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A month long standoff ends between Elsevier and South Korean universities

ScienceDirect is a database of more than 3500 academic journals and books, which is published by world’s no.1 academic publisher Elsevier. The publisher Elsevier is headquartered in Amsterdam, Netherlands. For more than a month, South Korean universities were opposing a steep price rise proposed by Elsevier.

Initially, Elsevier had proposed a price hike of 4.5%, which was severely opposed by a consortium of top South Korean universities. On January 12, 2018, a settlement was finally achieved between South Korean universities and Elsevier.

South Korean universities have agreed to a price rise of about 3.5–3.9%.  In the initial proposal, Elsevier was compelling South Korean universities to compulsorily prescribe to its lesser known journals, as part of their ScienceDirect package deal. In future, South Korean universities would negotiate further for more concessions.

According to Lee Chang Won, secretary general of the Korea University & College Library Association, Elsevier currently provides a flat rate system. Therefore, universities have to pay for digital content of all journals, including the ones that are read least by viewers.

Lee Chang Won led the consortium of South Korean universities along with Korean Council for University Education (KCUE). Previously, South Korean universities accepted whatever rate increase was imposed by Elsevier, but they can no longer do the same due to budget cuts in library expenditure.

The consortium of 300 university and college libraries was formed in May 2017 by negotiating with 42 providers of databases. This group sought concessions on open-access journals and other less-read journals, which were included in the ScienceDirect package of Elsevier.

When Elsevier authorities refused to oblige, the consortium boycotted Elsevier and refused to renew contracts. During the period of negotiations, Elsevier provided access to all its products. Following negotiations, individual universities will now have to renew their one-year license at 3.9%; moreover, their three-year contract would be increased by 3.5%, 3.6%, and 3.7% above the baseline. These terms and conditions have been agreed by the consortium of universities in South Korea.

For 2019 contracts, negotiations would continue about pricing and other details between the consortium of South Korean universities and Elsevier, the publisher. According to Sogang’s Kim, the consortium is keen on signing a multi-year contract with Elsevier, wherein the annual increase of fees would be in the range 3.5–3.9%. This annual rate of increase in subscription fees is well above the international level of 2%. ScienceDirect journals are expensive but indispensable for academicians, rights from professors to post-doc scholars.

The month-long standoff between South Korean universities and Elsevier is akin to similar dispute between the consortium of German universities and Elsevier in 2017. At that point of time, electronic journals of Elsevier were not accessible to more than 60 universities in Germany as Elsevier had temporarily suspended access; however, the publisher restored access few weeks later though negotiations are still going on between consortium of German universities and Elsevier. Meanwhile, more than 200 universities in Germany have ceased their contract with Elsevier.

 

 

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New methods approved by FDA for treating digestive tract cancers

The drug Lutathera (lutetium Lu 177 dotatate) was approved by US FDA for treating  neuroendocrine tumors that originate in the gastrointestinal tract and pancreas (GEP-NETs). This is an important breakthrough as it is the first radioactive drug to have been approved by the FDA. It is now a novel treatment for GEP-NETs.

Lutathera drug was found to be quite effective in treating adult patients with GEP-NETs. The treatment options for GEP-NETs were limited as it is a rare type of cancer and the conventional therapy was not successful in preventing the proliferation of this cancer. With US FDA approving the drug Lutathera, it is a ray of hope for patients diagnosed with these rare type of cancer.

It also establishes that US FDA is now open to considering data from alternative therapies, which can provide hope to patients with this rare type of cancer. GEP-NETs develop not only in the pancreas but also in different parts of the digestive system, such as stomach, colon, intestine, and rectum.

Statistical data suggests that the diagnosis of GEP-NETs has been low each year. Only one out of 27,000 people develop this cancer in the United States of America. Lutathera is a radiopharmaceutical drug. It exerts its therapeutic activity by clinging to the somatostatin receptor, which is a component of cell and is present in certain types of tumors.

