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  1. Article ; Online: Organ-specific aging in the plasma proteome predicts disease.

    Duggan, Michael R / Walker, Keenan A

    Trends in molecular medicine

    2024  Volume 30, Issue 5, Page(s) 423–424

    Abstract: In their recent Nature paper, Oh et al. use 4979 plasma proteins collected across multiple cohorts, publicly available gene expression data, and machine learning models to identify 11 organ-specific aging scores that are linked to organ-specific disease ... ...

    Abstract In their recent Nature paper, Oh et al. use 4979 plasma proteins collected across multiple cohorts, publicly available gene expression data, and machine learning models to identify 11 organ-specific aging scores that are linked to organ-specific disease and mortality risk, including heart failure, cognitive decline, and Alzheimer's disease.
    MeSH term(s) Humans ; Aging/blood ; Proteome/analysis ; Blood Proteins/genetics ; Blood Proteins/metabolism ; Organ Specificity ; Machine Learning ; Alzheimer Disease/blood ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Biomarkers/blood ; Heart Failure/blood ; Heart Failure/genetics
    Chemical Substances Proteome ; Blood Proteins ; Biomarkers
    Language English
    Publishing date 2024-01-31
    Publishing country England
    Document type Journal Article
    ZDB-ID 2036490-8
    ISSN 1471-499X ; 1471-4914
    ISSN (online) 1471-499X
    ISSN 1471-4914
    DOI 10.1016/j.molmed.2024.01.005
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  2. Article ; Online: Plasma biomarkers for Alzheimer's and related dementias: A review and outlook for clinical neuropsychology.

    Dark, Heather E / Duggan, Michael R / Walker, Keenan A

    Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists

    2024  Volume 39, Issue 3, Page(s) 313–324

    Abstract: Recent technological advances have improved the sensitivity and specificity of blood-based biomarkers for Alzheimer's disease and related dementias. Accurate quantification of amyloid-ß peptide, phosphorylated tau (pTau) isoforms, as well as markers of ... ...

    Abstract Recent technological advances have improved the sensitivity and specificity of blood-based biomarkers for Alzheimer's disease and related dementias. Accurate quantification of amyloid-ß peptide, phosphorylated tau (pTau) isoforms, as well as markers of neurodegeneration (neurofilament light chain [NfL]) and neuro-immune activation (glial fibrillary acidic protein [GFAP] and chitinase-3-like protein 1 [YKL-40]) in blood has allowed researchers to characterize neurobiological processes at scale in a cost-effective and minimally invasive manner. Although currently used primarily for research purposes, these blood-based biomarkers have the potential to be highly impactful in the clinical setting - aiding in diagnosis, predicting disease risk, and monitoring disease progression. Whereas plasma NfL has shown promise as a non-specific marker of neuronal injury, plasma pTau181, pTau217, pTau231, and GFAP have demonstrated desirable levels of sensitivity and specificity for identification of individuals with Alzheimer's disease pathology and Alzheimer's dementia. In this forward looking review, we (i) provide an overview of the most commonly used blood-based biomarkers for Alzheimer's disease and related dementias, (ii) discuss how comorbid medical conditions, demographic, and genetic factors can inform the interpretation of these biomarkers, (iii) describe ongoing efforts to move blood-based biomarkers into the clinic, and (iv) highlight the central role that clinical neuropsychologists may play in contextualizing and communicating blood-based biomarker results for patients.
    MeSH term(s) Humans ; Alzheimer Disease/blood ; Alzheimer Disease/diagnosis ; Biomarkers/blood ; Neuropsychology ; Dementia/diagnosis ; Dementia/blood ; tau Proteins/blood ; Amyloid beta-Peptides/blood
    Chemical Substances Biomarkers ; tau Proteins ; Amyloid beta-Peptides
    Language English
    Publishing date 2024-03-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 632972-x
    ISSN 1873-5843 ; 0887-6177
    ISSN (online) 1873-5843
    ISSN 0887-6177
    DOI 10.1093/arclin/acae019
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  3. Article ; Online: From Practice to Public Health: Broadening Neuropsychology's Reach & Value-An Introduction to the National Academy of Neuropsychology's 2022 Annual Conference Special Issue.

