Champagne and Cognitive Health

A new study reveals that drinking champagne, anywhere from 1 to 3 glasses per week, could benefit your memory and postpone the onset of dementia, Parkinson’s, Alzheimer’s and other degenerative brain disorders. The study was recently published in the journal Antioxidants and Redox Signalling.

The research team, consisting of scientists from the University of Reading, in the United Kingdom, discovered that the phenolic compounds that are found in champagne are responsible for improving spatial memory. This is the type of memory involved in the gathering of information related to the environment. According to the research team, these phenolic compounds modulate signals from the cortex and hippocampus, the areas of the brain related to learning and memorizing. The compounds were also found to adjust the effect of several proteins that are directly connected to the memorizing process. Previous studies have shown that the levels of these particular proteins drop with aging, thus causing the memorizing process to be less effective. This, in turn, leads to the worsening of one’s memory and is considered to be one of the causes for the onset of dementia. Their study reveals that the phenolic compounds found in champagne can slow down the loss of these proteins, thus also slowing down the aging process of the brain.

When compared to other products that contain phenolic compounds, such as white wine, champagne has the highest levels. Champagne is predominantly derived from Pinot noir and Pinot Meunier, which are types of red grapes, and Chardonnay, a type of white grapes. The phenolic compounds found in these particular types of grapes are considered to be the one that have the most beneficial effects on the brain. One of the authors of the study, professor Jeremy Spencer, notes that “These exciting results illustrate for the first time that the moderate consumption of champagne has the potential to influence cognitive functioning, such as memory. Several precedent studies have shown that flavonoids, the compounds found in red wine, also have beneficial effects on the human organism, if consumed moderately.

The current study shows that even though champagne doesn’t contain flavonoids, its effect on the brain function and brain aging process is still present, being achieved by the phenolic acids. Professor Spencer advocates on a moderate consumption of alcohol, due to the fact that their study results show that even small quantities of champagne per week can be effective. The main author of the study, David Vauzour, adds that their future studies will focus on the transition of these studies to human models. Currently, the effect has been achieved through intake of other foods rich in polyphenol, such as cocoa and blueberries. Precedent studies that were conducted by research teams from the University of Reading showed that 2 glasses of champagne per day have favorable effects on both the heart and circulation and could be responsible for lowering the risk of cardiac arrest and other cardiovascular disorders.

New Type 2 Diabetes Therapy Possibilities

A research team from the HSPH (Harvard School of Public Health) reveals a hormone that controls the regulation of glucose and the way the liver metabolizes it. Through the use of an experimental new technology, the researchers discovered that if this hormone is switched off, a better control over the production of glucose in the liver can be achieved. Their discovery, published in the journal Cell Metabolism on the 7th of May, could lead to new future type 2 diabetes treatments.

The senior author of the study, professor Gökhan Hotamisligil, says that until now the mechanism underlying the liver glucose production has been puzzling researchers. “We now have identified aP2 as a novel hormone released from fat cells that controls this critical function”, added Hotamisligil. Researchers suggest that the link between the liver and the adipose tissue could have developed in order to aid the organism in case of severe nutrient deprivation. On the other hand, in obese patients, these fat cells appear to lose their capability of controlling the connection with the liver, thus increasing the amount of aP2, causing the liver to increase its production of glucose. The result of this process is the rise of blood glucose, which in time leads to the onset of type 2 diabetes.

Diabetes

More than 26 million United States citizens are currently affected by type 2 diabetes and other metabolic diseases. These disorders are closely linked to a higher risk of stroke, heart disease and several other health complications. Diabetes is most often linked to insulin resistance and obesity, the majority of type 2 diabetes cases being related to the failure of insulin action. Even so, scientists around the world have noticed that not all of the obese patients suffer from type 2 diabetes and that type 2 diabetes does not occur in all of the patients who are resistant to insulin. On the contrary, the majority of patients who suffer from severe obesity are not diabetic.