After clinging to  the receptor, the drug gets into the cell and exudes radiation to damage cancerous activity. The drug Lutathera was approved by two research studies: a randomized clinical trial was conducted on 229 patients, who were diagnosed with a certain type of advanced GEP-NET. These patients elicited a positive response to the drug.

In this clinical trial, a combination of Lutathera and octreotide drug was administered to some patients, while the remaining patients only received   octreotide drug. After providing treatment to patients, researchers measured the period of time for which tumors did not show any signs of grow or development. This period was defined as progression-free survival of patients.

Patients who consumed a combination of Lutathera and octreotide drugs had a longer period of progression-free survival as compared to patients who only consumed the drug octreotide. Moreover, the possibility of the growth of tumors or death was lower in patients who received both the drugs: Lutathera and octreotide .

The second research study was performed on 1,214 patients in Netherlands. These patients were diagnosed with tumors showing positive response to somatostatins, including GEP-NETS. The drug Lutathera was administered at a single site in these patients.

In a clinical trial that included 360 patients with GEP-NETs, it was found that tumors  either shrunk completely or partially in about 16 percent of included patients . These patients also received the drug Lutathera initially, and their responses were monitored by the US FDA.

The drug Lutathera has following side-effects: the white blood cells decrease sharply in patients (lymphopenia); the levels of enzymes become high in certain organs (increased GGT, AST and/or ALT); some patients may develop nausea and vomiting; there could be a sudden spike in blood sugar levels (hyperglycemia), and the levels of potassium become low in the blood (hypokalemia).

The drug Lutathera has following serious side-effects: blood cells may decrease sharply in numbers (myelosuppression); certain types of blood or bone marrow cancers may develop in patients(secondary myelodysplastic syndrome and leukemia);  some patients may witness a serious damage to their kidneys (renal toxicity); some patients may suffer from permanent liver damage (hepatotoxicity); the hormonal levels may become abnormal in the human body (neuroendocrine hormonal crises), and infertility.

The drug Lutathera can harm the fetus developing in the womb of a pregnant mother; therefore, pregnant women are educated about the potential damage caused to the fetus by this drug . In general, radiation exposure is provided to patients before administering the drug.

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Guidelines to include feedback of patients in clinical trials

 

The impact of treatment on participants and their quality of life must be assessed more comprehensively, so it is imperative to make changes in international guidelines. The safety of participating patients and integrity of data collected depends on the protocols used for describing a clinical trial: objectives, design, methodology, statistical consideration, and organization.

Current protocols do not emphasize much on patient-reported outcomes (PROs). Most researchers have recommended that feedback must be collected from patients on how clinical trial affects overall quality of life.

According to a noted medical researcher at the University of Birmingham, feedback received from patients participating in a clinical trial can hold valuable information for following purposes: pharmaceutical labeling claims, clinical guidelines, health policy, shared-decision making.

Most clinical trials currently do not include information on quality of life and symptom data. This data must be collected to provide patient-centered care and to develop specific protocol guidelines.

Recommended changes to current protocols of clinical trials were published in the Journal of American Medical Association. This information was a joint-collaboration across universities of Toronto, Sydney, and Birmingham. It is important to understand the impact clinical trials have on cancer patients.

With this information, patients can then decide which line of treatment is most suitable for them. The side-effects of cancer treatments are often long-lasting and most clinical trials do not include this line of information. A cancer patient receiving treatment may live for years but their quality of life is severely impacted with these side-effects.

Patient-related outcomes (PROs) are classified as primary or secondary in clinical trial protocols; these outcomes need to be included in the current checklist guidelines of clinical trial protocol.

The PRO specific issues are as follows: trial rationale, eligibility criteria, objective, intervention, assessment time-points, proxy completion, and strategies for minimizing missing data.

The guidance prescribed in PROs is not prescriptive, but it provides a pathway for implementing a careful planning of PRO components of trials. Thus, PRO trial design improves, and the rationale for assessing PRO is improved. Thus, high quality analysis is ensured and reported, thereby improving the evidence base of PRO on a global scale.

