Revealing The Gut-brain Connection: The Effects of Microbiota Extend Beyond Digestion | Chapter 9 | Pharmaceutical Science: New Insights and Developments Vol. 9

 

The gut microbiome is a dynamic internal ecosystem that plays a crucial role in shaping our overall health. A balanced gut microbiome aids in digestion, nutrient absorption, immune function, mental clarity, and emotional regulation, and protects against diseases such as diabetes, neurodegenerative disorders, and autoimmune conditions. Comprising bacteria, viruses, fungi, and other microorganisms, this vast ecosystem is essential but often overlooked in its impact on health. It transforms dietary components into important neurotransmitters and antioxidants, including serotonin and indole-3-propionic acid (IPA). However, factors like poor diet, excessive hygiene, stress, and antibiotic use can disrupt this delicate balance by decreasing microbial diversity and impairing function. The gut microbiota is linked not only to digestive diseases but also to mental health conditions. This chapter emphasises the influence of stress, probiotics, circadian rhythms, diet, and environmental exposures on the gut microbiota’s interaction with brain function via the gut-brain axis—a bidirectional communication system. It explores how gut microbes affect the nervous system through neurotransmitters, the endocrine system, immune mechanisms, and microbial metabolites. Additionally, it discusses how alterations in gut microbiota may be involved in psychiatric disorders such as major depressive disorder (MDD), schizophrenia (SCZ), bipolar disorder (BD), autism spectrum disorder (ASD), and attention-deficit hyperactivity disorder (ADHD).

 

 

Author(s) Details

Chandrasekar R
Department of Pharmacognosy, Faculty of Pharmacy, Seven Hills College of Pharmacy, Tirupati, AP, India.

 

Pooja R.P
Department of Pharmacognosy, Seven Hills College of Pharmacy, Tirupati, AP, India.

 

Sadhana A
Department of Pharmacognosy, Seven Hills College of Pharmacy, Tirupati, AP, India.

 

Snehalatha K
Department of Pharmacognosy, Seven Hills College of Pharmacy, Tirupati, AP, India.

 

Prasanna Venkatesh J
Department of Pharmacognosy, Seven Hills College of Pharmacy, Tirupati, AP, India.

 

Selvakumar M
Department of Pharmacognosy, Seven Hills College of Pharmacy, Tirupati, AP, India.

 

Sivagami B

Department of Pharmaceutical Analysis, Faculty of Pharmacy, Seven Hills College of Pharmacy, Tirupati, AP, India.

 

Kumanan R
Department of Pharmacognosy, Faculty of Pharmacy, Devaki Amma Memorial College of Pharmacy, Malappuram, 673634, Kerala, India.

 

Please see the book here :- https://doi.org/10.9734/bpi/psnid/v9/6889

Potential Peptide Biomarkers and Etiological Factors in the Cerebrospinal Fluid of Amyotrophic Lateral Sclerosis Patients | Chapter 3 | Medicine and Medical Research: New Perspectives Vol. 10

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by the loss of upper and lower motor neurons, which eventually may lead to death. In spite of intensive research on the molecular and cellular mechanisms involved in the etiology of ALS initiation and progression, it is, unfortunately, poorly understood and there is no efficient specific/decisive treatment for ALS patients. Critical to the mission of developing effective therapies for ALS is the discovery of biomarkers that can illuminate mechanisms of neurodegeneration and have diagnostic, prognostic, or pharmacodynamic value. Here, we merged unbiased discovery-based approaches and targeted quantitative comparative analyses to identify proteins that are altered in cerebrospinal fluid (CSF) from patients with ALS. This study aims to identify specific peptides in the cerebrospinal fluid (CSF) of ALS patients and to examine their potential relevance to the etiology of this disease. Peptides were identified by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Motor activity of mice was tested by the Rota-rod test and peptide-induced inflammation was assessed by induction nitric oxide synthase activity in BV2 microglia cells. Analysis of CSF samples of ALS patients (n = 15) detected two peptides, C-terminal fragments of transthyretin and osteopontin, which were absent in a control group (n = 15). In addition to being potential biomarker candidates, the relevance of these peptides to the disease etiology was tested by assessing their effects on motor activity in mice and inflammation model in cell culture. Intranasal administration of the peptides reduced motor activity in the Rota-rod test and activated lipopolysaccharide-induced inflammation in BV2 microglia cells. The mechanism of action of the neurotoxic activity may be direct cytotoxicity to neuronal cells causing necrotic/apoptotic effect and/or via LPS coactivation of microglia and elicitation of inflammatory response resulting in neuronal damage. Future studies are needed to explore the mechanism of action of these neurotoxic peptides.

