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  1. Article ; Online: Hippocampal subfield pathologic Burden in Lewy body diseases versus Alzheimer's disease.

    Coughlin, David G / Grossman, Murray / Trojanowski, John Q / Irwin, David J

    Neuropathology and applied neurobiology

    2021  Volume 47, Issue 5, Page(s) 707–708

    MeSH term(s) Alzheimer Disease ; Hippocampus ; Humans ; Lewy Body Disease
    Language English
    Publishing date 2021-02-15
    Publishing country England
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80371-6
    ISSN 1365-2990 ; 0305-1846
    ISSN (online) 1365-2990
    ISSN 0305-1846
    DOI 10.1111/nan.12698
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    Zs.A 1241: Show issues Location:
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  2. Article ; Online: Polypathologic Associations with Gray Matter Atrophy in Neurodegenerative Disease.

    Phillips, Jeffrey S / Robinson, John L / Cousins, Katheryn A Q / Wolk, David A / Lee, Edward B / McMillan, Corey T / Trojanowski, John Q / Grossman, Murray / Irwin, David J

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

    2024  Volume 44, Issue 6

    Abstract: Mixed pathologies are common in neurodegenerative disease; however, antemortem imaging rarely captures copathologic effects on brain atrophy due to a lack of validated biomarkers for non-Alzheimer's pathologies. We leveraged a dataset comprising ... ...

    Abstract Mixed pathologies are common in neurodegenerative disease; however, antemortem imaging rarely captures copathologic effects on brain atrophy due to a lack of validated biomarkers for non-Alzheimer's pathologies. We leveraged a dataset comprising antemortem MRI and postmortem histopathology to assess polypathologic associations with atrophy in a clinically heterogeneous sample of 125 human dementia patients (41 female, 84 male) with T1-weighted MRI ≤ 5 years before death and postmortem ordinal ratings of amyloid-[Formula: see text], tau, TDP-43, and [Formula: see text]-synuclein. Regional volumes were related to pathology using linear mixed-effects models; approximately 25% of data were held out for testing. We contrasted a polypathologic model comprising independent factors for each proteinopathy with two alternatives: a model that attributed atrophy entirely to the protein(s) associated with the patient's primary diagnosis and a protein-agnostic model based on the sum of ordinal scores for all pathology types. Model fits were evaluated using log-likelihood and correlations between observed and fitted volume scores. Additionally, we performed exploratory analyses relating atrophy to gliosis, neuronal loss, and angiopathy. The polypathologic model provided superior fits in the training and testing datasets. Tau, TDP-43, and [Formula: see text]-synuclein burden were inversely associated with regional volumes, but amyloid-[Formula: see text] was not. Gliosis and neuronal loss explained residual variance in and mediated the effects of tau, TDP-43, and [Formula: see text]-synuclein on atrophy. Regional brain atrophy reflects not only the primary molecular pathology but also co-occurring proteinopathies; inflammatory immune responses may independently contribute to degeneration. Our findings underscore the importance of antemortem biomarkers for detecting mixed pathology.
    MeSH term(s) Humans ; Male ; Female ; Neurodegenerative Diseases/diagnostic imaging ; Neurodegenerative Diseases/pathology ; Gray Matter/pathology ; tau Proteins/metabolism ; Gliosis/pathology ; Atrophy/pathology ; Amyloid ; Synucleins ; DNA-Binding Proteins/metabolism ; Biomarkers ; Alzheimer Disease/pathology
    Chemical Substances tau Proteins ; Amyloid ; Synucleins ; DNA-Binding Proteins ; Biomarkers
    Language English
    Publishing date 2024-02-07
    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.0808-23.2023
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    Zs.A 1668: Show issues Location:
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  3. Article ; Online: Apraxia of Speech in the Spontaneous Speech of Nonfluent/Agrammatic Primary Progressive Aphasia.

    Ash, Sharon / Nevler, Naomi / Irwin, David J / Shellikeri, Sanjana / Rascovsky, Katya / Shaw, Leslie / Lee, Edward B / Trojanowski, John Q / Grossman, Murray

    Journal of Alzheimer's disease reports

    2023  Volume 7, Issue 1, Page(s) 589–604

    Abstract: Background: Apraxia of speech (AOS) is a core feature of nonfluent/agrammatic primary progressive aphasia (naPPA), but its precise characteristics and the prevalence of AOS features in spontaneous speech are debated.: Objective: To assess the ... ...