Clinicians can use PROs effectively to make right decisions, thereby improving the line of recovery and treatment. This is a more effective strategy for comprehensively reporting personal experiences of patients with serious illness.

More guidelines must be consistently presented to help both patients and clinicians and to improve the outcome of prognosis. By improving the reporting of PRO data, the outcomes of patients with chronic diseases can be improved tremendously.

 

 

 

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First clinical trial on lung stem cell transplantation in China

A significant breakthrough has been achieved by researchers working at China’s Tongji University. They have managed to develop an innovative technology for regenerating human lungs. In a successful clinical trial, an autologous transplantation of stem cells was carried out in the lungs. The main goal was to regenerate damaged lungs of patients.

This study was reported in the noted scientific journal named “Protein & Cell” . This journal is published by Springer Nature. The team of researchers headed by professor Zuo successfully identified p63+/Krt5+ adult stem cells in the lungs of experimental mice. These stem cells were later regenerated into bronchioles, alveoli, and other pulmonary structures.

Following this successful breakthrough, these researchers from Tongji University are now working together with a team of scientists at the Kiangnan Stem Cell Institute to apply the same discovery to human cells as the earlier clinical trial was successful on mice.

Human lungs are completely different from the lungs of mice, both in terms of anatomy and developmental processes. Therefore, chronic pulmonary disorders can be solved by directly investigating human lungs.

An SOX9+ marker was used to label the category of basal cells, which could be cloned into stem cells of the lung in human beings. Professor Ren Tao is a renowned physician who works at the Shanghai East Hospital.

The main goal was to produce lung stem cells from a small sample of basal cells. For this purpose, lung bronchoscopy was performed by a team of researchers headed by Professor Ren Tao.

Lung stem cells were obtained from about 0.2% of cells isolated from each brush. A scaled expansion was conducted in a well maintained fashion to ensure that the cells were genetically stable and to retain their distinct molecular phenotype.

To determine the ability with which lung stem cells could regenerate tissues of lungs in vivo, the researchers transplanted GFP-labeled, lung stem cells of humans into the damaged lungs of experimental mice.

The team of researchers then waited for three weeks after completing the transplantation. At this stage, a “human-mouse chimeric organ” was formed by integrating lung stem cells of humans into a large area of mice lungs.

By performing histological analysis, the transplanted stem cells were regenerated into structures resembling the bronchioles and alveoli of lungs in mice. Researchers observed a host of rising capillaries in the regenerated components of human lungs.

In other words, the team of researchers successfully regenerated respiratory units that were functional in nature. This was confirmed by gold-nanoparticle tracking. After performing stem cell transplantation successfully, new human alveoli were formed in place of fibrotic section of injured lungs.

Lung function in mice was significantly restored by conducting arterial blood gas test.The first clinical trial was performed successfully by a team of researchers from the following organizations: Southwest Hospital of China Army University and Regend Therapeutics.

An autologous transplantation of lung stem cells was performed on patients diagnosed with bronchiectasis. In this condition, the bronchial structure of the lungs is permanently damaged. Two patients were included in this study in March 2016 following strict supervision by ethical committees.

The generated lung stem cells were transplanted into patients’ lung by performing bronchoscopy. These patients were then monitored for one year continuously. Coughing, dyspnea, and other respiratory issues were alleviated in these patients, one year after transplantation.

The dilated structures showed almost complete recovery as per CT images. After the transplantation, it took three months for the patients to show a significant improvement in lung function. Thereafter, they showed further signs of recovery till one year.

 

 

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New structure of key protein holds clues for better drug design

The scientists working at the Scripps Research Institute (TSRI) have elucidated the molecular structure of  a key protein, which is used extensively in drug design. With this discovery, scientists can now develop to new ways to combat infectious diseases. They have discovered the structure of the protein named A2A adenosine receptor (A2aAR), which is a member of the G-protein-coupled receptor (GPCR) family. Approximately 40 percent of all approved pharmaceutical drugs use this protein as target molecule.

