scholarly journals Young at Gut—Turning Back the Clock with the Gut Microbiome

2021 ◽  
Vol 9 (3) ◽  
pp. 555
Author(s):  
Harish Narasimhan ◽  
Clarissa C. Ren ◽  
Sharvari Deshpande ◽  
Kristyn E. Sylvia
Keyword(s):  
Gut Microbiome ◽  
Past Century ◽  
Low Grade ◽  
Gut Dysbiosis ◽  
The Past ◽  
Health Measures ◽  
Aging Populations ◽  
Secretory Phenotype ◽  
The Brain

Over the past century, we have witnessed an increase in life-expectancy due to public health measures; however, we have also seen an increase in susceptibility to chronic disease and frailty. Microbiome dysfunction may be linked to many of the conditions that increase in prevalence with age, including type 2 diabetes, cardiovascular disease, Alzheimer’s disease, and cancer, suggesting the need for further research on these connections. Moreover, because both non-modifiable (e.g., age, sex, genetics) and environmental (e.g., diet, infection) factors can influence the microbiome, there are vast opportunities for the use of interventions related to the microbiome to promote lifespan and healthspan in aging populations. To understand the mechanisms mediating many of the interventions discussed in this review, we also provide an overview of the gut microbiome’s relationships with the immune system, aging, and the brain. Importantly, we explore how inflammageing (low-grade chronic inflammation that often develops with age), systemic inflammation, and senescent cells may arise from and relate to the gut microbiome. Furthermore, we explore in detail the complex gut–brain axis and the evidence surrounding how gut dysbiosis may be implicated in several age-associated neurodegenerative diseases. We also examine current research on potential interventions for healthspan and lifespan as they relate to the changes taking place in the microbiome during aging; and we begin to explore how the reduction in senescent cells and senescence-associated secretory phenotype (SASP) interplay with the microbiome during the aging process and highlight avenues for further research in this area.

scholarly journals The Gut Microbiota and Healthy Aging: A Mini-Review

Gerontology ◽  
2018 ◽  
Vol 64 (6) ◽  
pp. 513-520 ◽  
Author(s):  
Sangkyu Kim ◽  
S. Michal Jazwinski
Keyword(s):  
Gut Microbiota ◽  
Individual Variation ◽  
Gut Microbiome ◽  
Chronological Age ◽  
Low Grade ◽  
Beneficial Effects ◽  
Gut Dysbiosis ◽  
Age Related ◽  
Host Health ◽  
Nutrient Signaling

The gut microbiota shows a wide inter-individual variation, but its within-individual variation is relatively stable over time. A functional core microbiome, provided by abundant bacterial taxa, seems to be common to various human hosts regardless of their gender, geographic location, and age. With advancing chronological age, the gut microbiota becomes more diverse and variable. However, when measures of biological age are used with adjustment for chronological age, overall richness decreases, while a certain group of bacteria associated with frailty increases. This highlights the importance of considering biological or functional measures of aging. Studies using model organisms indicate that age-related gut dysbiosis may contribute to unhealthy aging and reduced longevity. The gut microbiome depends on the host nutrient signaling pathways for its beneficial effects on host health and lifespan, and gut dysbiosis disrupting the interdependence may diminish the beneficial effects or even have reverse effects. Gut dysbiosis can trigger the innate immune response and chronic low-grade inflammation, leading to many age-related degenerative pathologies and unhealthy aging. The gut microbiota communicates with the host through various biomolecules, nutrient signaling-independent pathways, and epigenetic mechanisms. Disturbance of these communications by age-related gut dysbiosis can affect the host health and lifespan. This may explain the impact of the gut microbiome on health and aging.

