Importance Of Antimicrobial Agents From Plants In Present: Fill & Download for Free

In Ancient India it was well understood that a person’s teeth had to be kept clean. In fact Ancient Indian’s also knew that they had to clean their tongue as well. At a time when most of the world could not write nor record numbers effectively, Ancient India had a very advanced system of Dentistry. At around 500 B.C. it known that Indian’s already had toothpaste. This paste had antimicrobial qualities and it was made from the Neem Plant or the Asana Plant. Even mouth ulcers were treated with botanicals and the Khadira plant was used for this purpose. The use of brushes was well understood, however most people used the twigs of medicinal plants. Amongst these the Pilu and Meswak varieties were common. There were many others as well which were more specialized and these plant varieties are well recorded. There are even records of filling cavities. In 2005 it was found that the profession of the Dentist existed far before anyone had expected. At a neolithic period site from Ancient India, the remains of several individuals which were dated to about 7000 B.C., showed filled cavities with lapis lazuli fashioned so finely, that such work is not seen in the West until 1500 A.D. in Europe. From 500 B.C. onwards dental tools are widely found in India. These tools show without a doubt, how advanced dental care was.During the time of the first Greek contacts with Ancient India beginning at in the 5th century B.C. , it was recorded that at the Indian University of Taxila, an Indian Scholar known as Charaka, was teaching the components of Surgery, Hygiene and dental health. His works would later be recorded in the Indian Treatise on the subject known as the Astanga Samgraha. From this time forward other texts would describe the techniques and the tools used. The botanical agents and their efficacy was also described. It is from this and the traditions we still see in India that a clear picture emerges of the state of Indian abilities in the medical field.In India, the ancient traditions of the distant past still carry through in large part. All over India, even with imported brands of tooth paste it is common to find an Ayurvedic variant. I have used several of these, including a variant by Colgate. But I find the simple and more true versions to be the neem based toothpaste which is made by various smaller Indian Companies. The use of medicinal plants really does work well, and even when judged against modern toothpaste Ancient India does indeed hold it’s own as these toothpastes succeed in keeping your dental health intact without the use of chemicals. The Datun (A medicinal Twig) which is also known as Miswak, is also very efficient at cleaning your teeth and dislodging particles. It is ecologically less harmful than modern brushes and it has natural medicinal properties. The fact that has been used in India since Ancient times is all the more remarkable.Excavated sites in India show that Ancient Indian’s did not suffer from inability to keep their teeth clean, nor from uncontrolled cavities, but rather from over use of their teeth. For the Ancient Diet, was far more based on rougher food than what is consumed today. Ancient Grains and food sources were not nearly milled down to modern standards. Nor were softer foods so widely available in the Ancient World. The use of one’s body was far different than today, and this included how food was eaten. The ground down nature of teeth is well seen and is nothing like the present day. Yet, we find that Ancient India even made dentures, though they are quite different than today.Ancient India and much of the Ancient World still surprise us. For people found solutions for the problems they faced even with far lesser technology. Much of what they achieved was based on far better ecological foot print than we find today. Their solutions live on, and today many in India are rediscovering natural remedies. The Datun, and plant based toothpastes of Ancient India have actually made a comeback in the past two decades. For an awareness is coming about that not everything that is “Modern” is better than what was discovered in the past. For those ideas and endeavors which were achieved in ages long ago should not simply be traded away, especially when they are effective and ecologically more sound.Hinduism Today MagazineMan Was Enduring the Dentist's Drill 9,000 Years Ago11 Ancient Inventions & Discoveries Of Science That India Gifted To The Rest Of The World

