Metformin alleviates the depression-like behaviors of elderly apoE4 mice via improving glucose metabolism and mitochondrial biogenesis

Lin, Yingbin; Dai, Xiaoman; Zhang, Jing; Chen, Xiaochun

doi:10.1016/j.bbr.2022.113772

Cited by 13 publications

(4 citation statements)

References 59 publications

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“…Consistent with this, the lifespan extension effect of metformin is not seen in male rats 232 or aged female mice. 233 Nevertheless, metformin relieves many aging-related diseases in rodent models, including cognitive impairment and neurodegeneration, 229 , 234 – 237 depression, 238 chronic kidney disease, 239 thymus degeneration, 240 aging-related cataract, 228 aging-related hearing loss, 241 mitochondrial dysfunction in aged hearts, 230 adipose tissue senescence and metabolic abnormalities, 242 , 243 and aging-related developmental and metabolic phenotypes. 244 …”

Section: Epigenetic Regulation Of Agingmentioning

confidence: 99%

Epigenetic regulation of aging: implications for interventions of aging and diseases

Wang

Liu

et al. 2022

Sig Transduct Target Ther

194

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Aging is accompanied by the decline of organismal functions and a series of prominent hallmarks, including genetic and epigenetic alterations. These aging-associated epigenetic changes include DNA methylation, histone modification, chromatin remodeling, non-coding RNA (ncRNA) regulation, and RNA modification, all of which participate in the regulation of the aging process, and hence contribute to aging-related diseases. Therefore, understanding the epigenetic mechanisms in aging will provide new avenues to develop strategies to delay aging. Indeed, aging interventions based on manipulating epigenetic mechanisms have led to the alleviation of aging or the extension of the lifespan in animal models. Small molecule-based therapies and reprogramming strategies that enable epigenetic rejuvenation have been developed for ameliorating or reversing aging-related conditions. In addition, adopting health-promoting activities, such as caloric restriction, exercise, and calibrating circadian rhythm, has been demonstrated to delay aging. Furthermore, various clinical trials for aging intervention are ongoing, providing more evidence of the safety and efficacy of these therapies. Here, we review recent work on the epigenetic regulation of aging and outline the advances in intervention strategies for aging and age-associated diseases. A better understanding of the critical roles of epigenetics in the aging process will lead to more clinical advances in the prevention of human aging and therapy of aging-related diseases.

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Section: Epigenetic Regulation Of Agingmentioning

confidence: 99%

Epigenetic regulation of aging: implications for interventions of aging and diseases

Wang

Liu

et al. 2022

Sig Transduct Target Ther

194

View full text Add to dashboard Cite

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“…Mitochondrial biogenesis is a process that leads to the creation of new mitochondria through the transcription of both nuclear and mitochondrial genes. Depressive‐like behaviours can be relieved by increasing mitochondrial biogenesis in elderly mice 43 . By controlling NRF1, PGC‐1α can integrate the mitochondrial genome.…”

Section: Discussionmentioning

confidence: 99%

“…Depressive-like behaviours can be relieved by increasing mitochondrial biogenesis in elderly mice. 43 By controlling NRF1, PGC-1α can integrate the mitochondrial genome. It does this by inducing TFAM to translocate to mitochondria, which increases the replication and expression of mtDNA.…”

Section: The Effect Of Cur On Mitochondrial Distribution and Mitophag...mentioning

confidence: 99%

Curcumin relieves corticosterone‐induced behaviour deficits via PGC‐1α‐mediated mitochondrial biogenesis and mitophagy

Zhang

Guo

et al. 2022

Clinical and Translational Dis

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Curcumin (CUR), an FDA‐approved natural product, has been found to be clinically effective in treating depression. However, the underlying mechanism remains elusive. PGC‐1α is a key factor in regulating mitochondrial health and depression. This study randomly divided C57BL/6 mice or cultured hippocampal neurons into four groups: CON, CORT, CORT + CUR and CORT + CUR + SR18292. The present study demonstrated that CUR was effective in suppressing CORT‐induced depressive‐like behaviour, as well as improving anxiety‐like behaviour and cognitive function. CUR was found to be effective in preventing oxidative stress induced by corticosterone (CORT), as evidenced by the restoration of Nrf2, NQO‐1, HO‐1, GCLC, SOD‐1 and DHE levels in cells. CUR inhibited the CORT‐induced perinuclear accumulation of mitochondria in vitro. Furthermore, CUR promoted mitochondrial biogenesis, potentially reversing the effect of CORT on NRF1, TFAM, PGC‐1α and the relative MT‐CO1/SDH‐A ratio. Lastly, the treatment of CUR normalized the CORT‐hindered mitophagy by upregulating the protein level of NIX, Beclin‐1, PINK1, Parkin and LC3II/LC3I, and enhancing the relative mt‐Keima signal. The protective effect of CUR was entirely negated by SR18292. CUR could regulate oxidative stress, mitochondrial biogenesis and mitophagy via PGC‐1α to achieve an anti‐depressive‐like function. This study would contribute to a greater understanding of how CUR alleviates depressive symptoms.

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“…Resveratrol, a naturally occurring polyphenolic antioxidant, is able to increase the mRNA expression of SIRT1 and PGC‐1α, and then promote mitochondrial biogenesis, eventually enhancing ATP level in the hippocampus of mice exposed to CUMS 31 . A study by Lin et al 100 . verified that Metformin significantly increases the mRNA levels of NRF1 and TFAM in the hippocampus of aged apoE4‐TR mice, performing the metformin‐mediated antidepressant‐like effect.…”

Section: Antidepressants and Mitochondriamentioning

confidence: 99%

Mitochondria in depression: The dysfunction of mitochondrial energy metabolism and quality control systems

Jiang,

Wang,

Sheng

2024

CNS Neurosci Ther

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BackgroundDepression is the most disabling neuropsychiatric disorder, causing difficulties in daily life activities and social interactions. The exact mechanisms of depression remain largely unclear. However, some studies have shown that mitochondrial dysfunction would play a crucial role in the occurrence and development of depression.AimsTo summarize the known knowledge about the role of mitochondrial dysfunction in the pathogenesis of depression.MethodsWe review the recent literature， including 105 articles, to summarize the mitochondrial energy metabolism and quality control systems in the occurrence and development of depression. Some antidepressants which may exert their effects by improving mitochondrial function are also discussed.ResultsImpaired brain energy metabolism and (or) damaged mitochondrial quality control systems have been reported not only in depression patients but in animal models of depression. Although the classical antidepressants have not been specially designed to target mitochondria, the evidence suggests that many antidepressants may exert their effects by improving mitochondrial function.ConclusionsThis brief review focuses on the findings that implicate mitochondrial dysfunction and the quality control systems as important etiological factors in the context of depressive disorders. It will help us to understand the various concepts of mitochondrial dysfunction in the pathogenesis of depression, and to explore novel and more targeted therapeutic approaches for depression.

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Metformin alleviates the depression-like behaviors of elderly apoE4 mice via improving glucose metabolism and mitochondrial biogenesis

Cited by 13 publications

References 59 publications

Epigenetic regulation of aging: implications for interventions of aging and diseases

Epigenetic regulation of aging: implications for interventions of aging and diseases

Curcumin relieves corticosterone‐induced behaviour deficits via PGC‐1α‐mediated mitochondrial biogenesis and mitophagy

Mitochondria in depression: The dysfunction of mitochondrial energy metabolism and quality control systems

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