The results imply that two potentially neurotoxic peptides are created, released, or penetrated the central nervous system during the beginning and progression of ALS, causing neuroinflammation and neurodegeneration.

 

Author (s) Details

 

Uri Wormser
Institute of Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 9112002, Israel.

 

Amnon Sintov

Department of Biomedical Engineering, Faculty of Engineering Sciences, Ben Gurion University of the Negev, Be’er Sheva 84105, Israel.

 

Marco Vinceti
Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41125 Modena, Italy and Department of Epidemiology, Boston University School of Public Health, Boston, MA 02118, USA.

 

Jessica Mandrioli
Department of Biomedical, Metabolic and Neural Sciences, Faculty of Medicine and Surgery, University of Modena and Reggio Emilia, 41125 Modena, Italy and Department of Neuroscience, Azienda Ospedaliero Universitaria di Modena, 41126 Modena, Italy.

 

Berta Brodsky
Institute of Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 9112002, Israel.

 

Elena Proscura
Institute of Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 9112002, Israel.

 

Yoram Finkelstein
Neurology and Toxicology Service and Unit, Shaare Zedek Medical Center, Jerusalem 9103102, Israel.

 

 

Please see the book here:- https://doi.org/10.9734/bpi/mmrnp/v10/2348

Photobiomodulation: An Emerging Non-Invasive Way to Treat Alzheimer's Disease Using Neuroprotective and Neurogenesis Strategies | Chapter 6 | Disease and Health: Research Developments Vol. 10

Amyloid-beta (Aβ) plaques, tau hyperphosphorylation, neuroinflammation, and synaptic dysfunction are characteristic features of Alzheimer's disease (AD), a neurodegenerative disorder that compromises cognitive performance. Notwithstanding extensive research endeavors, there remain limited efficacious therapeutic alternatives for AD. Low-level light therapy (LLLT) within the red and near-infrared spectrum is employed in photobiomodulation (PBM), a non-invasive method that has demonstrated potential as a neuroprotective intervention, influences mitochondrial activity, modifies reactive oxygen species (ROS), regulates calcium homeostasis, and diminishes neuroinflammation—crucial elements in AD pathophysiology. Recent investigations demonstrate that PBM mitigates Aβ toxicity by augmenting mitochondrial function and facilitating Aβ elimination. Furthermore, PBM aids in maintaining the integrity of the blood-brain barrier, enhances cerebral blood flow, and facilitates neurovascular coupling, all of which are vital for neuronal health. This chapter examines how PBM alleviates cellular and molecular dysfunctions associated with AD, emphasizing its impact on oxidative stress, energy metabolism, and synaptic plasticity. Furthermore, it explores the possibility of incorporating PBM into multimodal therapeutic approaches for AD. This chapter underscores the revolutionary capacity of PBM in enhancing neurotherapeutic strategies for AD.

 

Author (s) Details

 

Hossein Chamkouri
School of Materials Science and Engineering, Hefei University of Technology, Hefei, 230009, China

 

Aoyun Li
School of Materials Science and Engineering, Hefei University of Technology, Hefei, 230009, China.

 

Zhanchuang Lu
School of Materials Science and Engineering, Hefei University of Technology, Hefei, 230009, China.

 

Li Cao
Department of Neurology, Anhui No. 2 Provincial People’s Hospital, Hefei, 230041, China.

 

Xianjun Xing

School of Mechanical Engineering, Hefei University of Technology, Hefei, 230009, Anhui Province,         PR China and Institute of Environment, Hefei Comprehensive National Science Center, Hefei, 230088, Anhui Province, PR China.

 

Changchun Chen
Department of Neurology, Anhui No. 2 Provincial People’s Hospital, Hefei, 230041, China.

 

Lei Chen
School of Materials Science and Engineering, Hefei University of Technology, Hefei, 230009, China and Intelligent Manufacturing Institute of HFUT, Hefei, 230051, China.

