Physical Training Protects Against Brain Toxicity in Mice Exposed to an Experimental Model of Glioblastoma

Costa, Amanda K.; Marqueze, Luis Felipe; Gattiboni, Bruna B.; Pedroso, Giulia S.; Vasconcellos, Franciane F.; Cunha, Eduardo B B; Justa, Hanna C.; Baldissera, Antonielle B.; Nagashima, Seigo; Noronha, Lúcia de; Radák, Zsolt; Fernandes, Luiz C.; Pinho, Ricardo A.

doi:10.1007/s11064-022-03685-y

Cited by 3 publications

(3 citation statements)

References 69 publications

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“…Transcription factors such as SP1 and NF-kB are mediators of inflammatory processes, and downregulation of these transcription factors not only suppresses inflammation but also decreases reactive oxygen species production (ROS) [ 4 ]. Here, we confirmed that exercise especially in conjunction with postbiotic treatment reduces the involvement of NF-kB [ 35 , 36 ] in the inflammatory process, and our data showed that this process plays a neuroprotective role in APP/PS1 model [ 10 ].…”

Section: Discussionsupporting

confidence: 79%

Exercise combined with postbiotics treatment results in synergistic improvement of mitochondrial function in the brain of male transgenic mice for Alzheimer’s disease

Kolonics,

Bori,

Torma

et al. 2023

BMC Neurosci

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Background It has been suggested that exercise training and postbiotic supplement could decelerate the progress of functional and biochemical deterioration in double transgenic mice overexpresses mutated forms of the genes for human amyloid precursor protein (APPsw) and presenilin 1 (m146L) (APP/PS1TG). Our earlier published data indicated that the mice performed better than controls on the Morris Maze Test parallel with decreased occurrence of amyloid-β plaques in the hippocampus. We investigated the neuroprotective and therapeutic effects of high-intensity training and postbiotic supplementation. Methods Thirty-two adult APP/PS1TG mice were randomly divided into four groups: (1) control, (2) high-intensity training (3) postbiotic, (4) combined (training and postbiotic) treatment for 20 weeks. In this study, the whole hemibrain without hippocampus was used to find molecular traits explaining improved brain function. We applied qualitative RT-PCR for gene expression, Western blot for protein level, and Zymography for LONP1 activity. Disaggregation analysis of Aβ-40 was performed in the presence of Lactobacillus acidophilus and Bifidobacterium longum lysate. Results We found that exercise training decreased Alzheimer’s Disease (AD)-related gene expression (NF-kB) that was not affected by postbiotic treatment. The preparation used for postbiotic treatment is composed of tyndallized Bifidobacterium longum and Lactobacillus acidophilus. Both of the postbiotics effectively disaggregated amyloid-β/Aβ-40 aggregates by chelating Zn2+ and Cu2+ ions. The postbiotic treatment decreased endogenous human APPTG protein expression and mouse APP gene expression in the hemibrains. In addition, the postbiotic treatment elevated mitochondrial LONP1 activity as well. Conclusion Our findings revealed distinct mechanisms behind improved memory performance in the whole brain: while exercise training modulates NF-kB signaling pathway regulating immune response until postbiotic diminishes APP gene expression, disaggregates pre-existing amyloid-β plaques and activates mitochondrial protein quality control in the region of brain out of hippocampus. Using the above treatments complements and efficiently slows down the development of AD.

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Section: Discussionsupporting

confidence: 79%

Exercise combined with postbiotics treatment results in synergistic improvement of mitochondrial function in the brain of male transgenic mice for Alzheimer’s disease

Kolonics,

Bori,

Torma

et al. 2023

BMC Neurosci

Self Cite

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show abstract

“…Transcription factors like SP1 and NF-kB are mediators of in ammatory process and downregulation of these transcription factors not just suppress in ammation but decrease production of reactive oxygen species (ROS) as well (4). Here we con rmed that exercise especially with postbiotic treatment decrease the involvement of NF-kB (35,36) in in ammation and our data showed that in APP/PS1 model this process has neuroprotective role (10).…”

Section: Discussionsupporting

confidence: 71%

Exercise combined with postbiotics treatment results in synergistic improvement of mitochondrial function in the brain of male transgenic mice for Alzheimer’s disease