“It was surprising to find that a critical hormone playing a pathological role in diabetes turned out to be the secreted form of aP2”, said professor Hotamisligil, whilst adding that the researcher community has known that aP2 is a hormone that resides in the human fat cells. The research team from Harvard raised the levels of the aP2 hormone from normal laboratory mouse models in order to match the high levels of aP2 in obese human patients. The result was the inhibition of the glucose metabolism. Furthermore, researchers lowered the levels of aP2 levels in mouse models suffering from obesity and diabetes, to the normal levels seen in healthy mice. Their second experiment led to the normalization of the glucose metabolism.

Consequent to their discovery, the research team concluded that the levels of the aP2 hormone is directly linked to diabetes, thus being a potential new target for future type 2 diabetes therapies. Researchers also added that they have found a possible therapeutic role for an antibody that would neutralize the effect of aP2. The lead author of the study, fellow Haiming Cao, concludes that their discovery is important due to the fact that it reveals new possibilities in diabetes therapies and increases the capabilities of physicians towards diabetes treatment.

Epilepsy Cure

A research team from the UCSF (University of California, San Francisco), in the United States, has revealed a new method to control the seizures of mouse models with epilepsy. Their study was recently published in the journal Nature Neuroscience. The method consists of a one-time implantation of MGE (medial ganglionic eminence) cells, responsible for the signal inhibition of the overactive nervous system. During precedent studies, researchers used several different types of cells but failed to stop the seizures.

Due to the limitations of current epilepsy medication, cell therapy became one of the most active fields of research. The leader of the study, professor Scott Baraban, affirms that current medication is only effective against the symptoms of the disease, and doesn’t address the causes. In addition, Baraban said that for most types of epilepsy, the currently available drugs have little to no therapeutic effect, whilst adding that “Our results are an encouraging step toward using inhibitory neurons for cell transplantation in adults with severe forms of epilepsy”. The findings of the current study are the first to report the stopping of seizures in mouse models with epilepsy.

Epilepsy

The extreme muscle twitches and contractions that appear during seizures are responsible for the loss of control for some patients, thus causing them to fall and injure themselves. The abnormality responsible for these symptoms are considered to be the overactive nervous cells that react at the same time. The research team from UCSF transplanted cells which are capable of inhibiting these overactive nervous cells, thus reducing the total number of seizures in half of the mouse models and totally eliminating the seizures in the other half of the studied mice. Most of the key experiments were conducted by postdoctoral fellow Robert Hunt, who reported that  prior to their current study, the research team discovered a method capable of producing human MGE-like cells in laboratory conditions.

Previous studies have shown that in most forms of epilepsy, the loss of inhibitory nerve cells within the hippocampus plays a key role in the evolution of the disease. The medial ganglionic eminence cells are precursor cells which are able to generate interneurons. These are mature nerve cells with inhibitory capacity. Researchers discovered that these transplanted cells integrate into the already existing nervous circuits.

The mouse model used by the researchers resembles a sever form of human epilepsy which is resistant to drugs, called mesial temporal lobe epilepsy. This particular form of epilepsy is believed to have its roots in the hippocampus. Researchers also tried to implant these cells into the amygdala, a region of the brain responsible for emotions and memories, however, this showed no results. The form of epilepsy studied in the current paper usually appears in adolescence, sometimes after a long period of time from the first seizure, which is most often caused by high fever. In mice, this was achieved through chemical exposure and is very similar to the human form. The main author of the study also notes that the mouse models which were treated with the aforementioned technique revealed less hyperactivity and less abnormal agitation, in addition to the fewer seizures.

Whole Genome Sequencing Reveals Insight into Pneumococcal Disease Causes

A new study published by a research team from the HSPH (Harvard School of Public Health), in the United States, in collaboration with WTSI (Wellcome Trust Sanger Institute), in the United Kingdom, reveals the first genome sequencing technology capable of tracking the various changes that occur in the bacterial population after a vaccine injection. The research team followed changes that occur in the pneumococcal bacteria family after the injection of a vaccine called “Prevnar”. The vaccine is currently related to a substantial reduction in pneumococcal diseases across the United States. The current study shows that this genome sequencing technology can be used to monitor the effects of various vaccines against different populations of bacteria, thus evaluating their effectiveness. The study was published yesterday, the 5th of May, in the online journal Nature Genetics.