Scientists have been studying the relationships between pathogens and dementia in general, and between pathogens and Alzheimer's in particular, for decades. Various pathogens are known to cause progressive dementias (some of which may respond to treatment if caught early enough), such as AIDS Dementia Complex, syphilis, neurocysticercosis, herpes encephalitis, and human prion diseases.The possibility that pathogens might somehow cause Alzheimer's itself, and that by preventing or treating a specific infection, we can prevent or treat Alzheimer's, is a fascinating concept, and many studies have been conducted on individual pathogens suspected of having a relationship. The number of potential candidates has been growing by leaps and bounds in recent years. The viruses that have been linked to an increased risk of Alzheimer's include HSV1 / HSV2, Epstein-Barr, cytomegalovirus, hepatitis C, varicella zoster, and HHV-6A and HHV-7 viruses. Other types of infectious pathogens, including Helicobacter pylori, chronic osteomyelitis, Chlamydophila pneumoniae, many spirochetes such as Borrelia burgdorferi, protozoan parasites such as Toxoplasma gondii, various periodontal pathogens, and various yeasts and fungal (e.g., (Alternaria, Botrytis, Candida, Cladosporium, and Malassezia species) are associated with an increased risk of Alzheimer's. Researchers have developed theories about a wide range of possible mechanisms that might lead from infection to Alzheimer's, some specific to a given species, and some generic to broad classes of pathogens.In certain cases, a mountain of evidence has been produced that goes far beyond simple epidemiological studies. Some research has even gotten as far as preliminary clinical trials in humans that appeared to support the contention that treating the suspect pathogen reversed or prevented the dementia. However, efforts to reproduce these results have been unsuccessful, and the reasons are not understood.I assume your question comes from the recent flap over news releases from Cortexyme about their work on Porphyromonas gingivalis, one of the key bacteria in chronic gum disease, and the fact that they have an investigational new drug (IND) in clinical trials. See, e.g.:We may finally know what causes Alzheimer’s – and how to stop itCortexyme, IncAnd speaking of a mountain of evidence, that's exactly what Cortexyme and their collaborators have produced:Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitorsTry plowing through that before you've had your morning coffee!But...It's all supportive evidence, produced in mice (if you know anything about me, you know how I feel about mice), and in vitro solution and cell tissue studies. What happens in model test animals (especially mice) and in vitro experiments may have little or nothing to do with what happens in the human body. Moreover, a lot of the evidence relies on the specificity of certain antibodies (such as the anti-gingipain antibodies) used in the experiments, and while antibodies may appear to be specific when tested against a narrow range of potential analytes in a relatively uncomplicated medium, they could quite conceivably (often do) cross-react with many and diverse epitopes in a complicated milieu such as brain tissue.However, just for the sake of argument, let's suppose that the evidence is all representative of what would happen inside the human body, and the antibodies are highly specific, and so on and so forth. Does that mean they've discovered what causes Alzheimer's and a way to cure, or at least, prevent it?No. Because it doesn't fit in with so many other things that we know about Alzheimer's. In fact, it doesn't fit in with so many other things we know about periodontal disease.Periodontal disease represents a group of oral inflammatory infections initiated by oral pathogens which exist as a complex biofilms on the tooth surface and cause destruction to tooth supporting tissues. The severity of this disease ranges from mild and reversible inflammation of the gingiva (gingivitis) to chronic destruction of connective tissues, the formation of periodontal pocket and ultimately result in loss of teeth. It is now widely accepted that a myriad of bacteria -- not just a single microorganism -- are involved in periodontal diseases. The onset of periodontal tissue inflammation is triggered by the colonization of the subgingival region by periodontal bacteria. On the tooth surfaces, for example, early or primary colonizers are mainly streptococci and actinomyces. Over time, the proportions of these Gram-positive facultatively anaerobic bacteria decrease, and eventually Gram-negative anaerobes become more established, especially at the interface of the teeth and gums. Complex interactions between bacterial flora and the host defense mechanisms (including, possibly, the deficiency of certain immunological factors in the host) significantly influence the balance between bacterial aggression and host protection and determines whether periodontal breakdown occurs. In light of these criteria, a number of experimental findings have indicated that the primary etiological agents of periodontal diseases are generally Gram-negative rods, including Actinobacillus actinomycetemcomitans, Tannerella forsythia, Prevotella, Fusobacterium, and P. gingivalis. None of these microbial species is capable of causing the destructive events involved in the periodontal disease progression on its own; rather, the etiology requires a concerted interaction of these microorganisms to establish their niches in the oral cavity.Among major periodontal pathogens, P. gingivalis appears to be one of the prime etiological agents in the pathogenesis and progression of periodontal