    Abstract Background: Apraxia of speech (AOS) is a core feature of nonfluent/agrammatic primary progressive aphasia (naPPA), but its precise characteristics and the prevalence of AOS features in spontaneous speech are debated.
    Objective: To assess the frequency of features of AOS in the spontaneous, connected speech of individuals with naPPA and to evaluate whether these features are associated with an underlying motor disorder such as corticobasal syndrome or progressive supranuclear palsy.
    Methods: We examined features of AOS in 30 patients with naPPA using a picture description task. We compared these patients to 22 individuals with behavioral variant frontotemporal dementia and 30 healthy controls. Each speech sample was evaluated perceptually for lengthened speech segments and quantitatively for speech sound distortions, pauses between and within words, and articulatory groping. We compared subgroups of naPPA with and without at least two features of AOS to assess the possible contribution of a motor impairment to speech production deficits.
    Results: naPPA patients produced both speech sound distortions and other speech sound errors. Speech segmentation was found in 27/30 (90%) of individuals. Distortions were identified in 8/30 (27%) of individuals, and other speech sound errors occurred in 18/30 (60%) of individuals. Frequent articulatory groping was observed in 6/30 (20%) of individuals. Lengthened segments were observed rarely. There were no differences in the frequencies of AOS features among naPPA subgroups as a function of extrapyramidal disease.
    Conclusion: Features of AOS occur with varying frequency in the spontaneous speech of individuals with naPPA, independently of an underlying motor disorder.
    Language English
    Publishing date 2023-06-08
    Publishing country Netherlands
    Document type Journal Article
    ISSN 2542-4823
    ISSN (online) 2542-4823
    DOI 10.3233/ADR-220089
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  4. Article ; Online: Transmission of α-synuclein seeds in neurodegenerative disease: recent developments.

    Karpowicz, Richard J / Trojanowski, John Q / Lee, Virginia M-Y

    Laboratory investigation; a journal of technical methods and pathology

    2019  Volume 99, Issue 7, Page(s) 971–981

    Abstract: Cell-to-cell transmission of proteopathic alpha-synuclein (α-syn) seeds is increasingly thought to underlie the progression of neurodegenerative diseases including Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and related ... ...

    Abstract Cell-to-cell transmission of proteopathic alpha-synuclein (α-syn) seeds is increasingly thought to underlie the progression of neurodegenerative diseases including Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and related synucleinopathies. As such, it is important to understand the chemical and biological relationships between cells and pathological aggregates of α-syn. This brief review updates our understanding of the templated spread of α-syn pathology in neurodegenerative disease from the perspective of proteopathic α-syn seeds, including how these seeds are processed by cells as well as their effects on cellular function. Recent advances in understanding the conformations of α-syn seeds are highlighted, and the possible structural basis for the observed heterogeneity of synucleinopathies is discussed. Finally, we propose the possibility that some known risk factors for synucleinopathies may in fact potentiate the cell-to-cell transmission of α-syn pathology via imbalances in interrelated cell biological processes.
    MeSH term(s) Animals ; Disease Progression ; Endocytosis ; Humans ; Synucleinopathies/etiology ; Synucleinopathies/metabolism ; alpha-Synuclein/metabolism
    Chemical Substances alpha-Synuclein
    Language English
    Publishing date 2019-02-13
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 80178-1
    ISSN 1530-0307 ; 0023-6837
    ISSN (online) 1530-0307
    ISSN 0023-6837
    DOI 10.1038/s41374-019-0195-z
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  5. Article ; Online: Correction to: Isoform-specific patterns of tau burden and neuronal degeneration in MAPT-associated frontotemporal lobar degeneration.

    Giannini, Lucia A A / Ohm, Daniel T / Rozemuller, Annemieke J M / Dratch, Laynie / Suh, EunRan / van Deerlin, Vivianna M / Trojanowski, John Q / Lee, Edward B / van Swieten, John C / Grossman, Murray / Seelaar, Harro / Irwin, David J

    Acta neuropathologica

    2023  Volume 145, Issue 5, Page(s) 711

    Language English
    Publishing date 2023-03-17
    Publishing country Germany
    Document type Published Erratum
    ZDB-ID 1079-0
    ISSN 1432-0533 ; 0001-6322
    ISSN (online) 1432-0533
    ISSN 0001-6322
    DOI 10.1007/s00401-023-02556-2
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  6. Article ; Online: Amyloid-Beta (Aβ) Plaques Promote Seeding and Spreading of Alpha-Synuclein and Tau in a Mouse Model of Lewy Body Disorders with Aβ Pathology.

    Bassil, Fares / Brown, Hannah J / Pattabhiraman, Shankar / Iwasyk, Joe E / Maghames, Chantal M / Meymand, Emily S / Cox, Timothy O / Riddle, Dawn M / Zhang, Bin / Trojanowski, John Q / Lee, Virginia M-Y

    Neuron

    2023  Volume 111, Issue 22, Page(s) 3699

    Language English
    Publishing date 2023-12-07
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2023.10.030
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  7. Article: Network Proteomics of the Lewy Body Dementia Brain Reveals Presynaptic Signatures Distinct from Alzheimer's Disease.

