral Variant Frontotemporal Dementia.

    Seeley, William W

    Continuum (Minneapolis, Minn.)

    2019  Volume 25, Issue 1, Page(s) 76–100

    Abstract: Purpose of review: This article describes the clinical, anatomic, genetic, and pathologic features of behavioral variant frontotemporal dementia (bvFTD) and discusses strategies to improve diagnostic accuracy, emphasizing common pitfalls to avoid. Key ... ...

    Abstract Purpose of review: This article describes the clinical, anatomic, genetic, and pathologic features of behavioral variant frontotemporal dementia (bvFTD) and discusses strategies to improve diagnostic accuracy, emphasizing common pitfalls to avoid. Key aspects of management and the future of diagnosis and care for the disorder are highlighted.
    Recent findings: BvFTD is a clinical syndrome, not a disease. Patients with the syndrome share core symptoms that reflect degeneration within the most consistently affected brain regions, but accompanying features vary and reflect the precise topography of regional degeneration. The clinician must distinguish a bvFTD syndrome from psychiatric illness and other neurodegenerative syndromes that feature a prominent behavioral component. Antemortem prediction of pathologic diagnosis remains imperfect but improves with careful attention to the clinical details. Management should emphasize prevention of caregiver distress, behavioral and environmental strategies, symptom-based psychopharmacology, and genetic counseling.
    Summary: BvFTD is an important and challenging dementia syndrome. Although disease-modifying treatments are lacking, clinicians can have a profound impact on a family coping with this disorder. Treatment trials are under way for some genetic forms of bvFTD. For sporadic disease, pathologic heterogeneity remains a major challenge, and ongoing research seeks to improve antemortem molecular diagnosis to facilitate therapeutic discovery.
    MeSH term(s) Alzheimer Disease/diagnosis ; Alzheimer Disease/pathology ; Behavior/physiology ; Brain/pathology ; Caregivers/psychology ; Female ; Frontotemporal Dementia/diagnosis ; Frontotemporal Dementia/pathology ; Humans ; Middle Aged ; Neuropsychological Tests
    Language English
    Publishing date 2019-02-17
    Publishing country United States
    Document type Case Reports ; Journal Article ; Review
    ISSN 1538-6899
    ISSN (online) 1538-6899
    DOI 10.1212/CON.0000000000000698
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  4. Article: Progranulin inhibits phospholipase sPLA2-IIA to control neuroinflammation.

    Du, Huan / Yang, Cha / Nana, Alissa L / Seeley, William W / Smolka, Marcus / Hu, Fenghua

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Mutations in the granulin ( ...

    Abstract Mutations in the granulin (
    Language English
    Publishing date 2023-04-06
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.04.06.535844
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  5. Article ; Online: Mapping Neurodegenerative Disease Onset and Progression.

    Seeley, William W

    Cold Spring Harbor perspectives in biology

    2017  Volume 9, Issue 8

    Abstract: Brain networks have been of long-standing interest to neurodegeneration researchers, including but not limited to investigators focusing on conventional prion diseases, which are known to propagate along neural pathways. Tools for human network mapping, ... ...

    Abstract Brain networks have been of long-standing interest to neurodegeneration researchers, including but not limited to investigators focusing on conventional prion diseases, which are known to propagate along neural pathways. Tools for human network mapping, however, remained inadequate, limiting our understanding of human brain network architecture and preventing clinical research applications. Until recently, neuropathological studies were the only viable approach to mapping disease onset and progression in humans but required large autopsy cohorts and laborious methods for whole-brain sectioning and staining. Despite important advantages, postmortem studies cannot address in vivo, physiological, or longitudinal questions and have limited potential to explore early-stage disease except for the most common disorders. Emerging in vivo network-based neuroimaging strategies have begun to address these issues, providing data that complement the neuropathological tradition. Overall, findings to date highlight several fundamental principles of neurodegenerative disease anatomy and pathogenesis, as well as some enduring mysteries. These principles and mysteries provide a road map for future research.
    MeSH term(s) Brain Mapping/methods ; Disease Progression ; Humans ; Neurodegenerative Diseases/diagnostic imaging ; Neurodegenerative Diseases/etiology
    Language English
    Publishing date 2017-08-01
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1943-0264
    ISSN (online) 1943-0264
    DOI 10.1101/cshperspect.a023622
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  6. Article ; Online: A dynamic gradient architecture generates brain activity states.

