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Special Issue "Brain Aging and Gut-Brain Axis"

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (10 September 2018)

Special Issue Editor

Guest Editor
PD Dr. M. Hasan Mohajeri

DSM Nutritional Products, DSM, Kaiseraugst, Switzerland;University of Zurich, Zurich, Switzerland
Website | E-Mail
Interests: brain development; aging; gut-brain coomunication; neurodegeneration; nutrition

Special Issue Information

Dear Colleagues,

Increased life expectancy in the 20th century has led to a dramatic demographic shift, increasing the need of the elderly population for long-term health care and services. The last decade of life is normally marked by age-related diseases, including maladies of the brain and the gut. Progressive brain-related disorders are age dependent and, thus, their prevalence increases with advanced age. Additionally, it is generally accepted that the brain and the gut are involved in a bidirectional communication influencing each other’s functions.

This Special Issue of Nutrients, entitled "Brain Aging and Gut–Brain Axis", encourages the submission of original research articles, reviews, and meta-analyses. Potential topics may include, but are not limited to:

  • Changes to brain metabolism during aging
  • Neurogenerative disorders vs. normal brain aging
  • How does neurodevelopment affect brain aging?
  • Changes of microbiome in aging
  • Influence of altering microbiome on brain function
  • Role of nutrients in modulating brain aging, affecting microbiome composition
  • Dysbiosis in the elderly and its effect on age-related brain functions
Dr. M. Hasan Mohajeri
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Aging brain, neurodegeneration
  • Microbiome metabolism
  • Brain-active nutrients
  • Mechanisms of brain aging
  • Dysbiosis in aging gut

Published Papers (5 papers)

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Research

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Open AccessArticle Long-Term Diet Supplementation with Lactobacillus paracasei K71 Prevents Age-Related Cognitive Decline in Senescence-Accelerated Mouse Prone 8
Nutrients 2018, 10(6), 762; https://doi.org/10.3390/nu10060762
Received: 28 May 2018 / Revised: 10 June 2018 / Accepted: 11 June 2018 / Published: 13 June 2018
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Abstract
This study aimed to assess the suppressive effect of long-term diet supplementation with Lactobacillus strains on cognitive decline in the senescence-accelerated mouse prone 8 (SAMP8) model. For 43 weeks, fourteen-week-old female SAMP8 mice were fed a standard diet containing 0.05% (w/
[...] Read more.
This study aimed to assess the suppressive effect of long-term diet supplementation with Lactobacillus strains on cognitive decline in the senescence-accelerated mouse prone 8 (SAMP8) model. For 43 weeks, fourteen-week-old female SAMP8 mice were fed a standard diet containing 0.05% (w/w) Lactobacillus casei subsp. casei 327 (L. 327) or Lactobacillusparacasei K71 (L. K71) derived from rice grains and sake lees, respectively. SAMP8 mice that were fed a L. K71-supplemented diet had better cognitive performance compared with the control and L. 327 groups in the Barnes maze and passive avoidance tests. An ELISA analysis revealed that the levels of serotonin were elevated in the serum and brain tissue of L. K71-fed mice. The protein expression levels of brain-derived neurotrophic factor (BDNF), cAMP response element binding protein (CREB), and phosphorylated CREB were evaluated using western blot. Long-term administration of L. K71 resulted in increased protein expression of BDNF and CREB phosphorylation in the hippocampus. These results suggest that prolonged intake of a diet supplemented with a Lactobacillus strain derived from sake lees may prevent age-dependent cognitive decline by upregulating BDNF expression in the hippocampus. Full article
(This article belongs to the Special Issue Brain Aging and Gut-Brain Axis)
Figures