    Del Bene, Victor A / Walker, Keenan A

    Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists

    2024  Volume 39, Issue 3, Page(s) 273–275

    Abstract: This special issue is centered around presentations from the National Academy of Neuropsychology 2022 Annual Conference. The theme of the conference, "From Practice to Public Health: Broadening Neuropsychology's Reach & Value" is pivotal for the field's ... ...

    Abstract This special issue is centered around presentations from the National Academy of Neuropsychology 2022 Annual Conference. The theme of the conference, "From Practice to Public Health: Broadening Neuropsychology's Reach & Value" is pivotal for the field's future. With an ever-shifting technological landscape and recent changes in clinical practice post-COVID, we are left wondering how neuropsychology will develop. How will we use biomedical and technological advances, such as blood-based Alzheimer's disease biomarkers or passive digital recordings, to improve clinical care and further expand our understanding of disease mechanisms? As neuropsychologists, how can we use our expertise to empirically inform public health policy? The diagnosis and treatment of post-acute sequelae of COVID-19, the identification and characterization of post-pandemic educational setbacks, and the adaptation of new technological and diagnostic advances into clinical practice workflows represent a vital set of new challenges and opportunities poised to disrupt traditional modes of practice. The articles in this special issue convey the role of neuropsychology in addressing these emerging issues and illustrate how and why neuropsychology is well positioned to be at the forefront of clinical practice and scientific advancements.
    MeSH term(s) Humans ; Neuropsychology ; COVID-19 ; Public Health ; Congresses as Topic ; Academies and Institutes
    Language English
    Publishing date 2024-03-23
    Publishing country United States
    Document type Introductory Journal Article ; Journal Article
    ZDB-ID 632972-x
    ISSN 1873-5843 ; 0887-6177
    ISSN (online) 1873-5843
    ISSN 0887-6177
    DOI 10.1093/arclin/acae012
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  4. Article ; Online: New IDEAS about amyloid, race and dementia disparities.

    Dark, Heather E / Walker, Keenan A

    Nature reviews. Neurology

    2022  Volume 19, Issue 1, Page(s) 5–6

    MeSH term(s) Humans ; Dementia/epidemiology ; Alzheimer Disease/epidemiology ; Amyloid ; Amyloid beta-Peptides
    Chemical Substances Amyloid ; Amyloid beta-Peptides
    Language English
    Publishing date 2022-11-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2491514-2
    ISSN 1759-4766 ; 1759-4758
    ISSN (online) 1759-4766
    ISSN 1759-4758
    DOI 10.1038/s41582-022-00748-0
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  5. Article ; Online: Reducing decoys focuses fighting microglia.

    Duggan, Michael R / Walker, Keenan A

    Nature aging

    2022  Volume 2, Issue 7, Page(s) 573–575

    Abstract: Genetic variation linked to lower levels of soluble ST2, a decoy cytokine receptor for IL-33, may protect against Alzheimer's disease in ... ...

    Abstract Genetic variation linked to lower levels of soluble ST2, a decoy cytokine receptor for IL-33, may protect against Alzheimer's disease in female
    MeSH term(s) Male ; Humans ; Female ; Alzheimer Disease/genetics ; Microglia/immunology ; Interleukin-1 Receptor-Like 1 Protein ; Cytokines ; Apolipoproteins E
    Chemical Substances Interleukin-1 Receptor-Like 1 Protein ; Cytokines ; Apolipoproteins E ; IL1RL1 protein, human
    Language English
    Publishing date 2022-07-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Comment
    ISSN 2662-8465
    ISSN (online) 2662-8465
    DOI 10.1038/s43587-022-00251-7
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  6. Article ; Online: Inflammation and neurodegeneration: chronicity matters.