Furthermore, scientists have uncovered the detailed signaling mechanism of the protein A2aAR, helping us understand the inner workings of this proteins. For example, an amino acid of A2aAR acts like a “toggle switch” and controls the signaling processes of the cell membrane. Journal Cell published this path-breaking discovery today. Based on imaging techniques, it can be inferred that shape of proteins changes.

The protein A2aAR and other molecules of the GPCR family are embedded into plasma membrane of human cells. A normal human body contains more than 800 GPCRs and each protein molecule regulates the metabolic functions of the human body. Scientists have reported that the protein A2aAR is associated with the regulation of blood flow and inflammation. The harmful effects of caffeine are also alleviated by the protein A2aAR. For treating Parkinson’s disease, A2aAR is a relatively new target. Moreover, the protein A2aAR is reported to be a relatively new target in the treatment of cancer.

In recent years, X-ray crystallography has been used to determine the three-dimensional structure of A2aAR protein in previous studies. The X-ray images show that A2aAR protein resembles a chain, and it crisscrosses the cell membrane. An opening is present on the side that faces out of the cell. For signaling associate proteins inside the cell, a section of the GPCR structure emerges out of the membrane and gets associated with drugs.

During inactive and active-like states, an outline of the receptor’s shape was provided by the crystal structure. When A2aAR was combined with new candidate compounds of the pharmaceutical industry, they acted as binding partners; however, no motion and changes in cell structure was observed.

In this study, researchers realized that they need to establish the molecular mechanism through which A2aAR works in combating diseases. Nuclear magnetic resonance (NMR) spectroscopy was used by researchers for investigation. In this process, strong magnetic fields were used to probe the samples.

By using NMR technique, the structure of proteins was determined by scientists. Scientists also investigated the dynamic properties of the solutions at temperatures prevalent in the human body. The team of researchers visualized the internal structural changes in the A2aAR proteins.

In this study, researchers investigated the effects of binding drugs with extracellular surface. Changes were observed in the structure of proteins and in the dynamics of the protein surface at an intracellular level. Thus, scientists discovered the mechanism of signal transfer through intracellular pathways. Chemists modified drugs and manipulated the switch to control A2aAR signals.

 

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Researchers develop a remote-controlled cancer immunotherapy system

An innovative ultrasound system has been developed to control genetic processes in live T cells of the immune system. This team of researchers can destroy cancer cells. By developing non-invasive immunotherapeutic strategies, cancer cells can be manipulated and destroyed.

An innovative approach was used to improve practical applications of mechanogenetics: a field of science that improves the expression of genetics and activity of cells. T cells were mechanically destroyed by ultrasound. To genetically control cells, mechanical signals were used.

In this study, it was found that mechanogenetics system could be remote controlled and T cells can be manipulated by chimeric antigen receptor (CAR). Cancer cells can be targeted and killed with this innovative approach.

Researchers have engineered CAR-T cells with mechano-sensors, genetically transducing modules. This innovative approach was termed as CAR-T cell therapy, which provided a paradigm shift for the treatment of cancer.

Life-threatening complications develop when CAR-T cells are non-specifically targeted. Precision and accuracy of CAR-T cell immunotherapy was improved in an unprecedented manner. This innovative immunotherapy was used to target solid tumors. At the same time, off-tumor activities were minimized.

Microbubbles were conjugated to streptavidin and they were attached to cell surface. Mechanical vibration and stimulation of Piezo1 ion channels was performed by microbubbles when they were exposed to ultrasound waves. This led to the entry of calcium ions into the cell, triggering the following downstream pathways: calcineurin activation, NFAT dephoshorylation and translocation into the nucleus.

With recognition and destruction of targeted cancer cells, chimeric antigen receptor (CAR) was used to initiate the expression of genes.

 

 

 

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Possible Cure for Drug-resistant malaria: toothpaste ingredient

Researchers at the University of Cambridge have an innovative cure for drug-resistant malaria. This ingredient is commonly found in toothpastes.