 

Please see the book here:- https://doi.org/10.9734/bpi/dhrd/v10/4884

Immunosenescence and Elderly: Importance of Immune System in Alzheimer’s Disease and Neurodegenerative Disorders | Chapter 1 | New Visions in Medicine and Medical Science Vol. 5

Alzheimer’s disease (AD) is a chronic multifactorial and complex neuro-degenerative disorder characterized by memory impairment and loss of cognitive ability which is a plight for the elderly. AD is an aging brain pathology, and maybe it is a combination of different diseases or various symptoms that are orchestrated in common. Alzheimer’s disease is the most common type of dementia and it may contribute to 60–70% of cases. Pathologically intracellular accumulation of abnormally phosphorylated Tau protein to form neurofibrillary tangles, extracellular amyloid-beta (Aβ) deposition to form senile plaques, neural disconnection, neural deaths and synaptic dysfunction within the brain are hallmark pathologies that characterize AD. The prevalence of the disease continues to increase globally due to the increase in longevity, quality of life, and medical treatment for chronic diseases that decrease mortality and enhance the survival among elderly. Medical awareness and accurate diagnosis of the disease also contribute to the high prevalence observed globally. Unfortunately, no magic treatment exists to modify the course of AD, and no available treatment is capable to mitigate the cognitive decline or reversing the pathology of the disease yet.

 

A Plethora of hypothesis beginning from cholinergic to the dominant Aβ cascade hypothesis to the abnormally excessive phosphorylated Tau protein were reported. Various explanations for the pathogenesis of AD such as abnormal excitation of glutamate system and mitochondrial dysfunction were also suggested. Despite the continuous stumble to deliver significant benefits and effective treatment for this agonizing global aging illness, multiprong approaches and strategies to ameliorate the disease course are urgently needed based on the knowledge of the underpinning pathogenesis of AD.

 

Immunosenescence is a procedure of immune deficit that appears with age (inflammaging process) and encompasses remodeling of lymphoid organs, leading to alterations in the immune function and neuroinflammation in advanced aging, which is closely linked to the outgrowth of infections, autoimmune diseases, and malignant cancers. It is well known that long-standing inflammation influence badly the brain over the course of a lifetime due to the senescence of the immune system.

 

Herein, we want to trace the role of the immune system in the pathogenesis of AD, thus we are going to explore alternative avenues, such as neuroimmune involvement in the pathogenesis of AD. Determination of the initial triggers engaged in neuroinflammation, which is an early episode of the presymptomatic stages of AD and contributes to the advancement of the disease and the underlying key mechanisms of brain damage that might help the development of therapeutic strategies to combat this devastating disease. In addition, this study represents how different aspects of the immune system, both in the brain and peripherally, behave to contribute to AD.

Author(s) Details:

Abdalla Bowirrat,
Department of Molecular Biology, Adelson School of Medicine, Ariel University, Ariel 40700, Israel.

Aia Bowirrat M. D.,
Department of Orthopedic Surgery, Hasharon Hospital, Rabin Medical Center, Petah Tikwa, Israel.

Please see the link here: https://stm.bookpi.org/NVMMS-V5/article/view/14150

Insulin Resistance Contributes to Neuroinflammation, Cognitive Decline and Brain Senescence in Congenic Obese LA/Ntul//-cp Rats | Chapter 9 | Advancement and New Understanding in Medical Science Vol. 7

Search for a suitable an animal model may prove to be more productive to determine if insulin resistance and its direct metabolic sequelae might be significant co-contributors to the neuronal declines that occur in NIDDM, obesity, and progression of dementia conditions. The burgeoning prevalence of obesity and overweight conditions from the age of adolescence and throughout the lifespan has reached epidemic proportions in industrialized nations throughout the globe. One of the most prevalent findings in obesity is the emergence of insulin resistance, which is linked to both a persistent inflammatory state and systemic hypoxia in adipose tissue. Insulin resistance impacts several aspects of substrate oxidation and oxidative free radical production in brain and somatic tissues, and it is likely that adipose tissue depots are the source of cytokine-linked chronic inflammation. In studies with aging congenic lean and obese rats chronic hyperinsulinemia and brain shrinkage has now been reported, albeit it in the absence of Type 2 diabetes (NIDDM), hypertension (HTN) or other comorbidities, thereby suggesting that aspects of disordered substrate metabolism including insulin resistance as commonly observed in obesity may be a key contributory factor in the development of a neuroinflammatory linked brain shrinkage with accompanying decreases in brain mass, protein and DNA content, and which were further compromised when fed an isocaloric high vs. a low glycemic insulinogenic diet containing sucrose vs. cornstarch respectively. These findings imply that in this strain of obese rats, chronic insulin resistance due to obesity, which is at least partially caused by dietary variables, is a plausible independent risk factor in the development of neuroinflammation, DNA damage, brain shrinkage, and neural senescence.

Author(s) Details:

Orien L. Tulp,
Colleges of Medicine and Graduate Studies, University of Science Arts and Technology, Montserrat, British West Indies, MSR1110 and the Einstein Medical Institute, North Palm Beach, FL 33409, USA.

Please see the link here: https://stm.bookpi.org/ANUMS-V7/article/view/13427