Metabolic Syndrome and Its Effect on the Brain: Possible Mechanism

2018 ◽  
Vol 17 (8) ◽  
pp. 595-603 ◽  
Author(s):  
Nurul ‘Ain Arshad ◽  
Teoh Seong Lin ◽  
Mohamad Fairuz Yahaya
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Neurodegenerative Diseases ◽  
Disease Type ◽  
Low Grade ◽  
Oxygen Species ◽  
Metabolic Factors ◽  
Low Grade Inflammation ◽  
The Brain

Background & Objective: Metabolic syndrome (MetS) is an interconnected group of physiological, biochemical, clinical and metabolic factors that directly increase the risk of cardiovascular disease, type 2 diabetes mellitus (T2DM) and mortality. Rising evidence suggests that MetS plays a significant role in the progression of Alzheimer’s disease and other neurodegenerative diseases. Nonetheless, the factors linking this association has not yet been elucidated. As we are facing an increasing incidence of obesity and T2DM in all stages of life, understanding the association of MetS and neurodegenerative diseases is crucial to lessen the burden of the disease. Conclusion: In this review, we will discuss the possible mechanisms which may relate the association between MetS and cognitive decline which include vascular damages, elevation of reactive oxygen species (ROS), insulin resistance and low-grade inflammation.

Catatonia: A window into the cerebral underpinnings of will

2002 ◽  
Vol 25 (5) ◽  
pp. 582-584 ◽  
Author(s):  
Ricardo de Oliveira-Souza ◽  
Jorge Moll ◽  
Fátima Azevedo Ignácio ◽  
Paul J. Eslingerc
Keyword(s):  
The Other ◽  
Past Century ◽  
Western Thought ◽  
Clinical Expression ◽  
The Past ◽  
Human Autonomy ◽  
The Will ◽  
The Brain

The will is one of the three pillars of the trilogy of mind that has pervaded Western thought for millennia, the other two being affectivity and cognition (Hilgard 1980). In the past century, the concept of will was imperceptibly replaced by the cognitive-oriented behavioral qualifiers “voluntary,” “goal-directed,” “purposive,” and “executive” (Tranel et al. 1994), and has lost much of its heuristic merits, which are related to the notion of “human autonomy” (Lhermitte 1986). We view catatonia as the clinical expression of impairment of the brain mechanisms that promote human will. Catatonia is to the brain systems engaged in will, as coma is to the reticular ascending systems that promote sleep and wakefulness (Plum 1991).

The Gut Microbiome, Metformin, and Aging

2021 ◽  
Vol 62 (1) ◽  
Author(s):  
Sri Nitya Reddy Induri ◽  
Payalben Kansara ◽  
Scott C. Thomas ◽  
Fangxi Xu ◽  
Deepak Saxena ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Healthy Aging ◽  
Bacterial Species ◽  
Annual Review ◽  
Publication Date ◽  
Low Grade ◽  
Host Interactions ◽  
Age Related ◽  
Low Grade Inflammation

Metformin has been extensively used for the treatment of type 2 diabetes, and it may also promote healthy aging. Despite its widespread use and versatility, metformin's mechanisms of action remain elusive. The gut typically harbors thousands of bacterial species, and as the concentration of metformin is much higher in the gut as compared to plasma, it is plausible that microbiome-drug-host interactions may influence the functions of metformin. Detrimental perturbations in the aging gut microbiome lead to the activation of the innate immune response concomitant with chronic low-grade inflammation. With the effectiveness of metformin in diabetes and antiaging varying among individuals, there is reason to believe that the gut microbiome plays a role in the efficacy of metformin. Metformin has been implicated in the promotion and maintenance of a healthy gut microbiome and reduces many age-related degenerative pathologies. Mechanistic understanding of metformin in the promotion of a healthy gut microbiome and aging will require a systems-level approach. Expected final online publication date for the Annual Review of Pharmacology and Toxicology, Volume 62 is January 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

scholarly journals Active Forgetting: Adaptation of Memory by Prefrontal Control

2021 ◽  
Vol 72 (1) ◽  
pp. 1-36 ◽  
Author(s):  
Michael C. Anderson ◽  
Justin C. Hulbert
Keyword(s):  
Emotional State ◽  
Memory Loss ◽  
Brain Structures ◽  
Past Century ◽  
Top Down ◽  
The Past ◽  
New Findings ◽  
Nonhuman Animals ◽  
The Brain

