Microdose Lithium Treatment Reduced Inflammatory Factors and Neurodegeneration in Organotypic Hippocampal Culture of Old SAMP-8 Mice

Toricelli, Mariana; Evangelista, Sebastiana Ribeiro; Buck, Hudson Sousa; Viel, Tânia Araújo

doi:10.1007/s10571-020-00916-0

Cited by 12 publications

(22 citation statements)

References 52 publications

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“…Lithium carbonate was dissolved in filtered tap water and offered ad libitum, per os, to the animals, resulting in a final dosage of 0.005 mg/animal/day, which can be considered to be in the microdose range as described earlier by the group of the authors (Nunes et al, 2013(Nunes et al, , 2015Toricelli et al, 2020Toricelli et al, , 2021, The cited dosage corresponds to 0.25 mg/kg. The quantity of water consumed by the lithium-treated and untreated groups was not significantly different (average liquid consumption of the untreated groups: 44 ± 0.6 ml/week; average liquid consumption of the treated groups: 44.2 ± 0.9 ml/week).…”

Section: Treatment With Microdoses Of Lithiummentioning

confidence: 99%

“…Classically, it is reported that lithium decreases oxidative stress and the activity of GSK-3β (Chalecka-Franaszek and Chuang, 1999 ), reducing the formation of the toxic oligomers of Aβ while increasing the expression of anti-apoptotic genes such as Bcl-2 (O'Leary et al, 2012 ), as well as BDNF expression (Forlenza et al, 2012 , 2019 ), promoting neuroprotection. When used in microdoses, lithium can promote memory preservation and decrease anxiety (Nunes et al, 2015 ) and neuroinflammation (Toricelli et al, 2020 ), and it also exhibits senolytic properties (Viel et al, 2020 ), verified both in AD animal models and in human-derived induced pluripotent stem cell (iPSCs) astrocytes.…”

Section: Introductionmentioning

confidence: 99%

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Combined Neuroprotective Strategies Blocked Neurodegeneration and Improved Brain Function in Senescence-Accelerated Mice

Malerba

Pereira

Pierrobon

et al. 2021

Front. Aging Neurosci.

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Increase in the quality of life, combined with drug strategies, has been studied as possibilities for improving memory and delaying the onset of neurodegenerative diseases. A previous study published by the group of the authors has shown that microdose lithium and enriched environment can improve memory in both mice and humans. To elucidate this relationship better, this study aimed to evaluate whether the chronic combination of these two strategies could increase healthy aging in Senescence Accelerated Mouse-Prone 8 (SAMP8). Animals were submitted to either one or both of these strategies until the age of 10 months when they were anesthetized and killed and their hippocampus was extracted. The untreated SAMP-8 group exhibited worse memory and reduced neuronal density with greater neurodegeneration and increased amyloid-β plaque density compared with the control group. Moreover, significant alterations in proteins related to long-term potentiation, such as, synaptophysin and brain-derived neurotrophic factor (BDNF), were observed in this group. The strategies used in the study maintained long-term memory, reduced anxiety, and increased neuroprotection. Both strategies were efficient in reducing neurodegeneration and increasing parameters related to memory maintenance. In many experiments, the combination of the two strategies was more effective in improving healthy aging. This study sheds light on the combination of strategies that choose to improve the quality of life and drugs with low side effects. Moreover, it opens perspectives for a new field of study for healthy aging.

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Section: Treatment With Microdoses Of Lithiummentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Combined Neuroprotective Strategies Blocked Neurodegeneration and Improved Brain Function in Senescence-Accelerated Mice

Malerba

Pereira

Pierrobon

et al. 2021

Front. Aging Neurosci.

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“…Organotypic hippocampal culture was prepared according to previous studies from our group [ 12 , 49 ]. Briefly, mice were anesthetized, euthanized by decapitation, their brains were rapidly removed, and 300 µm sagittal slices (6–9 per brain) were taken using a vibratome (Leica VT1000S, Wetzlar, Germany) and dissected to isolate the hippocampus.…”

Section: Methodsmentioning

confidence: 99%

“…Cell death evaluation was done using propidium iodide staining, a widely accepted, simple, and reliable assay to evaluate cell death in organotypic hippocampal slice cultures [ 12 , 49 , 50 ]. For that, hippocampi slices were washed with 1 mL of PBS, sufficient to withdraw the residual culture medium, and incubated with 1 µg/mL of propidium iodide (Sigma-Aldrich, Saint Louis, MO, USA) during 15 min in absence of light.…”