disease. However, while it is often found in subgingival plaque samples from patients with chronic periodontitis, it is not always present -- studies have shown that about 40–100% of adult periodontitis patients have been infected with P. gingivalis. Moreover, some strains of P. gingivalis are considered to be non-invasive, based on their inability to form abscesses in a mouse model; and it has been demonstrated that the invasive strains of P. gingivalis possesses more pathogenic activities than the non-invasive strains both in vitro and in vivo. Invasive P. gingivalis strains express many different virulence factors with a wide range of activities, not just gingipains. To date, numerous studies have been done to elucidate the mechanism of virulence compounds secreted by P. gingivalis and the cellular interactions with the host. Improved understanding of the these interactions at the molecular and cellular level, may ultimately have relevance to the overall well-being of the host. In recent years, the use of plant-derived natural compounds has gained more attention to attenuate the action of P. gingivalis. For example, quercetin, resveratrol, and its related compounds, catechin, epicatechin, orcinol, and 4-allylphenol, were found to exhibit an inhibitory effect on the activity of P. gingivalis fimbriae; and polyphenols of Myrothamnus flabellifolia were shown to reduce P. gingivalis adhesion and invasion up to about 50% by interacting with bacterial outer membrane proteins. This anti-adhesive effect is also accompanied by cytoprotective effects which relate to cytokine secretion.Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum LineThe virulence factors that Cortexyme is targeting for treating P. gingivalis are gingipains, i.e., cysteine proteases that are essential for P. gingivalis survival and pathogenicity, playing critical roles in host colonization, inactivation of host defenses, iron and nutrient acquisition, and tissue destruction. Gingipains have been shown to mediate the toxicity of P. gingivalis in endothelial cells, fibroblasts, and epithelial cells. Although P. gingivalis has a plethora of virulence factors, much of its pathogenicity is surprisingly related to the overall immunosuppression of the host. While gingipains can contribute to immunosuppression, many other P. gingivalis virulence factors play a wide range of roles in immunosuppression, as well.https://www.tandfonline.com/doi/full/10.3402/jom.v8.33029In addition, P. gingivalis is not alone in being responsible for disease development, neither in periodontal nor in systemic diseases or dementia. Although it can modulate the growth of other bacteria in the subgingival biofilm, periodontitis and its related systemic diseases are not the effect of a single bacterium. Each bacterium in a cluster with quorum sensing-like properties may affect the responses induced by others and vice versa. In fact, a "biofilm concept of Alzheimer's senile plaques" has been proposed as an alternative platform for answering the question on whether microbes are the causative agents of Alzheimer's.Can an Infection Hypothesis Explain the Beta Amyloid Hypothesis of Alzheimer’s Disease?Periodontitis, Microbiomes and their Role in Alzheimer’s DiseaseItzhaki and colleagues claim that HSV1 causes Alzheimer's by direct viral action as well as by virus-induced inflammation, and that the use of anti-viral medications to treat severe active HSV infections can decrease the risk of dementia. However, despite all the evidence they've produced so far, they have failed to persuade me that they have a solid case.Is Alzheimer's or dementia actually caused by a virus like HSV?Similarly, it makes me very squeamish that Cortexyme and colleagues are focusing on a specific pathogen as the cause of Alzheimer's, and a specific drug target that's apparently unique to that bacterial species (i.e., its gingipains) as the cure or prevention.The Alzheimer's brain harbors its own, and apparently diverse, microbiome. The diversity of microbes that have been documented in Alzheimer's brains could be a reflection of the brain donors' other microbiomes (mouth, skin, GI tract), co-morbid states, geographical location, age, diet, oral function (e.g., denture wearing), and lifestyle. Since age is the major risk factor for developing Alzheimer's, evolving microbiomes may provide dynamics of the microbial communities over time. Pathogens may enter the brain via diverse routes. Many viruses can enter the brain via olfactory neural pathways to the basal forebrain, a route also employed by C. pneumoniae, for example. Disruption of the blood-brain barrier (BBB) appears to be an early feature of Alzheimer's, which may facilitate pathogen entry into the brain and/or be caused by certain pathogens or by bacterial cell wall components such as lipopolysaccharide (LPS) or lipoteichoic acid from repeated peripheral bacterial infections (a feature of the elderly population). The BBB can also be damaged by viral infection (vaccinia or HSV-1) or by P. gingivalis. Other pathogens such as B. burgdorferi, C. pneumoniae, or Cryptococcus neoformans (C. neoformans) have found other ways to circumvent this barrier.Periodontal disease has long been established as a major risk factor for Alzheimer's, and many researchers have been actively investigating it. Many of those studies have found a great deal of diversity in the oral microbiome associated with periodontal disease that ends up in the Alzheimer's brain. Some common examples of bacteria in the periodontal microbiome include not only P. gingivalis, but also Tannerella forsythia, Prevotella intermedia, Eikenella corrodens, Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans, and T. denticola.In fact, some of the best-documented bacterial species associated with periodontal disease were not observed in a 2017 study using 16S ribosomal gene-specific Next generation sequencing (NGS) of extracted brain tissue. Before that study, evidence had relied on methods that require prior knowledge of which bacterial species to look for, and specific methods for detecting the presence of those species. This new study allowed the researchers to determine what actually is in the samples, without going after specific species -- and also enabled the detection of bacteria which cannot be cultured. The researchers noted that these "missing" species could be present at low copy numbers or in discreet areas not sampled cannot be discounted; further sampling and NGS-based experiments exploring more rRNA gene variable regions, different PCR conditions and systematic analysis of 16S DNA in different areas of the brain are required in order to provide a fuller assessment. There are other considerations also: for instance, the cohort assessed in this study was not selected based on periodontal or any other disease; future studies would require specific cohorts selected for the presence and absence of periodontal or other disease. Additionally, any infection which initiates the neuropathology of Alzheimer's may occur 15-20 years pre-mortem; therefore, the bacteria identified in the post-mortem Alzheimer's brain may be due to secondary infection after the blood-brain barrier (BBB) breakdown rather than being the causative agent. In addition, patient cohorts from different geographical regions may differ in their gut, mouth and brain microbiomes. Species vary between global regions and ethnic groups; for example, Spanish periodontitis patients are more likely to harbor oral P. gingivalis than in Netherlands, where A. actinomycetemcomitans is more evident. Furthermore, whereas up to 90% of North American samples of Alzheimer's brains contained C. pneumoniae, in another study from North European patients, C. pneumoniae could not be detected. Similarly, in the 2017 16S ribosomal NGS study, C. pneumoniae was completely absent, as were E. coli K99 and some other periodontal species previously associated with Alzheimer's (as well as some other non-oral bacteria commonly associated with Alzheimer's.)16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem BrainSo. Many diverse pathogens have been implicated in Alzheimer's disease in epidemiological studies. Preliminary microbiome studies using unbiased next-generation sequencing have identified many fungi in Alzheimer's brains (Alternaria, Botrytis, Candida, Cladosporium, and Malassezia species) as well as the better studied viruses and bacteria. Many of these viruses, bacteria (or their LPS), fungi, and protozoa increase Aβ production in vitro or in vivo. Several of these pathogens also evoke tau phosphorylation.There are many passionate champions of individual pathogens as the single causative agent for Alzheimer's. Each has some supporting evidence, several have extensive supporting evidence ... but there are flaws or holes in their arguments. The diversity of viruses, bacteria, and fungi contributing to Alzheimer's, Aβ deposition, or dementia suggests a polymicrobial relationship with these conditions. Ergo, rather than a single pathogen being the cause of Alzheimer's, some researchers are beginning to study overall pathogen load as the cause. Some have started by studying viral load, and found that viral load -- rather than specific strains -- was tied to increased expression of components of the amyloid pathway in people with preclinical Alzheimer's. This fits with the related hypothesis that Aβ normally functions as an endogenous antimicrobial defense. Several researchers have reported that the peptide erects a physical barrier against invading bacteria and fungi, cocooning them in amyloid fibrils. Others have reported that Aβ40/42 can prevent HSV-1 entry into cells, and that Aβ can bind and agglutinate HSV-1 and HHV-6 in cells and in mice, preventing acute encephalitis.And this brings us to the "antimicrobial protection hypothesis of Alzheimer's." This is a very intriguing concept that seems to fit so many aspects of Alzheimer's, including the beta amyloid hypothesis, and the possible relationships between many and diverse pathogens and Alzheimer's pathology.Until recently, Aβ had been considered to be a functionless catabolic byproduct; and the pathways leading to Aβ generation were believed to be intrinsically