SLAB51 Probiotic Formulation Activates SIRT1 Pathway Promoting Antioxidant and Neuroprotective Effects in an AD Mouse Model

Bonfili, Laura; Cecarini, Valentina; Cuccioloni, Massimiliano; Angeletti, Mauro; Berardi, Sara; Scarpona, Silvia; Rossi, Giacomo; Eleuteri, Anna Maria

doi:10.1007/s12035-018-0973-4

Cited by 208 publications

(156 citation statements)

References 74 publications

Supporting

Mentioning

145

Contrasting

Unclassified

Order By: Relevance

“…Lastly, Bonfili et al (2017) determined that the expression levels of Beclin 1 and LC-II, autophagy regulator genes, significantly increased. More recently, Bonfili et al (2018) have investigated how SLAB51 activates antioxidative and neuroprotective mechanisms in 3xTg-AD mice, and determined SLAB51 activated Sirtuin 1 pathway (SIRT1: an NAD + -dependent protein deacetylase). They confirmed this finding by indicating an increase in acetylation level of SIRT1's substrate RARb.…”

Section: Regulation Of Neuronal Proteolysismentioning

confidence: 99%

The role of gut microbiota in pathogenesis of Alzheimer's disease

Bostancıklıoğlu

2019

Journal of Applied Microbiology

151

View full text Add to dashboard Cite

This paper describes the effects of the gut microbiota on the pathogenesis of Alzheimer's pathology by evaluating the current original key findings and identifying gaps in the knowledge required for validation. The diversity of the gut microbiota declines in the elderly and in patients with Alzheimer's disease (AD). Restoring the diversity with probiotic treatment alleviates the psychiatric and histopathological findings. This presents a problem: How does gut microbiota interact with the pathogenesis of AD? The starting point of this comprehensive review is addressing the role of bacterial metabolites and neurotransmitters in the brain under various conditions, ranging from a healthy state to ageing and disease. In the light of current literature, we describe three different linkages between the present gut microbiome hypothesis and the other major theories for the pathogenesis of AD as follows: bacterial metabolites and amyloids can trigger central nervous system inflammation and cerebrovascular degeneration; impaired gut microbiome flora inhibits the autophagy‐mediated protein clearance process; and gut microbiomes can change the neurotransmitter levels in the brain through the vagal afferent fibres.

show abstract

Section: Regulation Of Neuronal Proteolysismentioning

confidence: 99%

The role of gut microbiota in pathogenesis of Alzheimer's disease

Bostancıklıoğlu

2019

Journal of Applied Microbiology

151

View full text Add to dashboard Cite

show abstract

“…Probiotics are defined as 'live microorganisms which when administered in adequate amounts confer a health benefit on the host' (FAO/WHO, 2006) and have been demonstrated to play a role in maintaining microbial homeostasis within the gut (Kumar et al, 2016;Umbrello and Esposito, 2016). Indeed, probiotic organisms have shown beneficial effects on neurodegenerative disorders (Akbari et al, 2016;Bonfili et al, 2017Bonfili et al, , 2018Kobayashi et al, 2017;Nimgampalle and Kuna, 2017) and animal studies with probiotics have shown clear neuroprotective effects (Ait-Belgnaoui et al, 2014;Distrutti et al, 2014;Möhle et al, 2016;Park et al, 2017). The aetiology of neurodegeneration is complex and the functional diversity of probiotics may facilitate the simultaneous targeting of multiple disease-related mechanisms (Elufioye et al, 2017;Faden and Stoica, 2007).…”

Section: Introductionmentioning

confidence: 99%

In vitro neuroprotective activities of two distinct probiotic consortia

Michael

Davies

Loxley

et al. 2019

View full text Add to dashboard Cite

Neurodegeneration has been linked to changes in the gut microbiota and this study compares the neuroprotective capability of two bacterial consortia, known as Lab4 and Lab4b, using the established SH-SY5Y neuronal cell model. Firstly, varying total antioxidant capacities (TAC) were identified in the intact cells from each consortia and their secreted metabolites, referred to as conditioned media (CM). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Crystal Violet (CV) assays of cell viability revealed that Lab4 CM and Lab4b CM could induce similar levels of proliferation in SH-SY5Y cells and, despite divergent TAC, possessed a comparable ability to protect undifferentiated and retinoic acid-differentiated cells from the cytotoxic actions of rotenone and undifferentiated cells from the cytotoxic actions of 1-methyl-4-phenylpyridinium iodide (MPP+). Lab4 CM and Lab4b CM also had the ability to attenuate rotenone-induced apoptosis and necrosis with Lab4b inducing the greater effect. Both consortia showed an analogous ability to attenuate intracellular reactive oxygen species accumulation in SH-SY5Y cells although the differential upregulation of genes encoding glutathione reductase and superoxide dismutase by Lab4 CM and Lab4b CM, respectively, implicates the involvement of consortia-specific antioxidative mechanisms of action. This study implicates Lab4 and Lab4b as potential neuroprotective agents and justifies their inclusion in further in vivo studies.

show abstract

“…First reports indicate successful application in animal models: Lactobacillus plantarum, for example, was able to restore cognition and levels of acetylcholine esterase in the brain of a D-galactose-evoked AD-like rat model [94]. Similar results were obtained from investigations using genetic AD mouse models with Bifidobacterium breve strain A1 [95], SLAB51 (probiotic formulation, [96]) but also with Lactobacillus acidophilus, Lactobacillus fermentum, Bifidobacterium lactis, and Bifidobacterium longum in rodent sporadic AD models due to amyloid-β injection [97][98][99]. As only one explorative intervention study reports on a small cohort of AD human patients [100], the usefulness in humans is still not proven.…”

Section: Therapeutic Strategies Derived From Microbes Against Human Amentioning

confidence: 64%

Amyloidogenic Peptides in Human Neuro-Degenerative Diseases and in Microorganisms: A Sorrow Shared Is a Sorrow Halved?

Endres

2020

Molecules

View full text Add to dashboard Cite

The term “amyloid” refers to proteinaceous deposits of peptides that might be generated from larger precursor proteins e.g., by proteolysis. Common to these peptides is a stable cross-β dominated secondary structure which allows self-assembly, leading to insoluble oligomers and lastly to fibrils. These highly ordered protein aggregates have been, for a long time, mainly associated with human neurodegenerative diseases such as Alzheimer’s disease (Amyloid-β peptides). However, they also exert physiological functions such as in release of deposited hormones in human beings. In the light of the rediscovery of our microbial commensals as important companions in health and disease, the fact that microbes also possess amyloidogenic peptides is intriguing. Transmission of amyloids by iatrogenic means or by consumption of contaminated meat from diseased animals is a well-known fact. What if also our microbial commensals might drive human amyloidosis or suffer from our aggregated amyloids? Moreover, as the microbial amyloids are evolutionarily older, we might learn from these organisms how to cope with the sword of Damocles forged of endogenous, potentially toxic peptides. This review summarizes knowledge about the interplay between human amyloids involved in neurodegenerative diseases and microbial amyloids.

show abstract

SLAB51 Probiotic Formulation Activates SIRT1 Pathway Promoting Antioxidant and Neuroprotective Effects in an AD Mouse Model

Cited by 208 publications

References 74 publications

The role of gut microbiota in pathogenesis of Alzheimer's disease

The role of gut microbiota in pathogenesis of Alzheimer's disease

In vitro neuroprotective activities of two distinct probiotic consortia

Amyloidogenic Peptides in Human Neuro-Degenerative Diseases and in Microorganisms: A Sorrow Shared Is a Sorrow Halved?

Contact Info

Product

Resources

About