A mosquito is the key carrier of malarial pathogens. Whenever such a mosquito bites a human being, these parasites are transferred into bloodstream of humans. Such parasites move through the liver for colonization and proliferation.

After proliferation and colonization in the liver, they attack red blood cells and multiply continuously. This further leads to potentially threatening illnesses.

In Africa and south-east Asia, more than a million people are affected by malaria. Although numerous medicines are commercially available in the market, it has been found that malarial parasites are mutating in recent times.

According to a recent study in the journal “Scientific Reports,” a team of researchers discovered that triclosan is the active ingredient that can fight “drug-resistant bacteria.” Triclosan obstructs the development of plaque bacteria with the help of the enzyme enoyl reductase (ENR). This enzyme was used for producing fatty acids.

To investigate therapeutic efficiency of triclosan, scientists attacked the culture of pathogens. They found that triclosan could target ENR, which is a virulent strain of pathogenic bacteria in the liver.

Triclosan suppresses the growth of parasites by completely inhibiting an enzyme, named DHFR. An anti-malarial drug named pyrimethamine targets DHFR; however, this target is also resisted by malarial parasites in Africa. Interestingly, triclosan could target even these parasites resistant to pyrimethamine.

In Africa and south-east Asia, a growing concern is the proliferation of drug-resistant malaria. The expression of ENR and DHFR was inhibited by triclosan. Triclosan is found to be effective on the parasite both in the liver and bloodstream. Thus, there is hope of a new drug against drug-resistant parasites.

This experimental research study was conducted in conjunction with robot scientist “Eve” in order to accelerate drug discovery process. With the help of artificial intelligence and machine learning, an innovative approach can be established for inventing new drugs.

 

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Innovative colitis treatment through precision editing of gut bacteria

Medical researchers at Southwestern Medical Center, Utah, performed precision editing on the bacterial colonies found in the gastrointestinal tract. This reduced the inflammation’s severity and colitis caused in experimental mice.

The primary strategy was to target cellular pathways associated with metabolic activities, which are associated with gastrointestinal inflammation. The main object was to prevent or reduce the inflammation caused in mice with colitis. At the same time, the control animals showed no signs of inflammation; the bacterial colonies in the gut were balanced and healthy.

This path-breaking discovery was published in latest issue of Nature magazine. A framework was developed from our results, and the bacterial species that line the gastrointestinal tract were precisely altered to reduce the inflammation caused by colitis and other forms of inflammatory bowel disease [IBD].

In this experimental study, we used a heavy metal called tungsten, which is dangerous when ingested in high doses. It should be noted that no heavy metal is safe for consumption. Our primary goal was to develop a novel therapy that induces a similar effect but within the acceptable limits of safety.

There is a diverse population of microbes, which form a thin line on the gastrointestinal tract. These microbes are essential for the maintenance of good health. They help in digestion, improve the immune system, and effectively combat all kinds of infections.

When there is an imbalance in microbial populations, these beneficial bacteria become a nuisance as they develop invasive qualities and drive out species that compete with them for space. It is difficult to understand the biology of gut microbiota because they are  highly diverse in nature.

In humans, several bacterial species are found in the gastrointestinal tract. The composition of species differs extensively for individuals. The composition of gut microbiota changes considerably, causing many chronically progressive diseases, such IBD, ulcerative colitis, and Crohn’s disease.

According to Centers for Disease Control and Prevention, at least 1 million adults are affected by IBD in the United States of America . Currently, there is no cure for such diseases. The gut microbiota also undergoes changes in patients with Type 2 diabetes, HIV-related intestinal disease, colon cancer, and necrotizing enterocolitis. These diseases are also observed in certain premature infants.

The bacteria found in the microbiota of the gastrointestinal tract belonged to enterobacteriaceae family, causing many inflammatory diseases.  In healthy gut, a small number of healthy bacteria are present. They belong to E.coli (Escherichia coli). These bacteria also protect pathogenic bacteria, such as Salmonella, which is responsible for food poisoning in humans. In mouse afflicted with colitis, there is an uncontrolled growth of enterobacteriaceae species.

