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  1. Article: Editorial: Mitochondria at the nexus of metabolism, aging, and disease.

    Mallilankaraman, Karthik Babu / Kennedy, Brian K / Sorrentino, Vincenzo / Luciani, Alessandro

    Frontiers in cell and developmental biology

    2024  Volume 11, Page(s) 1356278

    Language English
    Publishing date 2024-01-11
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2023.1356278
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  2. Article ; Online: Investigating the biology of yeast aging by single-cell RNA-seq.

    Zhang, Yi / Zhang, Xiannian / Kennedy, Brian K

    Aging

    2023  Volume 15, Issue 15, Page(s) 7340–7342

    MeSH term(s) Humans ; Saccharomyces cerevisiae/genetics ; Single-Cell Gene Expression Analysis ; Aging/genetics ; Biology ; Sequence Analysis, RNA ; Gene Expression Profiling
    Language English
    Publishing date 2023-08-14
    Publishing country United States
    Document type Editorial
    ISSN 1945-4589
    ISSN (online) 1945-4589
    DOI 10.18632/aging.204991
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  3. Article ; Online: Editorial

    Karthik Babu Mallilankaraman / Brian K. Kennedy / Vincenzo Sorrentino / Alessandro Luciani

    Frontiers in Cell and Developmental Biology, Vol

    Mitochondria at the nexus of metabolism, aging, and disease

    2024  Volume 11

    Keywords ageing ; metabolism ; mitochondrial dysfuncion ; mitophagy ; metabolic disease ; dietary intervention ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2024-01-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: A concerted increase in readthrough and intron retention drives transposon expression during aging and senescence.

    Pabis, Kamil / Barardo, Diogo / Sirbu, Olga / Selvarajoo, Kumar / Gruber, Jan / Kennedy, Brian K

    eLife

    2024  Volume 12

    Abstract: Aging and senescence are characterized by pervasive transcriptional dysfunction, including increased expression of transposons and introns. Our aim was to elucidate mechanisms behind this increased expression. Most transposons are found within genes and ... ...

    Abstract Aging and senescence are characterized by pervasive transcriptional dysfunction, including increased expression of transposons and introns. Our aim was to elucidate mechanisms behind this increased expression. Most transposons are found within genes and introns, with a large minority being close to genes. This raises the possibility that transcriptional readthrough and intron retention are responsible for age-related changes in transposon expression rather than expression of autonomous transposons. To test this, we compiled public RNA-seq datasets from aged human fibroblasts, replicative and drug-induced senescence in human cells, and RNA-seq from aging mice and senescent mouse cells. Indeed, our reanalysis revealed a correlation between transposons expression, intron retention, and transcriptional readthrough across samples and within samples. Both intron retention and readthrough increased with aging or cellular senescence and these transcriptional defects were more pronounced in human samples as compared to those of mice. In support of a causal connection between readthrough and transposon expression, analysis of models showing induced transcriptional readthrough confirmed that they also show elevated transposon expression. Taken together, our data suggest that elevated transposon reads during aging seen in various RNA-seq dataset are concomitant with multiple transcriptional defects. Intron retention and transcriptional readthrough are the most likely explanation for the expression of transposable elements that lack a functional promoter.
    MeSH term(s) Animals ; Mice ; Humans ; Aged ; Introns ; RNA-Seq ; Aging/genetics ; Promoter Regions, Genetic ; DNA Transposable Elements/genetics
    Chemical Substances DNA Transposable Elements
    Language English
    Publishing date 2024-04-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.87811
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  5. Article ; Online: Aging inverts the effects of p75

    Wang, Zijun / Kennedy, Brian K / Wong, Lik-Wei / Sajikumar, Sreedharan

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2023  Volume 37, Issue 8, Page(s) e23067

    Abstract: Age-induced impairments in learning and memory are in part caused by changes to hippocampal synaptic plasticity during aging. The p75 neurotrophin receptor ( ... ...

    Abstract Age-induced impairments in learning and memory are in part caused by changes to hippocampal synaptic plasticity during aging. The p75 neurotrophin receptor (p75
    MeSH term(s) Animals ; Male ; Mice ; Aging ; Hippocampus/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Neuronal Plasticity ; Neurons/metabolism ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Ngfr protein, mouse
    Language English
    Publishing date 2023-07-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202201640RRR
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  6. Article ; Online: H

    Arumugam, Thiruma V / Kennedy, Brian K

    Cell

    2018  Volume 173, Issue 1, Page(s) 8–10

    Abstract: ... ...

    Abstract H
    MeSH term(s) NAD ; Sirtuin 1
    Chemical Substances NAD (0U46U6E8UK) ; Sirtuin 1 (EC 3.5.1.-)
    Language English
    Publishing date 2018-03-23
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2018.03.011
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    Zs.MG 58: Show issues

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  7. Article ; Online: Aging: Mechanisms, Measures, and Interventions.

    Chung, Maxey C M / Kennedy, Brian K

    Proteomics

    2020  Volume 20, Issue 5-6, Page(s) e1800336

    MeSH term(s) Aging ; Animals ; Body Temperature Regulation ; Computational Biology ; Homeostasis ; Humans ; Longevity ; Metabolic Diseases/etiology ; Microbiota ; Oxidative Stress ; Resilience, Psychological ; Stress, Physiological
    Keywords covid19
    Language English
    Publishing date 2020-03-31
    Publishing country Germany
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2032093-0
    ISSN 1615-9861 ; 1615-9853
    ISSN (online) 1615-9861
    ISSN 1615-9853
    DOI 10.1002/pmic.201800336
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    Zs.A 5386: Show issues Location:
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  8. Article ; Online: A mechanistic perspective on the health promoting effects of alcohol - A focus on epigenetics modification.

