Reduced serum SIRT1 levels in patients with Parkinson’s disease: a cross-sectional study in China

Zhu, Yuting; Zhu, Xiangyang; Zhou, Yong; Zhang, Dongmei

doi:10.1007/s10072-020-04711-z

Cited by 20 publications

(7 citation statements)

References 28 publications

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“…Chen and colleagues revealed that SIRT1 protects DNs against MPTP-induced injury through the improvement of mitochondrial function, reduction of the apoptotic process, and activation of PGC-1α (Zhang et al 2018 ). In this state, the experimental study of the PD model showed that mutated SIRT1 failed to protect DNs (Donmez et al 2012 ; Chen et al 2019 ; Zhu et al 2021 ). Thus, SIRT1-mediated mitochondrial biogenesis could be a possible mechanistic way for the neuroprotective effect of SIRT1 against PD neuropathology.…”

Section: Sirt1 In Pdmentioning

confidence: 99%

“…A case–control study illustrated that SIRT1 mRNA level was reduced in the peripheral blood of PD patients (Maszlag-Török et al 2021 ). An extended study involving PD with dementia and healthy controls illustrated that SIRT1 expression significantly differed between PD patients with dementia compared to the healthy controls (Zhu et al 2021 ). SIRT1 expression was reduced in the frontal and temporal lobes of PD patients with dementia (Bose and Beal 2016 ).…”

Section: Sirt1 In Pdmentioning

confidence: 99%

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SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

et al. 2022

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Silent information regulator (SIRT) has distinctive enzymatic activities and physiological functions to control cell-cycle progression, gene expression, and DNA stability by targeting histone and non-histone proteins. SIRT1 enhances synaptic formation and synaptic activity, and therefore, can reduce the progression of various degenerative brain diseases including Parkinson’s disease (PD). SIRT1 activity is decreased by aging with a subsequent increased risk for the development of degenerative brain diseases. Inhibition of SIRT1 promotes inflammatory reactions since SIRT1 inhibits transcription of nuclear factor kappa B (NF-κB) which also inhibits SIRT1 activation via activation of microRNA and miR-34a which reduce NAD synthesis. SIRT1 is highly expressed in microglia as well as neurons, and has antioxidant and anti-inflammatory effects. Therefore, this review aimed to find the possible role of SIRT1 in PD neuropathology. SIRT1 has neuroprotective effects; therefore, downregulation of SIRT1 during aging promotes p53 expression and may increase the vulnerability of neuronal cell deaths. PD neuropathology is linked with the sequence of inflammatory changes and the release of pro-inflammatory cytokines due to the activation of inflammatory signaling pathways. In addition, oxidative stress, inflammatory disorders, mitochondrial dysfunction, and apoptosis contribute mutually to PD neuropathology. Thus, SIRT1 and SIRT1 activators play a crucial role in the mitigation of PD neuropathology through the amelioration of oxidative stress, inflammatory disorders, mitochondrial dysfunction, apoptosis, and inflammatory signaling pathways.

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Section: Sirt1 In Pdmentioning

confidence: 99%

Section: Sirt1 In Pdmentioning

confidence: 99%

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

et al. 2022

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“…A loss of SIRT1 activity, but not total SIRT activity has been described for cortical tissue samples from patients with PD and other Lewy body diseases (Singh et al, 2017). PD-associated polymorphisms in the SIRT1 gene (Zhang et al, 2012; Maszlag-Török et al, 2021) have also been reported, along with reduced SIRT1 mRNA levels in peripheral blood cells (Maszlag-Török et al, 2021) and reduced SIRT1 protein levels in serum from PD patients (Zhu et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Adaptive epigenetic regulation of neuronal metabolism by a mitochondrial redox signal

Baeken,

Kötzner,

Richly

et al. 2023

Preprint

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Different signaling pathways connect the mitochondrion with the transcriptional machinery in the nucleus. Redox events are thought to play a substantial role along this axis, however, many open questions about their specificity, quantitative importance and mode of action remain. Here, we have employed subtoxic doses of the complex I inhibitor MPP+in human neuronal LUHMES cells to characterize the contribution of scavengeable redox signals to mito-nuclear communication. MPP+evoked a broadly targeted transcriptional induction of nuclear-encoded respiratory chain complex (RCC) subunits. Nanomolar doses of phenothiazine (PHT), a mitochondrially active antioxidant, attenuated these transcriptional effects by approximately half, but did not modulate the bioenergetic markers ATP, NAD+, NADH, lactate, or glucose. Transcriptional induction by MPP+was accompanied by a loss of nuclear 5-methyl-cytosine and an increase in histone H3K14 acetylation, both of which were entirely prevented by PHT. Inhibitor and PHT reversibility experiments suggested that these alterations were mediated by lowered DNMT3B and SIRT1 levels, respectively. Analysis of MPTP-treated mice recapitulated the PHT-reversible induction of histone acetylation and DNMT3B suppression in vivo. Moreover, PHT completely abrogated the statistical significance of the association of MPP+with the selective induction of mitochondrially imported proteins and RCC subunits. We conclude that the mitochondrion employs a redox signal to announce impending, but not yet acute mitochondrial distress to the nucleus, in order to selectively upregulate mito-metabolic genes via chromatin reorganization. Our results have implications for the interpretation of the observed epigenetic changes in Parkinson’s disease and other neurodegenerative disorders.

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“…Another regulatory function of SIRT1 involves the direct interaction with other regulatory proteins. High concentrations of SIRT1 in serum are correlated to better cognition in Parkinson's disease (PD) patients (Chen et al, 2021;Zhu et al, 2021). It has been described that SIRT1 deacetylates peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), a key regulator of mitochondrial biogenesis and potential target for therapy in PD patients (Nemoto et al, 2005;Zheng et al, 2010;Wang et al, 2015).…”

Section: Sirtuin Regulation Of Gene Expressionmentioning

confidence: 99%

Sirtuins and cognition: implications for learning and memory in neurological disorders

et al. 2022

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Sirtuins are an evolutionarily conserved family of regulatory proteins that function in an NAD+ -dependent manner. The mammalian family of sirtuins is composed of seven histone deacetylase and ADP-ribosyltransferase proteins (SIRT1-SIRT7) that are found throughout the different cellular compartments of the cell. Sirtuins in the brain have received considerable attention in cognition due to their role in a plethora of metabolic and age-related diseases and their ability to induce neuroprotection. More recently, sirtuins have been shown to play a role in normal physiological cognitive function, and aberrant sirtuin function is seen in pathological cellular states. Sirtuins are believed to play a role in cognition through enhancing synaptic plasticity, influencing epigenetic regulation, and playing key roles in molecular pathways involved with oxidative stress affecting mitochondrial function. This review aims to discuss recent advances in the understanding of the role of mammalian sirtuins in cognitive function and the therapeutic potential of targeting sirtuins to ameliorate cognitive deficits in neurological disorders.

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Reduced serum SIRT1 levels in patients with Parkinson’s disease: a cross-sectional study in China

Cited by 20 publications

References 28 publications

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

Adaptive epigenetic regulation of neuronal metabolism by a mitochondrial redox signal

Sirtuins and cognition: implications for learning and memory in neurological disorders

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