Energizing Mitochondria to Prevent Mobility Loss in Aging: Rationale and Hypotheses DOI
Qu Tian, Philip R. Lee, Keenan A. Walker

и другие.

Exercise and Sport Sciences Reviews, Год журнала: 2023, Номер 51(3), С. 96 - 102

Опубликована: Апрель 14, 2023

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 musculoskeletal central nervous systems. Mitochondrial could a therapeutic target to prevent aging.

Язык: Английский

Targeting the JAK2-STAT3 pathway to inhibit cGAS-STING activation improves neuronal senescence after ischemic stroke DOI

Wei Zhang,

Meijie Xu,

Fangyu Chen

и другие.

Experimental Neurology, Год журнала: 2023, Номер 368, С. 114474 - 114474

Опубликована: Июль 5, 2023

Язык: Английский

Процитировано

23

Neuroinflammaging: A Tight Line Between Normal Aging and Age-Related Neurodegenerative Disorders DOI Creative Commons
Luca Soraci, Andrea Corsonello, Ersilia Paparazzo

и другие.

Aging and Disease, Год журнала: 2024, Номер unknown

Опубликована: Янв. 1, 2024

Aging in the healthy brain is characterized by a low-grade, chronic, and sterile inflammatory process known as neuroinflammaging. This condition, mainly consisting an up-regulation of response at level, contributes to pathogenesis age-related neurodegenerative disorders. Development this proinflammatory state involves interaction between genetic environmental factors, able induce epigenetic modifications. Indeed, exposure compounds, drugs, infections, can contribute modifications DNA methylome, histone fold proteins, nucleosome positioning, leading modulation neuroinflammatory responses. Furthermore, some modifiers, which combine interact during life course, modeling epigenome dynamics sustain, or dampen phenotype. The aim review summarize current knowledge about neuroinflammaging with particular focus on mechanisms underlying onset progression cascades central nervous system; furthermore, we describe diagnostic biomarkers that may increase accuracy help tailor therapeutic strategies patients diseases.

Язык: Английский

Процитировано

10

Immunophenotypes in psychosis: is it a premature inflamm-aging disorder? DOI Creative Commons
Song Chen, Yunlong Tan, Li Tian

и другие.

Molecular Psychiatry, Год журнала: 2024, Номер 29(9), С. 2834 - 2848

Опубликована: Март 26, 2024

Immunopsychiatric field has rapidly accumulated evidence demonstrating the involvement of both innate and adaptive immune components in psychotic disorders such as schizophrenia. Nevertheless, researchers are facing dilemmas discrepant findings immunophenotypes outside inside brains patients, discovered by recent meta-analyses. These discrepancies make interpretations interrogations on their roles psychosis remain vague even controversial, regarding whether certain cells more activated or less so, they causal consequential, beneficial harmful for psychosis. Addressing these issues is not at all trivial, either brain an enormously heterogeneous plastic cell population, falling into a vast range lineages subgroups, functioning differently malleably context-dependent manners. This review aims to overview currently known patients with psychosis, provocatively suggest premature "burnout" inflamm-aging initiated since organ development potential primary mechanism behind pathogenesis disorders.

Язык: Английский

Процитировано

9

Association between the systemic immune-inflammation index and sarcopenia: a systematic review and meta-analysis DOI Creative Commons

Siye Xie,

Qi Wu

Journal of Orthopaedic Surgery and Research, Год журнала: 2024, Номер 19(1)

Опубликована: Май 28, 2024

Sarcopenia is associated with increased morbidity and mortality. The systemic immune-inflammation index (SII) has been correlated to a variety of disorders. present study conducted systematic review meta-analysis investigate the relationship between SII sarcopenia.

Язык: Английский

Процитировано

9

Multifunctional scaffolds for bone repair following age-related biological decline: Promising prospects for smart biomaterial-driven technologies DOI
Jonathan Schwartzman,

Max McCall,

Yasmine Ghattas

и другие.

Biomaterials, Год журнала: 2024, Номер 311, С. 122683 - 122683

Опубликована: Июнь 28, 2024

Язык: Английский

Процитировано

9

The transcription factor STAT3 and aging: an intermediate medium DOI

Min Shi,

H Li,

Runyu Liang

и другие.

Biogerontology, Год журнала: 2025, Номер 26(2)

Опубликована: Фев. 7, 2025

Язык: Английский

Процитировано

1

Aging-related hyperphosphatemia triggers the release of TNF-α from macrophages, promoting indicators of sarcopenia through the reduction of IL-15 expression in skeletal muscle DOI Creative Commons
Elena Alcalde‐Estévez,

Ariadna Moreno-Piedra,

Ana Asenjo‐Bueno

и другие.

Life Sciences, Год журнала: 2025, Номер 368, С. 123507 - 123507

Опубликована: Фев. 25, 2025

Язык: Английский

Процитировано

1

Impact of Geroscience on Therapeutic Strategies for Older Adults With Cardiovascular Disease DOI Creative Commons
Daniel E. Forman, George A. Kuchel, John C. Newman

и другие.

Journal of the American College of Cardiology, Год журнала: 2023, Номер 82(7), С. 631 - 647

Опубликована: Июнь 28, 2023

Язык: Английский

Процитировано

20

Mitochondrial OGG1 expression reduces age-associated neuroinflammation by regulating cytosolic mitochondrial DNA DOI Creative Commons
Mansoor Hussain,

Xixia Chu,

Burcin Duan Sahbaz

и другие.

Free Radical Biology and Medicine, Год журнала: 2023, Номер 203, С. 34 - 44

Опубликована: Апрель 1, 2023

Язык: Английский

Процитировано

18

Skeletal muscle mitochondrial function predicts cognitive impairment and is associated with biomarkers of Alzheimer's disease and neurodegeneration DOI
Qu Tian, Murat Bilgel, Keenan A. Walker

и другие.

Alzheimer s & Dementia, Год журнала: 2023, Номер 19(10), С. 4436 - 4445

Опубликована: Авг. 2, 2023

Abstract INTRODUCTION Mitochondrial dysfunction is implicated in the pathophysiology of many chronic diseases. Whether it related to cognitive impairment and pathological markers unknown. METHODS We examined associations vivo skeletal muscle mitochondrial function (post‐exercise recovery rate phosphocreatine [kPCr] via magnetic resonance [MR] spectroscopy with future mild (MCI) or dementia, positron emission tomography (PET) blood biomarkers Alzheimer's disease [AD] neurodegeneration (i.e., Pittsburgh Compound‐B [PiB] distribution volume ratio [DVR] for amyloid beta [Aβ], flortaucipir (FTP) standardized uptake value [SUVR] tau, Aβ 42 / 40 ratio, phosphorylated tau 181 [p‐tau181], neurofilament light chain [NfL], glial fibrillary acidic protein [GFAP]). RESULTS After covariate adjustment, each standard deviation (SD) higher kPCr level was associated 52% lower hazards developing MCI/dementia, 59% odds being PiB positive specific DVR frontal, parietal, temporal regions, cingulate cortex pallidum. Higher also plasma GFAP. DISCUSSION In aging, may play a vital role AD changes neuroinflammation. Highlights risk (MCI)/dementia. tracer uptake. key (AD) neurodegeneration.

Язык: Английский

Процитировано

18