In a paper published by Cell Host & Microbe, it was reported that cellular energy was produced by Enterobacteriaceae family. Gut bacteria uses this energy for improving growth and obtaining nutrients. Unique metabolic pathways were used to improve the growth and drive out beneficial bacteria at the time of illness.

These unique pathways are used to improve inflammation in gut. In current study, tungsten was used to inhibit the pathways obstructing metabolism. An inflammation develops due to incessant growth of pathogenic bacteria.

These researchers have reported that bacteria absorbed tungsten, and they developed an important cofactor of bacteria. Due to the inflammation, enterobacteriaceae lost its capacity to generate energy.

A soluble salt of tungsten was orally administered to patients. The useful bacteria were not affected in this innovative experiment. This is because a particular the cofactor could not govern the metabolism of beneficial bacteria.

The proliferation of enterobacteriaceae was stopped in our current experiment. When enterobacteriaceae  species were present in correct ratios, colonization would be resisted by bacterial pathogens.

By controlling the proliferation of bacteria, inflammatory episodes were prevented completely. With miniscule experimental evidence, it can be postulated that diseases of the gut worsen due to changes in the composition of microbiota.

In this study, it was found that the inflammation of the gut was reduced and a normal state was achieved by using tungsten treatment. In most experiments, tungsten was used to rectify a molecular target. This treatment was therapeutic for patients. At the same time, tungsten is the heavy metal that provokes neurological and reproductive diseases.

Conventional approaches are focused on treating bacterial pathogens. However, this path-breaking research is quite useful to harness bacteria in the normal gut. The composition and the function of gut microbiota was controlled.

Most doctors prescribe broad spectrum antibiotics. The final objective is to tarnish numerous bacteria in the gut. Whenever a patient visits the clinic in a critical state, most doctors prescribe antibiotics and do not conduct tests to identify the specific pathogens in the human body. In such a scenario,  the prescribed antibiotics have broad-spectrum activity, killing most pathogens and beneficial bacteria.

Only one family of bacteria, enterobacteriaceae, was targeted in our study. Although results are promising, more studies must be conducted to identify potential therapies that cause human diseases.

 

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How Accessible Publishing has Revolutionized Academic Publishing

The world of scientific publishing has undergone a metamorphosis in recent times. The key ingredients here are “authentication” and “piracy” in scholarly communications. Many people have come up with “inclusiveness of scholarly communications,” for disabled people. There seems to be a lacuna in the world of scientific publications, given the “professional” and “educational” spheres of education. In a highly connected world, knowledge must be disseminated through “journals,” “books,” and “databases.”

At one end, most academicians are of the view that

knowledge must grow with highly authoritative communications being accessible to readers. At the other end, publishers argue about “copyright infringement” with new challenges towards tackling piracy and digital infringement. Accessibility is still an issue for scholarly communications.

According to the National Institute of Health, there are more than 285 million people with some form of physical, cognitive, and educational challenge in the USA. Nevertheless, the enrollment of disabled masses is just 10–20% across colleges in the USA. People with disabilities are a sizeable population if we take into consideration that they can be perennial customers of scholarly communications.

“Accessibility” is still an issue here for most publishers. Publishers are concerned about “return on investment” while catering to such people. Accessible publishing is not really avenue for making great revenues. However, people with disabilities are now being considered for inclusiveness and diversity. They are provided with “navigable, feature-rich content” through various innovative publishers: DAISY and ReadSpeaker.

Accessible publishing is far superior given the fact that it can improve the “quality” and “interoperability” of metadata. With proliferation of machine learning and search engine optimization (SEO), general discoverability of such innovative publications is improved significantly. Publishers and technological evangelists provide deciphering workflow with maximum accessibility to all stages of publications, right from manuscript selection, improvement, and publications. Right from increasing submissions to improving usage, measurable benefits can be availed through “accessible publishing.”