    Brown, Jesse A / Lee, Alex J / Pasquini, Lorenzo / Seeley, William W

    NeuroImage

    2022  Volume 261, Page(s) 119526

    Abstract: The human brain exhibits a diverse yet constrained range of activity states. While these states can be faithfully represented in a low-dimensional latent space, our understanding of the constitutive functional anatomy is still evolving. Here we applied ... ...

    Abstract The human brain exhibits a diverse yet constrained range of activity states. While these states can be faithfully represented in a low-dimensional latent space, our understanding of the constitutive functional anatomy is still evolving. Here we applied dimensionality reduction to task-free and task fMRI data to address whether latent dimensions reflect intrinsic systems and if so, how these systems may interact to generate different activity states. We find that each dimension represents a dynamic activity gradient, including a primary unipolar sensory-association gradient underlying the global signal. The gradients appear stable across individuals and cognitive states, while recapitulating key functional connectivity properties including anticorrelation, modularity, and regional hubness. We then use dynamical systems modeling to show that gradients causally interact via state-specific coupling parameters to create distinct brain activity patterns. Together, these findings indicate that a set of dynamic, intrinsic spatial gradients interact to determine the repertoire of possible brain activity states.
    MeSH term(s) Brain/diagnostic imaging ; Brain Mapping/methods ; Humans ; Magnetic Resonance Imaging/methods ; Nerve Net/diagnostic imaging
    Language English
    Publishing date 2022-07-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1147767-2
    ISSN 1095-9572 ; 1053-8119
    ISSN (online) 1095-9572
    ISSN 1053-8119
    DOI 10.1016/j.neuroimage.2022.119526
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    Zs.A 3664: Show issues Location:
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  7. Article ; Online: Mutant tau and stress lead to downregulation of long noncoding RNA, SNHG8.

    Bhagat, Reshma / Minaya, Miguel A / Renganathan, Arun / Mehra, Muneshwar / Marsh, Jacob / Martinez, Rita / Eteleeb, Abdallah M / Nana, Alissa L / Spina, Salvatore / Seeley, William W / Grinberg, Lea T / Karch, Celeste M

    Molecular psychiatry

    2024  Volume 28, Issue 11, Page(s) 4489

    MeSH term(s) RNA, Long Noncoding/genetics ; Down-Regulation
    Chemical Substances RNA, Long Noncoding
    Language English
    Publishing date 2024-03-05
    Publishing country England
    Document type Journal Article
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-023-02328-0
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    Zs.A 4812: Show issues Location:
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  8. Article ; Online: Three-Dimensional Imaging of Fibrinogen and Neurovascular Alterations in Alzheimer's Disease.

    Merlini, Mario / Sozmen, Elif G / Subramanian, Keshav S / Nana, Alissa L / Seeley, William W / Akassoglou, Katerina

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2561, Page(s) 87–101

    Abstract: Cerebrovascular dysfunction is a hallmark of Alzheimer's disease (AD) that is linked to cognitive decline. However, blood-brain barrier (BBB) disruption in AD is focal and requires sensitive methods to detect extravasated blood proteins and vasculature ... ...

    Abstract Cerebrovascular dysfunction is a hallmark of Alzheimer's disease (AD) that is linked to cognitive decline. However, blood-brain barrier (BBB) disruption in AD is focal and requires sensitive methods to detect extravasated blood proteins and vasculature in large brain volumes. Fibrinogen, a blood coagulation factor, is deposited in AD brains at sites of BBB disruption and cerebrovascular damage. This chapter presents the methodology of fibrinogen immunolabeling-enabled three-dimensional (3D) imaging of solvent-cleared organs (iDISCO) which, when combined with immunolabeling of amyloid β (Aβ) and vasculature, enables sensitive detection of focal BBB vascular abnormalities, and reveals the spatial distribution of Aβ plaques and fibrin deposits, in large tissue volumes from cleared human brains. Overall, fibrinogen iDISCO enables the investigation of neurovascular and neuroimmune mechanisms driving neurodegeneration in disease.
    MeSH term(s) Humans ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Fibrinogen/metabolism ; Imaging, Three-Dimensional ; Plaque, Amyloid
    Chemical Substances Amyloid beta-Peptides ; Fibrinogen (9001-32-5)
    Language English
    Publishing date 2022-11-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2655-9_5
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  9. Article ; Online: Progranulin deficiency results in sex-dependent alterations in microglia in response to demyelination.