    Walker, Keenan A

    Aging

    2018  Volume 11, Issue 1, Page(s) 3–4

    MeSH term(s) Alzheimer Disease/etiology ; Alzheimer Disease/pathology ; Brain/pathology ; Humans ; Inflammation/complications ; Inflammation/pathology
    Language English
    Publishing date 2018-12-15
    Publishing country United States
    Document type Editorial
    ISSN 1945-4589
    ISSN (online) 1945-4589
    DOI 10.18632/aging.101704
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  7. Article: The Role of Chronic Infection in Alzheimer's Disease: Instigators, Co-conspirators, or Bystanders?

    Butler, Lauren / Walker, Keenan A

    Current clinical microbiology reports

    2021  Volume 8, Issue 4, Page(s) 199–212

    Abstract: Purpose of review: Herein, we provide a critical review of the clinical and translational research examining the relationship between viral and bacterial pathogens and Alzheimer's disease. In addition, we provide an overview of the biological pathways ... ...

    Abstract Purpose of review: Herein, we provide a critical review of the clinical and translational research examining the relationship between viral and bacterial pathogens and Alzheimer's disease. In addition, we provide an overview of the biological pathways through which chronic infection may contribute to Alzheimer's disease.
    Recent findings: Dementia due to Alzheimer's disease is a leading cause of disability among older adults in developed countries, yet knowledge of the causative factors that promote Alzheimer's disease pathogenesis remains incomplete. Over the past several decades, numerous studies have demonstrated an association of chronic viral and bacterial infection with Alzheimer's disease. Implicated infectious agents include numerous herpesviruses (HSV-1, HHV-6, HHV-7) and various gastric, enteric, and oral bacterial species, as well as
    Summary: Evidence supports the association between multiple pathogens and Alzheimer's disease risk. Whether these pathogens play a causal role in Alzheimer's pathophysiology remains an open question. We propose that the host immune response to active or latent infection in the periphery or in the brain triggers or accelerates the Alzheimer's disease processes, including the accumulation of amyloid-ß and pathogenic tau, and neuroinflammation. While recent research suggests that such theories are plausible, additional longitudinal studies linking microorganisms to Aß and phospho-tau development, neuroinflammation, and clinically defined Alzheimer's dementia are needed.
    Language English
    Publishing date 2021-04-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2786543-5
    ISSN 2196-5471
    ISSN 2196-5471
    DOI 10.1007/s40588-021-00168-6
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  8. Article ; Online: Energizing Mitochondria to Prevent Mobility Loss in Aging: Rationale and Hypotheses.

    Tian, Qu / Lee, Philip R / Walker, Keenan A / Ferrucci, Luigi

    Exercise and sport sciences reviews

    2023  Volume 51, Issue 3, Page(s) 96–102

    Abstract: Based on recent studies from our group and others, we hypothesize that mitochondrial dysfunction during aging may be the root cause of mobility decline through deficits in the musculoskeletal and central nervous systems. Mitochondrial dysfunction could ... ...

    Abstract Based on recent studies from our group and others, we hypothesize that mitochondrial dysfunction during aging may be the root cause of mobility decline through deficits in the musculoskeletal and central nervous systems. Mitochondrial dysfunction could be a therapeutic target to prevent mobility decline in aging.
    MeSH term(s) Humans ; Aging/physiology ; Mitochondria/physiology
    Language English
    Publishing date 2023-04-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 187040-3
    ISSN 1538-3008 ; 0091-6331
    ISSN (online) 1538-3008
    ISSN 0091-6331
    DOI 10.1249/JES.0000000000000315
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  9. Article ; Online: Connecting aging biology and inflammation in the omics era.

    Walker, Keenan A / Basisty, Nathan / Wilson, David M / Ferrucci, Luigi

    The Journal of clinical investigation

    2022  Volume 132, Issue 14

    Abstract: Aging is characterized by the accumulation of damage to macromolecules and cell architecture that triggers a proinflammatory state in blood and solid tissues, termed inflammaging. Inflammaging has been implicated in the pathogenesis of many age- ... ...