    Shantaraman, Anantharaman / Dammer, Eric B / Ugochukwu, Obiadada / Duong, Duc M / Yin, Luming / Carter, E Kathleen / Gearing, Marla / Chen-Plotkin, Alice / Lee, Edward B / Trojanowski, John Q / Bennett, David A / Lah, James J / Levey, Allan I / Seyfried, Nicholas T / Higginbotham, Lenora

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Lewy body dementia (LBD), a class of disorders comprising Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB), features substantial clinical and pathological overlap with Alzheimer's disease (AD). The identification of biomarkers ... ...

    Abstract Lewy body dementia (LBD), a class of disorders comprising Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB), features substantial clinical and pathological overlap with Alzheimer's disease (AD). The identification of biomarkers unique to LBD pathophysiology could meaningfully advance its diagnosis, monitoring, and treatment. Using quantitative mass spectrometry (MS), we measured over 9,000 proteins across 138 dorsolateral prefrontal cortex (DLPFC) tissues from a University of Pennsylvania autopsy collection comprising control, Parkinson's disease (PD), PDD, and DLB diagnoses. We then analyzed co-expression network protein alterations in those with LBD, validated these disease signatures in two independent LBD datasets, and compared these findings to those observed in network analyses of AD cases. The LBD network revealed numerous groups or "modules" of co-expressed proteins significantly altered in PDD and DLB, representing synaptic, metabolic, and inflammatory pathophysiology. A comparison of validated LBD signatures to those of AD identified distinct differences between the two diseases. Notably, synuclein-associated presynaptic modules were elevated in LBD but decreased in AD relative to controls. We also found that glial-associated matrisome signatures consistently elevated in AD were more variably altered in LBD, ultimately stratifying those LBD cases with low versus high burdens of concurrent beta-amyloid deposition. In conclusion, unbiased network proteomic analysis revealed diverse pathophysiological changes in the LBD frontal cortex distinct from alterations in AD. These results highlight the LBD brain network proteome as a promising source of biomarkers that could enhance clinical recognition and management.
    Language English
    Publishing date 2024-01-24
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.23.576728
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  8. Article ; Online: Antemortem network analysis of spreading pathology in autopsy-confirmed frontotemporal degeneration.

    Chen, Min / Burke, Sarah / Olm, Christopher A / Irwin, David J / Massimo, Lauren / Lee, Edward B / Trojanowski, John Q / Gee, James C / Grossman, Murray

    Brain communications

    2023  Volume 5, Issue 3, Page(s) fcad147

    Abstract: Despite well-articulated hypotheses of spreading pathology in animal models of neurodegenerative disease, the basis for spreading neurodegenerative pathology in humans has been difficult to ascertain. In this study, we used graph theoretic analyses of ... ...

    Abstract Despite well-articulated hypotheses of spreading pathology in animal models of neurodegenerative disease, the basis for spreading neurodegenerative pathology in humans has been difficult to ascertain. In this study, we used graph theoretic analyses of structural networks in antemortem, multimodal MRI from autopsy-confirmed cases to examine spreading pathology in sporadic frontotemporal lobar degeneration. We defined phases of progressive cortical atrophy on T
    Language English
    Publishing date 2023-05-12
    Publishing country England
    Document type Journal Article
    ISSN 2632-1297
    ISSN (online) 2632-1297
    DOI 10.1093/braincomms/fcad147
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  9. Article ; Online: Cerebrospinal fluid biomarker panel of synaptic dysfunction in Alzheimer's disease and other neurodegenerative disorders.

    Nilsson, Johanna / Cousins, Katheryn A Q / Gobom, Johan / Portelius, Erik / Chen-Plotkin, Alice / Shaw, Leslie M / Grossman, Murray / Irwin, David J / Trojanowski, John Q / Zetterberg, Henrik / Blennow, Kaj / Brinkmalm, Ann

    Alzheimer's & dementia : the journal of the Alzheimer's Association

    2022  Volume 19, Issue 5, Page(s) 1775–1784

    Abstract: Introduction: Synaptic degeneration is a key part of the pathophysiology of neurodegenerative diseases, and biomarkers reflecting the pathological alterations are greatly needed.: Method: Seventeen synaptic proteins were quantified in a pathology- ... ...