Kolonics¹,

Bori²,

Torma³

et al. 2023

Preprint

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Background It has been suggested that exercise training and postbiotic supplement could decelerate the progress of functional and biochemical deterioration in double transgenic mice overexpresses mutated forms of the genes for human amyloid precursor protein (APPsw) and presenilin 1 (m146L) (APP/PS1TG). Our earlier published data indicated that the mice performed better than controls on the Morris Maze Test parallel with decreased occurrence of amyloid-β plaques in the hippocampus. We investigated the neuroprotective and therapeutic effects of high-intensity training and postbiotic supplementation. Methods Thirty-two adult APP/PS1 TG mice were randomly divided into four groups: 1. control, 2. high-intensity training 3. postbiotic, 4. combined (training and postbiotic) treatment for 20 weeks. In this study, the whole hemibrain without hippocampus was used to find molecular traits explaining improved brain function. We applied qualitative RT-PCR for gene expression, Western blot for protein level, and Zymography for LONP1 activity. Disaggregation analysis of Ab-40 was performed in the presence of Lactobacillus acidophilus and Bifidobacterium longum lysate. Results We found that exercise training decreased Alzheimer’s Disease (AD)-related gene expression (NF-kB) that was not affected by postbiotic treatment. The preparation used for postbiotic treatment is composed of tyndallized Bifidobacterium longum and Lactobacillus acidophilus. Both of the postbiotics effectively disaggregated amyloid-β/Aβ-40 aggregates by chelating Zn2+ and Cu2+ ions. The postbiotic treatment decreased endogenous human APPTG protein expression and mouse APP gene expression in the hemibrains. In addition, the postbiotic treatment elevated mitochondrial LONP1 activity as well. Conclusion Our findings revealed distinct mechanisms behind improved memory performance in the whole brain: while exercise training modulates NF-kB signaling pathway regulating immune response until postbiotic diminishes APP gene expression, disaggregates pre-existing amyloid-β plaques and activates mitochondrial protein quality control in the region of brain out of hippocampus. Using the above treatments complements and efficiently slows down the development of AD.

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“…Since temporal muscle thickness is highly correlated with muscle strength [ 37 ], it may be of particular interest to counteract general muscle wasting with appropriate interventions. Benefits from physical activity have also been shown in mouse models of glioma [ 38 – 40 ]. Tantillo et al, e.g., report on reduced tumor proliferation rates as well as later onset of motor deficits by voluntary physical exercise in glioma-bearing mice [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Conceptual development of an intensive exercise program for glioma patients (ActiNO): summary of clinical experience

et al. 2023

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Purpose Exercise proved to reduce cancer-related symptoms and prolong survival in some cancer types. However, brain tumor patients are often advised against strenuous exercise. Here, we summarize our experience with a submaximal exercise program for glioma patients: ActiNO (Active in Neuro-Oncology). Methods Glioma patients were invited to participate in the program. Since 2011, a sports scientist individualized two one-hour sessions per week adapted to the patients’ symptoms. One session consisted of bicycle ergometry (average workload: 75% of maximum heart rate), the other of whole-body resistance training. Both sessions were further complimented by coordinative elements. Cardiorespiratory fitness was assessed using the ”Physical Work Capacity” procedure. Patients were followed up regularly to assess adherence to the program and disease activity. Results Until December 2019, 45 glioma patients, median-aged 49 years (IQR 42–59), were included in the analysis. Most patients suffered from glioblastoma (58%), followed by diffuse lower-grade astrocytoma (29%). In overall 1828 training sessions, two minor epileptic events occurred (1 speech arrest; 1 focal seizure). During fitness assessment, all patients achieved at least 75% of their age-adjusted maximum heart rate. Peak workload averaged 172 W (95% CI 156–187). Median survival of participating glioblastoma patients was 24.1 months (95% CI 8.6–39.5). Conclusion This supervised training program with submaximal exertion was feasible and safe in glioma regardless of WHO grading. Based on these experiences, we initiated a prospective multicenter study to objectify improvements in physical performance and quality of life in patients with glioblastoma.

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Physical Training Protects Against Brain Toxicity in Mice Exposed to an Experimental Model of Glioblastoma

Cited by 3 publications

References 69 publications

Exercise combined with postbiotics treatment results in synergistic improvement of mitochondrial function in the brain of male transgenic mice for Alzheimer’s disease

Exercise combined with postbiotics treatment results in synergistic improvement of mitochondrial function in the brain of male transgenic mice for Alzheimer’s disease

Exercise combined with postbiotics treatment results in synergistic improvement of mitochondrial function in the brain of male transgenic mice for Alzheimer’s disease

Conceptual development of an intensive exercise program for glioma patients (ActiNO): summary of clinical experience

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