    Abstract Aging is characterized by the accumulation of damage to macromolecules and cell architecture that triggers a proinflammatory state in blood and solid tissues, termed inflammaging. Inflammaging has been implicated in the pathogenesis of many age-associated chronic diseases as well as loss of physical and cognitive function. The search for mechanisms that underlie inflammaging focused initially on the hallmarks of aging, but it is rapidly expanding in multiple directions. Here, we discuss the threads connecting cellular senescence and mitochondrial dysfunction to impaired mitophagy and DNA damage, which may act as a hub for inflammaging. We explore the emerging multi-omics efforts that aspire to define the complexity of inflammaging - and identify molecular signatures and novel targets for interventions aimed at counteracting excessive inflammation and its deleterious consequences while preserving the physiological immune response. Finally, we review the emerging evidence that inflammation is involved in brain aging and neurodegenerative diseases. Our goal is to broaden the research agenda for inflammaging with an eye on new therapeutic opportunities.
    MeSH term(s) Aging/genetics ; Biology ; Cellular Senescence/physiology ; DNA Damage ; Humans ; Inflammation/pathology
    Language English
    Publishing date 2022-07-15
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI158448
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  10. Article ; Online: Plasma metabolomic markers underlying skeletal muscle mitochondrial function relationships with cognition and motor function.

    Tian, Qu / Greig, Erin E / Walker, Keenan A / Fishbein, Kenneth W / Spencer, Richard G / Resnick, Susan M / Ferrucci, Luigi

    Age and ageing

    2024  Volume 53, Issue 4

    Abstract: Background: Lower skeletal muscle mitochondrial function is associated with future cognitive impairment and mobility decline, but the biological underpinnings for these associations are unclear. We examined metabolomic markers underlying skeletal muscle ...

    Abstract Background: Lower skeletal muscle mitochondrial function is associated with future cognitive impairment and mobility decline, but the biological underpinnings for these associations are unclear. We examined metabolomic markers underlying skeletal muscle mitochondrial function, cognition and motor function.
    Methods: We analysed data from 560 participants from the Baltimore Longitudinal Study of Aging (mean age: 68.4 years, 56% women, 28% Black) who had data on skeletal muscle oxidative capacity (post-exercise recovery rate of phosphocreatine, kPCr) via 31P magnetic resonance spectroscopy and targeted plasma metabolomics using LASSO model. We then examined which kPCr-related markers were also associated with cognition and motor function in a larger sample (n = 918, mean age: 69.4, 55% women, 27% Black).
    Results: The LASSO model revealed 24 metabolites significantly predicting kPCr, with the top 5 being asymmetric dimethylarginine, lactic acid, lysophosphatidylcholine a C18:1, indoleacetic acid and triacylglyceride (17:1_34:3), also significant in multivariable linear regression. The kPCr metabolite score was associated with cognitive or motor function, with 2.5-minute usual gait speed showing the strongest association (r = 0.182). Five lipids (lysophosphatidylcholine a C18:1, phosphatidylcholine ae C42:3, cholesteryl ester 18:1, sphingomyelin C26:0, octadecenoic acid) and 2 amino acids (leucine, cystine) were associated with both cognitive and motor function measures.
    Conclusion: Our findings add evidence to the hypothesis that mitochondrial function is implicated in the pathogenesis of cognitive and physical decline with aging and suggest that targeting specific metabolites may prevent cognitive and mobility decline through their effects on mitochondria. Future omics studies are warranted to confirm these findings and explore mechanisms underlying mitochondrial dysfunction in aging phenotypes.
    MeSH term(s) Female ; Humans ; Aged ; Male ; Longitudinal Studies ; Lysophosphatidylcholines ; Muscle, Skeletal ; Cognition ; Cognitive Dysfunction
    Chemical Substances Lysophosphatidylcholines
    Language English
    Publishing date 2024-03-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 186788-x
    ISSN 1468-2834 ; 0002-0729
    ISSN (online) 1468-2834
    ISSN 0002-0729
    DOI 10.1093/ageing/afae079
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