    Guan, Shou Ping / Kumar, Shermila N / Fann, David Y / Kennedy, Brian K

    Alcohol (Fayetteville, N.Y.)

    2022  Volume 107, Page(s) 91–96

    Abstract: While the detrimental effects of binge drinking are well recognized, low-to-moderate alcohol consumption may be beneficial to health, although the underlying mechanism(s) remains elusive. In this opinion article, we will examine the effects of low dose ... ...

    Abstract While the detrimental effects of binge drinking are well recognized, low-to-moderate alcohol consumption may be beneficial to health, although the underlying mechanism(s) remains elusive. In this opinion article, we will examine the effects of low dose alcohol consumption from the perspective of epigenetic modulation. Biochemically, alcohol is metabolized into acetate and subsequently to acetyl-coA, which can modulate histone acetylation levels. While elevated levels of acetyl-CoA are detrimental for longevity, we argue that diminished acetyl-CoA also negatively affects fatty acid biosynthesis and histone acetylation, which play a critical role in gene expression and, ultimately, health span. Since mitochondrial function and glucose metabolism, which provide the main source of nucleocytoplasmic acetyl-CoA, are compromised with age, alcohol-derived acetate could be an alternative source of acetyl-CoA to compensate. Hence, the health benefits of low ethanol consumption may be more pronounced after midlife, since mitochondrial function and/or glucose metabolism are diminished in this phase of the life course. Indeed, various clinical alcohol consumption studies concur with this notion, and have shown that a low dose of regular alcohol intake after midlife brings about various health and survival benefits. The requirement for regular alcohol intake may also reflect the transient nature of ethanol-induced histone acetylation. Conversely, ethanol may also stimulate carcinogenesis by inhibiting DNA methylation, as it was shown to reduce various pathways leading to DNA and histone methylation. However, unlike acetylation, where ethanol directly increases the substrate for acetylation, this effect was only observed in the high alcohol exposure cohort. While alcohol-derived acetate may be beneficial for health after midlife, various detrimental effects of alcohol consumption remain, and hence, we do not advocate excessive drinking to increase acetate. This opinion article establishes a possible role of ethanol-derived acetate in achieving homeostasis and sustaining an organism's health span.
    MeSH term(s) Humans ; Histones/metabolism ; Acetyl Coenzyme A/genetics ; Acetyl Coenzyme A/metabolism ; Ethanol ; Epigenesis, Genetic ; DNA Methylation ; Acetates/metabolism ; Glucose ; Health Promotion ; Acetylation
    Chemical Substances Histones ; Acetyl Coenzyme A (72-89-9) ; Ethanol (3K9958V90M) ; Acetates ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2022-08-18
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 605912-0
    ISSN 1873-6823 ; 0741-8329
    ISSN (online) 1873-6823
    ISSN 0741-8329
    DOI 10.1016/j.alcohol.2022.07.009
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  9. Article ; Online: Accelerated aging in schizophrenia and related disorders: Future research.

    Kirkpatrick, Brian / Kennedy, Brian K

    Schizophrenia research

    2017  Volume 196, Page(s) 4–8

    Abstract: Several lines of evidence suggest schizophrenia is a segmental progeria, that is, some but not all aspects of accelerated aging may be present. However, the evidence has not been consistent. Problems with matching and confounding may account for some of ... ...

    Abstract Several lines of evidence suggest schizophrenia is a segmental progeria, that is, some but not all aspects of accelerated aging may be present. However, the evidence has not been consistent. Problems with matching and confounding may account for some of these discrepancies. Given the etiopathophysiological heterogeneity of schizophrenia, it is possible that only a specific pathophysiological group within schizophrenia is associated with progeroid features, while others are not, or that one group is associated with a particular segment of aging features, while other progeroid features are found in another pathophysiological subgroup. In the aging research field, significant progress has been made in identifying the molecular pathways that confer aging: epigenetic changes, inflammation, proteostasis, adult stem cell function, metabolic changes, and adaptation to stress, and macromolecular damage. In addition to replication and clarification of existing kinds of evidence, examining these aging pathways would improve our understanding of progeria in schizophrenia.
    MeSH term(s) Aging/metabolism ; Biomedical Research ; Humans ; Schizophrenia/metabolism
    Language English
    Publishing date 2017-07-06
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 639422-x
    ISSN 1573-2509 ; 0920-9964
    ISSN (online) 1573-2509
    ISSN 0920-9964
    DOI 10.1016/j.schres.2017.06.034
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  10. Article ; Online: Aging mechanisms and interventions that impact senior health: Introduction to a special issue on Geroscience.

    Leng, Sean X / Liu, Baohua / Kennedy, Brian K

    Aging medicine (Milton (N.S.W))

    2019  Volume 2, Issue 3, Page(s) 126–129

    Language English
    Publishing date 2019-09-20
    Publishing country Australia
    Document type Editorial
    ISSN 2475-0360
    ISSN (online) 2475-0360
    DOI 10.1002/agm2.12086
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