Over the past century, psychologists have discussed whether forgetting might arise from active mechanisms that promote memory loss to achieve various functions, such as minimizing errors, facilitating learning, or regulating one's emotional state. The past decade has witnessed a great expansion in knowledge about the brain mechanisms underlying active forgetting in its varying forms. A core discovery concerns the role of the prefrontal cortex in exerting top-down control over mnemonic activity in the hippocampus and other brain structures, often via inhibitory control. New findings reveal that such processes not only induce forgetting of specific memories but also can suppress the operation of mnemonic processes more broadly, triggering windows of anterograde and retrograde amnesia in healthy people. Recent work extends active forgetting to nonhuman animals, presaging the development of a multilevel mechanistic account that spans the cognitive, systems, network, and even cellular levels. This work reveals how organisms adapt their memories to their cognitive and emotional goals and has implications for understanding vulnerability to psychiatric disorders.

scholarly journals Elevated Fecal pH Indicates a Profound Change in the Breastfed Infant Gut Microbiome Due to Reduction of Bifidobacterium over the Past Century

mSphere ◽  
2018 ◽  
Vol 3 (2) ◽  
Author(s):  
Bethany M. Henrick ◽  
Andra A. Hutton ◽  
Michelle C. Palumbo ◽  
Giorgio Casaburi ◽  
Ryan D. Mitchell ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Species Abundance ◽  
Breastfed Infant ◽  
Past Century ◽  
Breastfed Infants ◽  
The Past ◽  
Gut Function ◽  
Infant Gut Microbiome ◽  
Fecal Ph ◽  
Rich Countries

ABSTRACT Historically, Bifidobacterium species were reported as abundant in the breastfed infant gut. However, recent studies in resource-rich countries show an increased abundance of taxa regarded as signatures of dysbiosis. It is unclear whether these differences are the product of genetics, geographic factors, or interventions such as formula feeding, antibiotics, and caesarean section. Fecal pH is strongly associated with Bifidobacterium abundance; thus, pH could be an indicator of its historical abundance. A review of 14 clinical studies published between 1926 and 2017, representing more than 312 healthy breastfed infants, demonstrated a change in fecal pH from 5.0 to 6.5 (adjusted r 2 = 0.61). This trend of increasing infant fecal pH over the past century is consistent with current reported discrepancies in Bifidobacterium species abundance in the gut microbiome in resource-rich countries compared to that in historical reports. Our analysis showed that increased fecal pH and abundance of members of the families Enterobacteriaceae , Clostridiaceae , Peptostreptococcaceae , and Veillonellaceae are associated, indicating that loss of highly specialized Bifidobacterium species may result in dysbiosis, the implications of which are not yet fully elucidated. Critical assessment of interventions that restore this ecosystem, measured by key parameters such as ecosystem productivity, gut function, and long-term health, are necessary to understand the magnitude of this change in human biology over the past century.

scholarly journals “Inflammaging” as a Druggable Target: A Senescence-Associated Secretory Phenotype—Centered View of Type 2 Diabetes

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Francesco Prattichizzo ◽  
Valeria De Nigris ◽  
Lucia La Sala ◽  
Antonio Domenico Procopio ◽  
Fabiola Olivieri ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Er Stress ◽  
Death Rate ◽  
Therapeutic Option ◽  
Diabetic Patients ◽  
Low Grade ◽  
Molecular Alterations ◽  
Inflammatory Score ◽  
Secretory Phenotype