Streptococcus Pneumoniae

“This gives an unprecedented insight into the bacteria living and transmitting among us”, noted the co-author of the study, associate professor William Hanage. He added that the technology allowed them to thoroughly investigate the bacteria populations, helping them understand the mechanisms that allow these bacteria to survive and continue to proliferate even when the compounds of a vaccine are present. The cause of pneumococcal disease is known as Streptococcus pneumoniae, a bacteria present in the superior respiratory system (throat & nose) of most people. The main pathways of transmission between infected patients include sneezing and coughing. Penumococal disease can lead to meningitis, pneumonia and several other respiratory illnesses, however, the pathogenesis of the disease isn’t yet completely understood.

The research team, led by associate professor Hanage, professor Lipsitch, from HSPH, and senior scientist Stephen Bentley, from WTSI, was aiming to understand the response of bacteria to vaccination. The technology used by researchers, called whole genome sequencing, can reveal the entire DNA coding of each bacterial strain. For the study, more than 616 samples of pneumococci were used. According to the researchers, the vaccine is responsible for the destruction of different parts of the bacteria, however, those parts are replaced by pre-existing bacteria types. This translates into a new family of bacteria, very similar to the original family, with only a few genes being affected by the vaccine.

Researchers affirm that these genetic modifications suffered by the bacterial DNA are responsible for the decreasing rates of the disease occurrence. “The widespread use of whole genome sequencing will allow better surveillance of bacterial populations and improve understanding of their evolution”, said professor Lipsitch. He also noted that during the study, the research team managed to identify the genes that are associated to the bacteria found in children at different ages. Stephen Bentley concludes that in the near future, researchers will be able to monitor the evolution of bacterial DNA in real-time.

 Higher Levels and Glutamate to Schizophrenia

According to a new study published in the April issue of the journal Neuron, a team of researchers from the CUMC (Columbia University Medical Center), in the United States, has discovered that higher levels of glutamate could be responsible for the onset of schizophrenia in predisposed patients. Glutamate is a neurotransmitter that plays a key role in the long-term increase in the strength of nerve impulses through previously used pathways. Glutamate also plays a part in the memory and learning processes.

The findings of the researchers include a treatment strategy that could possibly slow down or even prevent the progression of schizophrenia and other psychotic disorders related to schizophrenia, and a possible diagnostic tool that would identify the patients who are at risk for schizophrenia. The senior author of the study, neurology professor Scot Small, reports that “Previous studies of schizophrenia have shown that hypermetabolism and atrophy of the hippocampus are among the most prominent changes in the patient’s brain”. Small also notes that his most recent study reveals that the aforementioned changes occur in the early stages of the disease, thus making an early diagnostic possible.

Schizophrenia

In order to locate the process, the research team from Columbia University used neuroimaging techniques in mouse models and human patients. Their first study involved a group of 25 patients who were at risk for the onset of schizophrenia. The research team studied their brains and the changes that occurred during the onset and development of the disease. A pattern was discovered in patients whose condition progressed towards schizophrenia: the activity of the glutamate neurotransmitter increased in the hippocampus first; Secondly, the metabolism of the hippocampus increased; thirdly the hippocampus atrophied.

Researchers used laboratory mouse models with schizophrenia in order to see if the increased levels of glutamate had other effects on the hippocampus as well. However, they discovered that the increase of glutamate had the same effect as it had on humans. Firstly the hippocampus became hypermetabolic and lastly, it began to atrophy.

In theory, the abnormal levels of the neurotransmitter and the hypermatabolism of the hippocampus can be seen through neuroimaging, thus being able to detect the early stages of schizophrenia. Treatment for patients with a high risk of schizophrenia onset could include the control of glutamate release. The president of the American Psychiatric Association, professor Jeffrey Lieberman, says that there have been treatment schemes for schizophrenia that were based on the reduction of glutamate levels, however, those schemes were only used on patients with a later stage of the disease, rather than an early stage. Professor Bita Moghaddam, from the University of Pittsburgh, affirms that if glutamate is responsible for the onset of schizophrenia, it could also explain why the psychotic episodes caused by the disease appear after periods of stress, due to the fact that glutamate levels increase during stress.