    Zhang, Tingting / Feng, Tuancheng / Wu, Kenton / Guo, Jennifer / Nana, Alissa L / Yang, Guang / Seeley, William W / Hu, Fenghua

    Acta neuropathologica

    2023  Volume 146, Issue 1, Page(s) 97–119

    Abstract: Heterozygous mutations in the granulin (GRN) gene, resulting in the haploinsufficiency of the progranulin (PGRN) protein, is a leading cause of frontotemporal lobar degeneration (FTLD). Complete loss of the PGRN protein causes neuronal ceroid ... ...

    Abstract Heterozygous mutations in the granulin (GRN) gene, resulting in the haploinsufficiency of the progranulin (PGRN) protein, is a leading cause of frontotemporal lobar degeneration (FTLD). Complete loss of the PGRN protein causes neuronal ceroid lipofuscinosis (NCL), a lysosomal storage disorder. Polymorphisms in the GRN gene have also been associated with several other neurodegenerative diseases, including Alzheimer's disease (AD), and Parkinson's disease (PD). PGRN deficiency has been shown to cause myelination defects previously, but how PGRN regulates myelination is unknown. Here, we report that PGRN deficiency leads to a sex-dependent myelination defect with male mice showing more severe demyelination in response to cuprizone treatment. This is accompanied by exacerbated microglial proliferation and activation in the male PGRN-deficient mice. Interestingly, both male and female PGRN-deficient mice show sustained microglial activation after cuprizone removal and a defect in remyelination. Specific ablation of PGRN in microglia results in similar sex-dependent phenotypes, confirming a microglial function of PGRN. Lipid droplets accumulate in microglia specifically in male PGRN-deficient mice. RNA-seq analysis and mitochondrial function assays reveal key differences in oxidative phosphorylation in male versus female microglia under PGRN deficiency. A significant decrease in myelination and accumulation of myelin debris and lipid droplets in microglia were found in the corpus callosum regions of FTLD patients with GRN mutations. Taken together, our data support that PGRN deficiency leads to sex-dependent alterations in microglia with subsequent myelination defects.
    MeSH term(s) Animals ; Female ; Male ; Mice ; Cuprizone/metabolism ; Demyelinating Diseases ; Frontotemporal Dementia/metabolism ; Frontotemporal Lobar Degeneration/genetics ; Intercellular Signaling Peptides and Proteins/metabolism ; Lysosomes/metabolism ; Microglia/metabolism ; Progranulins/genetics
    Chemical Substances Cuprizone (5N16U7E0AO) ; Intercellular Signaling Peptides and Proteins ; Progranulins ; Grn protein, mouse
    Language English
    Publishing date 2023-04-30
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1079-0
    ISSN 1432-0533 ; 0001-6322
    ISSN (online) 1432-0533
    ISSN 0001-6322
    DOI 10.1007/s00401-023-02578-w
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  10. Article ; Online: Divergent network connectivity changes in healthy APOE ε4 carriers: disinhibition or compensation?

    Seeley, William W

    Archives of neurology

    2011  Volume 68, Issue 9, Page(s) 1107–1108

    MeSH term(s) Apolipoprotein E4/genetics ; Brain/physiology ; Cognition/physiology ; Female ; Humans ; Male ; Nerve Net/physiology ; Protein Isoforms/genetics
    Chemical Substances Apolipoprotein E4 ; Protein Isoforms
    Language English
    Publishing date 2011-09
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 80049-1
    ISSN 1538-3687 ; 0003-9942
    ISSN (online) 1538-3687
    ISSN 0003-9942
    DOI 10.1001/archneurol.2011.202
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