pathological. Now Aβ has been identified as an antimicrobial peptide (AMP.) AMPs are the first line of defense against pathogens and act as potent broad-spectrum antibiotics and immunomodulators that target bacteria, mycobacteria, enveloped viruses, fungi, and protozoans, and in some cases, transformed or cancerous host cells. AMPs are widely expressed and are abundant in brain and other immunoprivileged tissues where actions of the adaptive immune system are constrained. Although AMPs are normally protective, AMP dysregulation can lead to host cell toxicity, chronic inflammation, and degenerative pathologies. Particularly germane to Aβ's role in Alzheimer's, AMPs are deposited as amyloid in several disorders, including senile seminal vesicle amyloid and isolated atrial amyloidosis, two of the most common human amyloidopathies.The protective role for Aβ in innate immunity employs a classic AMP mechanism. When pathogens get into the brain, they activate the production of soluble Aβ proteins which bind to microbial cell wall carbohydrates. Developing protofibrils inhibit pathogen adhesion to host cells. Propagating Aβ fibrils mediate agglutination and final entrapment of microbes. That network of fibers entombs the microbes so they can't infect the cell. It then forms a plaque. This new model posits that in Alzheimer's, normally protective antimicrobial pathways mediated by Aβ oligomerization are overactivated, either by real or incorrectly perceived infection. Ongoing Aβ deposition drives neuroinflammation, leading to neuropathology and widespread neuronal death. Consistent with this model, Salmonella infections of the brains of transgenic 5XFAD mice resulted in rapid seeding and accelerated Aβ deposition, which closely co-localized with the invading bacteria.Overall, the findings raise the intriguing possibility that Aβ may play a protective role in innate immunity. What might drive widespread Aβ deposition in Alzheimer's, however, remains unclear. Among sterile inflammatory diseases, dysregulated innate immune responses rather than infections are emerging as drivers of pathology. Notably, two of the three confirmed AMP amyloidopathies are not linked to obvious infections. However, a large body of data accrued over nearly a century suggests that genuine infection may also play a role in Alzheimer's etiology. The findings to date do not constitute direct evidence of a role for infection in Alzheimer's etiology. However, they do suggest a possible mechanism for pathogen-driven Aβ amyloidosis. The data also suggest the possibility that a range of microbial organisms may be able to induce Aβ deposition, a possible reason for why a single pathogen species has not yet been identified that is overwhelmingly associated with Alzheimer's.This model differs in several important ways from the "pathogen hypothesis" championed by researchers such as Itzhaki and those at Cortexyme. A key insight is that it's not direct killing of brain cells by specific strains of pathogens that causes Alzheimer's; rather, it's the body's innate immune response to the pathogens that leads to brain-damaging neuroinflammation. And while the "pathogen hypothesis" is typically offered as an alternative to the Aβ hypothesis, the "antimicrobial protection hypothesis" is not an alternative, but rather fits within the Aβ-tau-inflammation paradigm. It fills in blanks, offering an explanation for how the process starts and for the true nature of Aβ. Circumstantial evidence for the importance of Aβ is significant; it appears to have developed some 400 million years ago and has not only survived evolutionary pressures to appear in humans today, but is present in 60 percent of vertebrates, including fish, reptiles, and birds.So. How reliable are the new claims linking Alzheimer's disease with chronic gum disease?The concept that chronic gum disease is linked to Alzheimer's is not new, at all, and there may, in fact, be a causal relationship. To claim, however, that Porphyromonas gingivalis, which is one of the key bacteria in periodontic gum disease, is the sole cause of Alzheimer's, and that by targeting small molecule drugs against a tiny handful of its virulence factors, it may be possible to treat or prevent Alzheimer's, is going way out on a limb and, I think, isn't supported by the research literature.

Not valuing things which are native to India. May be because of our educational system, or might be the fact that people give more unnecessary importance to “foreign” things just for the sake of it. There are many but i’ll take this as an example which I read on twitter recently. This is about NEEM ! Neem contains a unique composition of organic and beneficial compounds, so products derived from it are very popular in alternative and herbal remedies. From tea and garnishes to skin salves and herbal supplements, it is considered as one of the most important and versatile plants in Indian culture The oil from the leaves can be extracted and used in a wide variety of medicines, while the leaves can be dried and used as an herb or even as a pest repellent. In many areas of India, the shoots and(more)