Effect of Sirt3 on hippocampal MnSOD activity, mitochondrial function, physiology, and cognition in an aged murine model

Allen, Antiño R.; Jones, A’Vonte; LoBianco, Francesca V.; Krager, Kimberly J.; Aykin-Burns, Nūkhet

doi:10.1016/j.bbr.2023.114335

Cited by 5 publications

(3 citation statements)

References 62 publications

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“…Reduced Sirt3 expression causes hyperacetylation of mitochondrial proteins linked with neuronal excitotoxicity and cell death [ 45 ]. The depletion of Sirt3 in mice showed cognitive impairments during the probe trial in the Morris water maze test [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Tat-heat shock protein 10 ameliorates age-related phenotypes by facilitating neuronal plasticity and reducing age-related genes in the hippocampus

Jung,

Kwon,

Hahn

et al. 2023

Aging

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We investigated the effects of heat shock protein 10 (HSP10) protein on memory function, hippocampal neurogenesis, and other related genes/proteins in adult and aged mice. To translocate the HSP10 protein into the hippocampus, the Tat-HSP10 fusion protein was synthesized, and Tat-HSP10, not HSP10, was successfully delivered into the hippocampus based on immunohistochemistry and western blotting. Tat-HSP10 (0.5 or 2.0 mg/kg) or HSP10 (control protein, 2.0 mg/kg) was administered daily to 3- and 21-month-old mice for 3 months, and observed the senescence maker P16 was significantly increased in aged mice and the treatment with Tat-HSP10 significantly decreased P16 expression in the hippocampus of aged mice. In novel object recognition and Morris water maze tests, aged mice demonstrated decreases in exploratory preferences, exploration time, distance moved, number of object contacts, and escape latency compared to adult mice. Treatment with Tat-HSP10 significantly improved exploratory preferences, the number of object contacts, and the time spent swimming in the target quadrant in aged mice but not adults. Administration of Tat-HSP10 increased the number of proliferating cells and differentiated neuroblasts in the dentate gyrus of adult and aged mice compared to controls, as determined by immunohistochemical staining for Ki67 and doublecortin, respectively. Additionally, Tat-HSP10 treatment significantly mitigated the reduction in sirtuin 1 mRNA level, N -methyl-D-aspartate receptor 1, and postsynaptic density 95 protein levels in the hippocampus of aged mice. In contrast, Tat-HSP10 treatment significantly increased sirtuin 3 protein levels in both adult and aged mouse hippocampus. These suggest that Tat-HSP10 can potentially reduce hippocampus-related aging phenotypes.

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Section: Discussionmentioning

confidence: 99%

Tat-heat shock protein 10 ameliorates age-related phenotypes by facilitating neuronal plasticity and reducing age-related genes in the hippocampus

Jung,

Kwon,

Hahn

et al. 2023

Aging

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Section: Molecular Mechanisms Of Brain Ageingmentioning

confidence: 99%

“…Their activity depends on nicotinamide adenine dinucleotide (NAD + ), whose levels seem to decrease with ageing, leading to mitochondrial deterioration and sirtuin activity reduction [87]. Moreover, SIRT3 was shown to be critical for neuronal proliferation in cell culture [88] and long-term memory function and cognition in the ageing mouse brain [89] Tightly related to the previous signalling pathways, AMPK was described to slow down ageing and increase life span in C. elegans by modulating the mitochondrial network [90], with its signalling declining with age. AMPK upregulates brain derived neurotrophic factor (BDNF), essential for synaptic transmission and memory consolidation [91] and plays neuroprotective roles by mitigating neuroinflammation and oxidative stress, being explored as a clinical target to promote longevity [92].…”

Section: Metabolic Dysregulationmentioning

confidence: 99%

Ageing in the brain: mechanisms and rejuvenating strategies

Gaspar-Silva

Trigo

Magalhaes

2023

Cell. Mol. Life Sci.

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Ageing is characterized by the progressive loss of cellular homeostasis, leading to an overall decline of the organism’s fitness. In the brain, ageing is highly associated with cognitive decline and neurodegenerative diseases. With the rise in life expectancy, characterizing the brain ageing process becomes fundamental for developing therapeutic interventions against the increased incidence of age-related neurodegenerative diseases and to aim for an increase in human life span and, more importantly, health span. In this review, we start by introducing the molecular/cellular hallmarks associated with brain ageing and their impact on brain cell populations. Subsequently, we assess emerging evidence on how systemic ageing translates into brain ageing. Finally, we revisit the mainstream and the novel rejuvenating strategies, discussing the most successful ones in delaying brain ageing and related diseases.

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Effects of moderate intensity training and lithium on spatial learning and memory in a rat model: The role of SIRT3 and PGC1-α expression levels and brain-derived neurotropic factor

Shoghi,

Safari,

Parsi-Moud

et al. 2024

Experimental Gerontology

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Effect of Sirt3 on hippocampal MnSOD activity, mitochondrial function, physiology, and cognition in an aged murine model

Cited by 5 publications

References 62 publications

Tat-heat shock protein 10 ameliorates age-related phenotypes by facilitating neuronal plasticity and reducing age-related genes in the hippocampus

Tat-heat shock protein 10 ameliorates age-related phenotypes by facilitating neuronal plasticity and reducing age-related genes in the hippocampus

Ageing in the brain: mechanisms and rejuvenating strategies

Effects of moderate intensity training and lithium on spatial learning and memory in a rat model: The role of SIRT3 and PGC1-α expression levels and brain-derived neurotropic factor

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