Succinate-Based Preparation Alleviates Manifestations of the Climacteric Syndrome in Women

Peskov, A.B.; Maevskii, E. I.; Uchitel, M. L.; Sakharova, N. Yu.; Сторонова, О. А.

doi:10.1007/s10517-005-0476-y

Cited by 3 publications

(2 citation statements)

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“…Succinic acid, a Krebs cycle-generated metabolite, donates electrons directly into complex II and thus could be used to bypass complex I [ 25 – 27 , 30 ] ( Fig 2A ). Additionally, succinic acid is inexpensive, endogenous and FDA-approved making it an attractive therapeutic [ 43 – 47 ]. A concentration of 0.75 mg/mL of succinic acid dissolved in the cage drinking water and administered ad libitum was chosen based on preliminary dose-response data.…”

Section: Resultsmentioning

confidence: 99%

Short-term succinic acid treatment mitigates cerebellar mitochondrial OXPHOS dysfunction, neurodegeneration and ataxia in a Purkinje-specific spinocerebellar ataxia type 1 (SCA1) mouse model

et al. 2017

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Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved motor behavior. Thus, exploration of mitochondrial dysfunction and its role in neurodegenerative ataxias, and warrants further investigation.

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Section: Resultsmentioning

confidence: 99%

Short-term succinic acid treatment mitigates cerebellar mitochondrial OXPHOS dysfunction, neurodegeneration and ataxia in a Purkinje-specific spinocerebellar ataxia type 1 (SCA1) mouse model

et al. 2017

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“…As the hypothalamus ages, the sensitivity to the sensor input begins to decline which results in dysregulation of feeding behavior ( 93 , 94 , 97 ). Internal or external signals that activate this pathway will thus be useful therapeutic targets in preventing weight gain, obesity, and other metabolic or cardiovascular diseases ( 97 – 99 ).…”

Section: Discovery Of Key Longevity Genes and Their Regulatory Pathwamentioning

confidence: 99%

Maintenance of Homeostasis in the Aging Hypothalamus: The Central and Peripheral Roles of Succinate

2015

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Aging is the phenotype resulting from accumulation of genetic, cellular, and molecular damages. Many factors have been identified as either the cause or consequence of agerelated decline in functions and repair mechanisms. The hypothalamus is the source and a target of many of these factors and hormones responsible for the overall homeostasis in the body. With advanced age, the sensitivity of the hypothalamus to various feedback signals begins to decline. In recent years, several aging-related genes have been identified and their signaling pathways elucidated. These gene products include mTOR, IKK-β/NF-κB complex, and HIF-1α, an important cellular survival signal. All of these activators/modulators of the aging process have also been identified in the hypothalamus and shown to play crucial roles in nutrient sensing, metabolic regulation, energy balance, reproductive function, and stress adaptation. This illustrates the central role of the hypothalamus in aging. Inside the mitochondria, succinate is one of the most prominent intermediates of the Krebs cycle. Succinate oxidation in mitochondria provides the most powerful energy output per unit time. Extra-mitochondrial succinate triggers a host of succinate receptor (SUCN1 or GPR91)-mediated signaling pathways in many peripheral tissues including the hypothalamus. One of the actions of succinate is to stabilize the hypoxia and cellular stress conditions by inducing the transcriptional regulator HIF-1α. Through these actions, it is hypothesized that succinate has the potential to restore the gradual but significant loss in functions associated with cellular senescence and systemic aging.

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Clinical Evaluation of Effectiveness and Safety of Combined Use of Dietary Supplements Amberen® and Smart B® in Women with Climacteric Syndrome in Perimenopause

Kachko,

Shulman,

Kuznetsova

et al. 2024

Adv Ther

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Succinate-Based Preparation Alleviates Manifestations of the Climacteric Syndrome in Women

Cited by 3 publications

References 0 publications

Short-term succinic acid treatment mitigates cerebellar mitochondrial OXPHOS dysfunction, neurodegeneration and ataxia in a Purkinje-specific spinocerebellar ataxia type 1 (SCA1) mouse model

Short-term succinic acid treatment mitigates cerebellar mitochondrial OXPHOS dysfunction, neurodegeneration and ataxia in a Purkinje-specific spinocerebellar ataxia type 1 (SCA1) mouse model

Maintenance of Homeostasis in the Aging Hypothalamus: The Central and Peripheral Roles of Succinate

Clinical Evaluation of Effectiveness and Safety of Combined Use of Dietary Supplements Amberen® and Smart B® in Women with Climacteric Syndrome in Perimenopause

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