Aging is a complex phenomenon driven by a variety of molecular alterations. A relevant feature of aging is chronic low-grade inflammation, termed “inflammaging.” In type 2 diabetes mellitus (T2DM), many elements of aging appear earlier or are overrepresented, including consistent inflammaging. T2DM patients have an increased death rate, associated with an incremented inflammatory score. The source of this inflammation is debated. Recently, the senescence-associated secretory phenotype (SASP) has been proposed as the main origin of inflammaging in both aging and T2DM. Different pathogenic mechanisms linked to T2DM progression and complications development have been linked to senescence and SASP, that is, oxidative stress and endoplasmic reticulum (ER) stress. Here we review the latest data connecting oxidative and ER stress with the SASP in the context of aging and T2DM, with emphasis on endothelial cells (ECs) and endothelial dysfunction. Moreover, since current medical practice is insufficient to completely suppress the increased death rate of diabetic patients, we propose a SASP-centered view of T2DM as a futuristic therapeutic option, possibly opening new prospects by moving the attention from one-organ studies of diabetes complications to a wider targeting of the aging process.

scholarly journals The Interaction between the Gut Microbiome and Bile Acids in Cardiometabolic Diseases

Metabolites ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 65
Author(s):  
Cengiz Callender ◽  
Ilias Attaye ◽  
Max Nieuwdorp
Keyword(s):  
Bile Acids ◽  
Gut Microbiome ◽  
Fatty Liver Disease ◽  
Metabolic Diseases ◽  
Comprehensive Overview ◽  
Endocrine Organ ◽  
Cardiometabolic Diseases ◽  
Signalling Molecules ◽  
The Past

Cardio-metabolic diseases (CMD) are a spectrum of diseases (e.g., type 2 diabetes, atherosclerosis, non-alcohol fatty liver disease (NAFLD), and metabolic syndrome) that are among the leading causes of morbidity and mortality worldwide. It has long been known that bile acids (BA), which are endogenously produced signalling molecules from cholesterol, can affect CMD risk and progression and directly affect the gut microbiome (GM). Moreover, studies focusing on the GM and CMD risk have dramatically increased in the past decade. It has also become clear that the GM can function as a “new” endocrine organ. BA and GM have a complex and interdependent relationship with several CMD pathways. This review aims to provide a comprehensive overview of the interplay between BA metabolism, the GM, and CMD risk and progression.

Dietary inulin alleviates diverse stages of type 2 diabetes mellitusviaanti-inflammation and modulating gut microbiota in db/db mice

2019 ◽  
Vol 10 (4) ◽  
pp. 1915-1927 ◽  
Author(s):  
Ke Li ◽  
Li Zhang ◽  
Jing Xue ◽  
Xiaoli Yang ◽  
Xiaoying Dong ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Gut Microbiota ◽  
Low Grade ◽  
Gut Dysbiosis ◽  
P Type ◽  
Low Grade Inflammation

Type 2 diabetes mellitus (T2DM) is closely correlated with chronic low-grade inflammation and gut dysbiosis.

scholarly journals Lipid Chaperones and Metabolic Inflammation

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Masato Furuhashi ◽  
Shutaro Ishimura ◽  
Hideki Ota ◽  
Tetsuji Miura
Keyword(s):  
Large Body ◽  
Metabolic Stress ◽  
Fatty Acid Binding Proteins ◽  
Low Grade ◽  
Oxygen Species ◽  
Fatty Acid Binding ◽  
Metabolic Inflammation ◽  
The Past ◽  
Inflammatory State

Over the past decade, a large body of evidence has emerged demonstrating an integration of metabolic and immune response pathways. It is now clear that obesity and associated disorders such as insulin resistance and type 2 diabetes are associated with a metabolically driven, low-grade, chronic inflammatory state, referred to as “metaflammation.” Several inflammatory cytokines as well as lipids and metabolic stress pathways can activate metaflammation, which targets metabolically critical organs and tissues including adipocytes and macrophages to adversely affect systemic homeostasis. On the other hand, inside the cell, fatty acid-binding proteins (FABPs), a family of lipid chaperones, as well as endoplasmic reticulum (ER) stress, and reactive oxygen species derived from mitochondria play significant roles in promotion of metabolically triggered inflammation. Here, we discuss the molecular and cellular basis of the roles of FABPs, especially FABP4 and FABP5, in metaflammation and related diseases including obesity, diabetes, and atherosclerosis.

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