Graphical abstract

Open AccessArticle Towards an Integrative Understanding of tRNA Aminoacylation–Diet–Host–Gut Microbiome Interactions in Neurodegeneration
Nutrients 2018, 10(4), 410; https://doi.org/10.3390/nu10040410
Received: 14 February 2018 / Revised: 19 March 2018 / Accepted: 22 March 2018 / Published: 26 March 2018
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Abstract
Transgenic mice used for Alzheimer’s disease (AD) preclinical experiments do not recapitulate the human disease. In our models, the dietary tryptophan metabolite tryptamine produced by human gut microbiome induces tryptophanyl-tRNA synthetase (TrpRS) deficiency with consequent neurodegeneration in cells and mice. Dietary supplements, antibiotics
[...] Read more.
Transgenic mice used for Alzheimer’s disease (AD) preclinical experiments do not recapitulate the human disease. In our models, the dietary tryptophan metabolite tryptamine produced by human gut microbiome induces tryptophanyl-tRNA synthetase (TrpRS) deficiency with consequent neurodegeneration in cells and mice. Dietary supplements, antibiotics and certain drugs increase tryptamine content in vivo. TrpRS catalyzes tryptophan attachment to tRNAtrp at initial step of protein biosynthesis. Tryptamine that easily crosses the blood–brain barrier induces vasculopathies, neurodegeneration and cell death via TrpRS competitive inhibition. TrpRS inhibitor tryptophanol produced by gut microbiome also induces neurodegeneration. TrpRS inhibition by tryptamine and its metabolites preventing tryptophan incorporation into proteins lead to protein biosynthesis impairment. Tryptophan, a least amino acid in food and proteins that cannot be synthesized by humans competes with frequent amino acids for the transport from blood to brain. Tryptophan is a vulnerable amino acid, which can be easily lost to protein biosynthesis. Some proteins marking neurodegenerative pathology, such as tau lack tryptophan. TrpRS exists in cytoplasmic (WARS) and mitochondrial (WARS2) forms. Pathogenic gene variants of both forms cause TrpRS deficiency with consequent intellectual and motor disabilities in humans. The diminished tryptophan-dependent protein biosynthesis in AD patients is a proof of our model-based disease concept. Full article
(This article belongs to the Special Issue Brain Aging and Gut-Brain Axis)
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Graphical abstract

Review

Jump to: Research

Open AccessReview The Gut-Brain Axis in Alzheimer’s Disease and Omega-3. A Critical Overview of Clinical Trials
Nutrients 2018, 10(9), 1267; https://doi.org/10.3390/nu10091267
Received: 24 August 2018 / Revised: 5 September 2018 / Accepted: 6 September 2018 / Published: 8 September 2018
PDF Full-text (1046 KB) | HTML Full-text | XML Full-text
Abstract
Despite intensive study, neurodegenerative diseases remain insufficiently understood, precluding rational design of therapeutic interventions that can reverse or even arrest the progressive loss of neurological function. In the last decade, several theories investigating the causes of neurodegenerative diseases have been formulated and a
[...] Read more.
Despite intensive study, neurodegenerative diseases remain insufficiently understood, precluding rational design of therapeutic interventions that can reverse or even arrest the progressive loss of neurological function. In the last decade, several theories investigating the causes of neurodegenerative diseases have been formulated and a condition or risk factor that can contribute is described by the gut-brain axis hypothesis: stress, unbalanced diet, and drugs impact altering microbiota composition which contributes to dysbiosis. An altered gut microbiota may lead to a dysbiotic condition and to a subsequent increase in intestinal permeability, causing the so-called leaky-gut syndrome. Herein, in this review we report recent findings in clinical trials on the risk factor of the gut-brain axis in Alzheimer’s disease and on the effect of omega-3 supplementation, in shifting gut microbiota balance towards an eubiosis status. Despite this promising effect, evidences reported in selected randomized clinical trials on the effect of omega-3 fatty acid on cognitive decline in Alzheimer’s disease are few. Only Mild Cognitive Impairment, a prodromal state that could precede the progress to Alzheimer’s disease could be affected by omega-3 FA supplementation. We report some of the critical issues which emerged from these studies. Randomized controlled trials in well-selected AD patients considering the critical points underlined in this review are warranted. Full article
(This article belongs to the Special Issue Brain Aging and Gut-Brain Axis)
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Figure 1