Accessible publishing is much easier today thanks to developments in technology although it does require some efforts out here. Technologies such as HTML, EPUB, etc., would be leveraged to provide the best practices in accessible publishing. Industry-standard workflow formats of publishing are now accessible to all readers. The mission of academic publishing would be to disseminate knowledge through “accessible publishing.” They can envision the horizon of many accessible publishers.

 

 

 

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In Mice with Alzheimer’s, memory loss is reversed with diabetic drug

According to a recently published paper in Brain Research, a diabetic drug could be used to reverse memory loss in mice with Alzheimer’s disease. This study was conducted at Lancaster University in the UK. Professor Christian Holscher was the lead researcher of this study. This is a promising line of treatment for Alzheimer’s disease, a common neurodegenerative disorder. The drug was conventionally used to treat patients with type 2 diabetes.

Memory loss and dementia are the most common signs of Alzheimer’s disease. According to Alzheimer’s Society, more than two million people would suffer from Alzheimer’s disease by 2051. This research study was partially funded by Alzheimer’s Society. It is alarming rate of increase and there has been no new treatment for Alzheimer’s disease in recent times.

Since the past 15 years, physicians have been prescribing the same medications for patients with Alzheimer’s disease. According to Dr Doug Brown at the Alzheimer’s Society, new drugs must be urgently developed to tackle the growing number of patients with Alzheimer’s disease. Patients with Alzheimer’s disease cannot lead normal lives as dementia progresses quickly, limiting their cognitive skills and memory.

Diabetic drug liraglutide was tested on mice with Alzheimer’s disease; however, its efficacy must be further tested on human patients with Alzheimer’s disease. Randomized clinical trial need to be carried out with this objective. “Triple agonist drugs” have also shown promising results on mice with Alzheimer’s disease. Nevertheless, much needs to be done in the area of research and development.

Liraglutide is a “triple receptor drug” that has been tested for the first time. Researchers found that this drug could offer protection against degeneration of brain cells. Growth factors GLP-1, GIP, and Glucagon are combined in the formulation of the diabetic drug liraglutide. Previous studies have reported that growth signaling factors get impaired in the brain of patients with Alzheimer’s disease.

In this research study, scientists used transgenic mice APP/PSI. In these mice, they observed the expression of mutated genes, which cause Alzheimer’s disease. The same genes also undergo mutation in humans with Alzheimer’s disease. This form of Alzheimer’s is inherited through genetic mutation.

Researchers found that even in the advanced stage of neurodegeneration, memory loss could be significantly reversed in transgenic mice. By administering liraglutide drug to these aged mice, they could not improve memory but also cognitive ability. By performing maze test, they found that growth factors were enhanced in the brain of aged transgenic mice.

These growth factors in the brain would ensure normally functioning of nerve cells, preventing them from undergoing degeneration. Moreover, the drug decreased the formation of amyloid plaques in the brain of patients with Alzheimer’s disease. Furthermore, oxidative stress and chronic inflammation were reduced with the administration of this drug. Finally, the rate of nerve cell loss decreased following the action of this drug.

According to Professor Holscher, clinical trials have been successfully conducted with an older version of this drug. The promising results suggested that this drug was suitable for treating patients with Alzheimer’s disease. Although this drug was originally developed to manage type 2 diabetes, many studies have reported about its neuro-protective effects.

Our study is unique in the fact that a novel triple drug shows promising results when used as a line of treatment for Alzheimer’s disease. However, further clinical trials must be conducted in a dose-dependent manner on humans, and its efficacy must be compared with existing drugs to know whether if the novel drug is superior to existing ones.

The risk of Alzheimer’s disease is high in patients with type 2 diabetes. Quite often, Alzheimer’s disease develops with the progression of type 2 diabetes. Owing to impaired insulin levels, cerebral degeneration occurs in patients with type 2 diabetes. This leads to the development of Alzheimer’s disease.

In the brain of patients with Alzheimer’s disease, scientists have found that there is no sensitivity to insulin. They believe that neurodegenerative disorders occur due to insulin desensistization in the brain. This is because insulin exhibits neuroprotective effects as it is a growth factor in human brain.