Neuronal Senescence in the Aged Brain

Chou, Shu-Min; Yen, Yi‐Hao; Fang, Yuan; Zhang, Su‐Chun; Chong, Cheong-Meng

doi:10.14336/ad.2023.0214

Cited by 21 publications

(5 citation statements)

References 147 publications

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“…Consequently, we believe that ferrosenescence may be more prevalent in SCZ then ferroptosis. Moreover, ferrosenescence may account for the other SCZ markers, including decreased brain volume, γ oscillations on EEG, and mitochondrial dysfunction [55][56][57][58].…”

Section: Ferrosenescence Vs Ferroptosismentioning

confidence: 99%

The Future of Antipsychotic Interventions: From Managing Symptoms to Improving Outcomes

Sfera,

Imran,

Sfera

et al. 2024

Preprint

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For the past 70 years, dopamine hypothesis has been the key working model in schizophrenia. This has contributed to the development of numerous inhibitors of dopaminergic signaling, antipsychotic drugs, which led to rapid symptom resolution but only marginal outcome improvement. Over the past decades, there was limited research on the quantifiable pathological changes in schizophrenia, including premature cellular/neuronal, senescence, brain volume loss, attenuation of gamma oscillations on electroencephalogram and oxidation of lipids in plasma and mitochondrial membranes. We surmise that aberrant activation of aryl hydrocarbon receptor by toxins derived from the gut microbes or the environment drives premature cellular, including neuronal, senescence, a hallmark of schizophrenia. Early brain aging promotes secondary changes, including impairment and loss of mitochondria, gray matter depletion, decreased gamma oscillations, and a compensatory metabolic shift to lactate and lactylation. The aim of this narrative review is twofold: 1. To summarize what is known about premature cellular/neuronal senescence in schizophrenia or schizophrenia-like disorders. 2. To discuss novel strategies for improving long-term outcome in severe mental illness with natural senotherapeutics, membrane lipid replacement, mitochondrial transplantation, microbial phenazines, novel antioxidant phenothiazines, inhibitors of glycogen synthase kinase-3 beta, and aryl hydrocarbon receptor.

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Section: Ferrosenescence Vs Ferroptosismentioning

confidence: 99%

The Future of Antipsychotic Interventions: From Managing Symptoms to Improving Outcomes

Sfera,

Imran,

Sfera

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…Cellular senescence is a complicated cellular state triggered by stressful damage and certain physiological processes (e.g., DNA damage, oncogene activation, oxidative stress, or exogenous toxicant exposure) and is characterized by prolonged and usually irreversible cell cycle arrest due to SASP, macromolecular damage, and metabolic alterations [33,34]. The process of cell proliferation arrest due to cellular senescence occurs gradually as telomere shortening and DNA damage accumulate [35].…”

Section: The Role Of Cellular Senescence In Agingmentioning

confidence: 99%

Targeting Cellular Senescence in Aging and Age-Related Diseases: Challenges, Considerations, and the Emerging Role of Senolytic and Senomorphic Therapies

2024

Aging dis

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Cellular senescence is characterized by the permanent arrest of cell proliferation and is a response to endogenous and exogenous stress. The continuous accumulation of senescent cells (SnCs) in the body leads to the development of aging and age-related diseases (such as neurodegenerative diseases, cancer, metabolic diseases, cardiovascular diseases, and osteoarthritis). In the face of the growing challenge of aging and age-related diseases, several compounds have received widespread attention for their potential to target SnCs. As a result, senolytics (compounds that selectively eliminate SnCs) and senomorphics (compounds that alter intercellular communication and modulate the behavior of SnCs) have become hot research topics in the field of anti-aging. In addition, strategies such as combination therapies and immune-based approaches have also made significant progress in the field of antiaging therapy. In this article, we discuss the latest research on anti-aging targeting SnCs and gain a deeper understanding of the mechanism of action and impact of different anti-aging strategies on aging and age-related diseases, with the aim of providing more effective references and therapeutic ideas for clinical anti-aging treatment in the face of the ever-grave challenges of aging and age-related diseases.

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“…Consequently, we believe that ferrosenescence may be more prevalent in SCZ than ferroptosis. Moreover, ferrosenescence may account for the other SCZ markers, including a decreased brain volume, γ-oscillations in EEGs, and mitochondrial dysfunction [ 55 , 56 , 57 , 58 ].…”

Section: Premature Cellular Senescence In Schizophreniamentioning

confidence: 99%

Novel Insights into Psychosis and Antipsychotic Interventions: From Managing Symptoms to Improving Outcomes

Sfera,

Imran,

Sfera

et al. 2024

IJMS

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For the past 70 years, the dopamine hypothesis has been the key working model in schizophrenia. This has contributed to the development of numerous inhibitors of dopaminergic signaling and antipsychotic drugs, which led to rapid symptom resolution but only marginal outcome improvement. Over the past decades, there has been limited research on the quantifiable pathological changes in schizophrenia, including premature cellular/neuronal senescence, brain volume loss, the attenuation of gamma oscillations in electroencephalograms, and the oxidation of lipids in the plasma and mitochondrial membranes. We surmise that the aberrant activation of the aryl hydrocarbon receptor by toxins derived from gut microbes or the environment drives premature cellular and neuronal senescence, a hallmark of schizophrenia. Early brain aging promotes secondary changes, including the impairment and loss of mitochondria, gray matter depletion, decreased gamma oscillations, and a compensatory metabolic shift to lactate and lactylation. The aim of this narrative review is twofold: (1) to summarize what is known about premature cellular/neuronal senescence in schizophrenia or schizophrenia-like disorders, and (2) to discuss novel strategies for improving long-term outcomes in severe mental illness with natural senotherapeutics, membrane lipid replacement, mitochondrial transplantation, microbial phenazines, novel antioxidant phenothiazines, inhibitors of glycogen synthase kinase-3 beta, and aryl hydrocarbon receptor antagonists.

show abstract

Neuronal Senescence in the Aged Brain

Cited by 21 publications

References 147 publications

The Future of Antipsychotic Interventions: From Managing Symptoms to Improving Outcomes

The Future of Antipsychotic Interventions: From Managing Symptoms to Improving Outcomes

Targeting Cellular Senescence in Aging and Age-Related Diseases: Challenges, Considerations, and the Emerging Role of Senolytic and Senomorphic Therapies

Novel Insights into Psychosis and Antipsychotic Interventions: From Managing Symptoms to Improving Outcomes

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