    Abstract Introduction: Synaptic degeneration is a key part of the pathophysiology of neurodegenerative diseases, and biomarkers reflecting the pathological alterations are greatly needed.
    Method: Seventeen synaptic proteins were quantified in a pathology-confirmed cerebrospinal fluid cohort of patients with Alzheimer's disease (AD; n = 63), frontotemporal lobar degeneration (FTLD; n = 53), and Lewy body spectrum of disorders (LBD; n = 21), as well as healthy controls (HC; n = 48).
    Results: Comparisons revealed four distinct patterns: markers decreased across all neurodegenerative conditions compared to HC (the neuronal pentraxins), markers increased across all neurodegenerative conditions (14-3-3 zeta/delta), markers selectively increased in AD compared to other neurodegenerative conditions (neurogranin and beta-synuclein), and markers selectively decreased in LBD and FTLD compared to HC and AD (AP2B1 and syntaxin-1B).
    Discussion: Several of the synaptic proteins may serve as biomarkers for synaptic dysfunction in AD, LBD, and FTLD. Additionally, differential patterns of synaptic protein alterations seem to be present across neurodegenerative diseases.
    Highlights: A panel of synaptic proteins were quantified in the cerebrospinal fluid using mass spectrometry. We compared Alzheimer's disease, frontotemporal degeneration, and Lewy body spectrum of disorders. Pathology was confirmed by autopsy or familial mutations. We discovered synaptic biomarkers for synaptic degeneration and cognitive decline. We found differential patterns of synaptic proteins across neurodegenerative diseases.
    MeSH term(s) Humans ; Alzheimer Disease/cerebrospinal fluid ; Neurodegenerative Diseases ; Frontotemporal Lobar Degeneration/genetics ; Neurogranin ; Biomarkers/cerebrospinal fluid ; tau Proteins/cerebrospinal fluid ; Amyloid beta-Peptides/cerebrospinal fluid
    Chemical Substances Neurogranin (132654-77-4) ; Biomarkers ; tau Proteins ; Amyloid beta-Peptides
    Language English
    Publishing date 2022-10-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2211627-8
    ISSN 1552-5279 ; 1552-5260
    ISSN (online) 1552-5279
    ISSN 1552-5260
    DOI 10.1002/alz.12809
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  10. Article ; Online: Association of CSF Aβ, amyloid PET, and cognition in cognitively unimpaired elderly adults.

    Guo, Tengfei / Shaw, Leslie M / Trojanowski, John Q / Jagust, William J / Landau, Susan M

    Neurology

    2020  Volume 95, Issue 15, Page(s) e2075–e2085

    Abstract: Objective: To compare CSF β-amyloid (Aβ) and florbetapir PET measurements in cognitively unimpaired (CU) elderly adults in order to detect the earliest abnormalities and compare their predictive effect for cognitive decline.: Methods: A total of 259 ... ...

    Abstract Objective: To compare CSF β-amyloid (Aβ) and florbetapir PET measurements in cognitively unimpaired (CU) elderly adults in order to detect the earliest abnormalities and compare their predictive effect for cognitive decline.
    Methods: A total of 259 CU individuals were categorized as abnormal (+) or normal (-) on CSF Aβ
    Results: The proportions of individuals in each discordant group were similar (8.1% CSF+/PET- and 7.7% CSF-/PET+). Among baseline Aβ-negative (CSF-/PET-) individuals with longitudinal CSF and PET measurements, a larger proportion subsequently worsened on CSF Aβ (odds ratio 4 [95% confidence interval (CI) 1.1, 22.1],
    Conclusions: The proportions of discordant PET and CSF Aβ-positive individuals were similar cross-sectionally. However, unambiguously Aβ-negative (CSF-/PET-) individuals are more likely to show subsequent worsening on CSF than PET, supporting the idea that CSF detects the earliest Aβ changes. In discordant cases, only PET abnormality predicted cognitive decline, suggesting that abnormal Aβ PET changes are a later phenomenon in cognitively normal individuals.
    MeSH term(s) Aged ; Amyloid beta-Peptides/cerebrospinal fluid ; Aniline Compounds/metabolism ; Biomarkers/cerebrospinal fluid ; Biomarkers/metabolism ; Brain/metabolism ; Cognitive Dysfunction/diagnosis ; Cognitive Dysfunction/diagnostic imaging ; Early Diagnosis ; Ethylene Glycols/metabolism ; Female ; Humans ; Longitudinal Studies ; Male ; Mass Spectrometry ; Neuropsychological Tests ; Peptide Fragments/cerebrospinal fluid ; Positron-Emission Tomography
    Chemical Substances Amyloid beta-Peptides ; Aniline Compounds ; Biomarkers ; Ethylene Glycols ; Peptide Fragments ; amyloid beta-protein (1-40) ; amyloid beta-protein (1-42) ; florbetapir (6867Q6IKOD)
    Language English
    Publishing date 2020-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 207147-2
    ISSN 1526-632X ; 0028-3878
    ISSN (online) 1526-632X
    ISSN 0028-3878
    DOI 10.1212/WNL.0000000000010596
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