Open AccessReview Changes of Colonic Bacterial Composition in Parkinson’s Disease and Other Neurodegenerative Diseases
Nutrients 2018, 10(6), 708; https://doi.org/10.3390/nu10060708
Received: 27 April 2018 / Revised: 28 May 2018 / Accepted: 30 May 2018 / Published: 1 June 2018
Cited by 1 | PDF Full-text (762 KB) | HTML Full-text | XML Full-text
Abstract
In recent years evidence has emerged that neurodegenerative diseases (NDs) are strongly associated with the microbiome composition in the gut. Parkinson’s disease (PD) is the most intensively studied neurodegenerative disease in this context. In this review, we performed a systematic evaluation of the
[...] Read more.
In recent years evidence has emerged that neurodegenerative diseases (NDs) are strongly associated with the microbiome composition in the gut. Parkinson’s disease (PD) is the most intensively studied neurodegenerative disease in this context. In this review, we performed a systematic evaluation of the published literature comparing changes in colonic microbiome in PD to the ones observed in other NDs including Alzheimer’s disease (AD), multiple system atrophy (MSA), multiple sclerosis (MS), neuromyelitis optica (NMO) and amyotrophic lateral sclerosis (ALS). To enhance the comparability of different studies, only human case-control studies were included. Several studies showed an increase of Lactobacillus, Bifidobacterium, Verrucomicrobiaceae and Akkermansia in PD. A decrease of Faecalibacterium spp., Coprococcus spp., Blautia spp., Prevotella spp. and Prevotellaceae was observed in PD. On a low taxonomic resolution, like the phylum level, the changes are not disease-specific and are inconsistent. However, on a higher taxonomic resolution like genus or species level, a minor overlap was observed between PD and MSA, both alpha synucleinopathies. We show that standardization of sample collection and analysis is necessary for ensuring the reproducibility and comparability of data. We also provide evidence that assessing the microbiota composition at high taxonomic resolution reveals changes in relative abundance that may be specific to or characteristic of one disease or disease group, and might evolve discriminative power. The interactions between bacterial species and strains and the co-abundances must be investigated before assumptions about the effects of specific bacteria on the host can be made with certainty. Full article
(This article belongs to the Special Issue Brain Aging and Gut-Brain Axis)
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Figure 1

Open AccessReview Polyphenols in Parkinson’s Disease: A Systematic Review of In Vivo Studies
Nutrients 2018, 10(5), 642; https://doi.org/10.3390/nu10050642
Received: 21 April 2018 / Revised: 14 May 2018 / Accepted: 16 May 2018 / Published: 19 May 2018
PDF Full-text (350 KB) | HTML Full-text | XML Full-text
Abstract
Parkinson’s disease (PD) is the second most common neurodegenerative disorder. However, therapeutic options treating only its symptoms are very disappointing. Therefore there is an ongoing search for compounds capable of tackling the multi-dimensional features of PD. Recently natural polyphenols have gained great interest
[...] Read more.
Parkinson’s disease (PD) is the second most common neurodegenerative disorder. However, therapeutic options treating only its symptoms are very disappointing. Therefore there is an ongoing search for compounds capable of tackling the multi-dimensional features of PD. Recently natural polyphenols have gained great interest as potential therapeutic agents. Herein, we have attempted to summarize results obtained in different animal models demonstrating their neuroprotective effects. The in vivo findings presented below are supported by human subject data and reports regarding the ability of polyphenols to cross the blood-brain barrier. The beneficial effects of polyphenols are demonstrated by the results of behavioral examinations, mainly related to motor and cognitive capabilities, histopathological and immunohistochemical examination concerning the protection of dopaminergic neurons, analyses of dopamine and the concentration of its metabolites, as well as mechanistic studies regarding the modulation of oxidative stress, neuroinflammation, cellular iron management, proteinopathy, and additionally the regulation of signaling pathways. Importantly, data about brain distribution of the metabolic derivatives of the reviewed polyphenols are crucial for the justification of their nutritional intake in neuroprotective intervention, as well as for the identification of potential targets for a novel therapeutic approach to Parkinson’s disease. Full article
(This article belongs to the Special Issue Brain Aging and Gut-Brain Axis)
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