Section: Methodsmentioning

confidence: 99%

Kinin B2 Receptor Activation Prevents the Evolution of Alzheimer’s Disease Pathological Characteristics in a Transgenic Mouse Model

et al. 2020

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Background: Alzheimer’s disease is mainly characterized by remarkable neurodegeneration in brain areas related to memory formation. This progressive neurodegeneration causes cognitive impairment, changes in behavior, functional disability, and even death. Our group has demonstrated changes in the kallikrein–kinin system (KKS) in Alzheimer’s disease (AD) experimental models, but there is a lack of evidence about the role of the KKS in Alzheimer’s disease. Aim: In order to answer this question, we evaluated the potential of the kinin B2 receptors (BKB2R) to modify AD characteristics, particularly memory impairment, neurodegeneration, and Aβ peptide deposition. Methods: To assess the effects of B2, we used transgenic Alzheimer’s disease mice treated with B2 receptor (B2R) agonists and antagonists, and performed behavioral and biochemical tests. In addition, we performed organotypic hippocampal culture of wild-type (WT) and transgenic (TG) animals, where the density of cytokines, neurotrophin BDNF, activated astrocyte marker S100B, and cell death were analyzed after treatments. Results: Treatment with the B2R agonist preserved the spatial memory of transgenic mice and decreased amyloid plaque deposition. In organotypic hippocampal culture, treatment with B2R agonist decreased cell death, neuroinflammation, and S100B levels, and increased BDNF release. Conclusions: Our results indicate that the kallikrein–kinin system plays a beneficial role in Alzheimer’s disease through B2R activation. The use of B2R agonists could, therefore, be a possible therapeutic option for patients diagnosed with Alzheimer’s disease.

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“…SAMP8 (Senescence Accelerated Prone Mouse 8) mice, developed from the AKR/J strain, are a rapid aging mouse model, which have the advantage of having short lifespans and experiencing accelerated aging processes. To compare SAMP8 mice with an accelerating senescence rate, SAMR1 (Senescence Accelerated Resistant Mouse 1) are usually utilized [ 31 , 32 , 33 ]. Compared with SAMR1mice, it has been reported that SAMP8 mice showed decreased muscle strength, muscle fiber size and muscle phosphocreatine level with aging [ 34 ].…”

Section: Introductionmentioning

confidence: 99%

Beneficial Effects of Walnut Oligopeptides on Muscle Loss in Senescence-Accelerated Mouse Prone-8 (SAMP8) Mice: Focusing on Mitochondrial Function

Fan

Hao

et al. 2022

Nutrients

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Aging-related muscle loss is a hallmark of aging and is the cause of some negative outcomes. An optimized diet and supplements have a positive effect in slowing down the process of muscle loss. This study was designed to evaluate the beneficial effects of walnut oligopeptides (WOPs) on aging-related muscle loss and explore the possible underlying mechanism in Senescence-Accelerated Mouse Prone 8 (SAMP8) Mice. SAMP8 mice were randomly divided into four groups (n = 15/group), including one group which was the SAMP8 age control group and three groups those were WOP intervention groups. Meanwhile, Senescence Accelerated Resistant Mouse 1 (SAMR1) mice (n = 12), which had normal senescence rates, were used as model controls. During the six-month intervention period, the age control and normal control groups were given sterilized water, while the three WOP intervention groups were given WOP solution with low (110 mg/kg·bw), medium (220 mg/kg·bw) and high concentrations (440 mg/kg·bw), respectively. The results showed that WOPs could significantly increase muscle mass and improve physical performance (wire hang and catwalk behavioral tests) in aging mice. Moreover, WOPs could significantly reduce the levels of IL-1β, IL-6 and TNF-α in serum and gastrocnemius tissues and increase the mitochondrial DNA content, as well as the expression levels of AMPK, PGC-1α, NRF-1 and TFAM in the gastrocnemius muscle of aging mice, which was speculated to be the specific mechanism related to mitochondrial function improvement and inflammation reduction. These results indicate that WOPs can improve aging-related muscle loss, in term of both muscle mass and physical performance, and WOP supplements seems to be potentially effective in elderly individuals.

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Microdose Lithium Treatment Reduced Inflammatory Factors and Neurodegeneration in Organotypic Hippocampal Culture of Old SAMP-8 Mice

Cited by 12 publications

References 52 publications

Combined Neuroprotective Strategies Blocked Neurodegeneration and Improved Brain Function in Senescence-Accelerated Mice

Combined Neuroprotective Strategies Blocked Neurodegeneration and Improved Brain Function in Senescence-Accelerated Mice

Kinin B2 Receptor Activation Prevents the Evolution of Alzheimer’s Disease Pathological Characteristics in a Transgenic Mouse Model

Beneficial Effects of Walnut Oligopeptides on Muscle Loss in Senescence-Accelerated Mouse Prone-8 (SAMP8) Mice: Focusing on Mitochondrial Function

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