New kidney cancer subtypes

Researchers at the Institute of Urologic Oncology and the Department of Urology at UCLA have discovered a new subtype of clear cell renal cancer. This discovery is a step forward in the development of personalized treatments designed according to the patient. Renal cancer represents about 3% of cancers in adults, and of the types of kidney cancer, renal cell carcinoma is the most common (it means about 80%). Nobody knows exactly what are the causes of kidney cancer but there have been put into question several risk factors such as smoking, obesity, hypertension, occupational exposure to various chemicals etc. It should be noted that there are several types of renal cell carcinoma,  but the most common subtype is clear cell renal carcinoma.

Renal Cancer

Renal tumors generally produce hematuria, that is blood in the urine, or back pain; sometimes the first signs are those due to complications. Besides the classic signs and symptoms ( pain, hematuria, tumor ) there can occur several paraneoplastic syndromes related to hematological, endocrine, cardiovascular system, liver, etc.. Therefore renal cancer patients may have prolonged fever, which does not respond to antibiotic treatment, or various haematological disorders (anemia), hypercalcemia, hypertension, Cushing’s syndrome, etc..

The new subtype of kidney cancer is the result of 10 years of study and experiments on the type of genetic mutations that cause these cancers. Dr. Allan Pantuck, a professor of urology and director of genitourinary oncology at UCLA’s Jonsson Comprehensive Cancer Center, said that there were evaluated thousands of renal cancers operated at UCLA. Generally the final diagnosis is made by pathologists who study biopsies samples under microscope. They also determine the stage of a tumor and the prognosis. But sometimes tumors that are similar under the microscop behave differently and have different prognosis. It is essential to establish the prognosis of a tumor in order to decide the type of treatment (for example, high-risk tumors require more aggressive treatment).

Researchers found that in clear cell renal cancer there were deletions in the short arm of chromosome 3 (3p) and the long arm of chromosome 14 (14q). Short arm of chromosome 3 contains a tumor suppressor gene while  the long arm of chromosome 14 contains a gene involved in hypoxia (HIF1 alpha genes). It was found that the loss of chromosome 3p is associated with a better prognosis, which has implications regarding the choice of treatment. Patients with such mutations do not require aggressive treatment. But patients that have mutations in both chromosome 3 and chromosome 14 have a much worse prognosis.

New technique to cancel out Parkinson tremors

Researchers at Oxford’s John Radcliffe Hospital have developed a new therapy that improves symptoms of Parkinson’s disease. Parkinson tremors may be cancelled out using a technique called transcranial alternating current stimulation  or TACS. Although it is present in only about 30% of patients, tremor in Parkinson’s disease is one of the major symptoms and it is one of the factors that affect quality of life significantly. Parkinson tremor is different from that which occurs in lesions of the cerebellum (that is intentional tremor), as it is a resting tremor that is emphasised during emotions,  diminishes during voluntary movements and disappears during sleep.

The discovery of a new technique to improve Parkinson tremor in patients is a significant advance in treating this debilitating disease because tremor is one of the symptoms that does not respond so well to medication. It should be noted however that deep brain stimulation can help control these symptoms, but it is an invasive procedure that involves placing an electrode deep in the brain through which electrical impulses are delivered. It should be noted that deep brain stimulation is applied only to certain patients according to age, health status, mental status, etc.. In addition, deep brain stimulation is a costly procedure that involves several risks and may lead to serious side effects such as bleeding, various neurological deficits, etc..

Parkinson Tremors

The new technique developed by researchers at Oxford’s John Radcliffe Hospital, unlike deep brain stimulation, does not involve so many risks as it consists of placing electrode pads outside the patient’s head. Transcranial alternating current stimulation, or TACS, refers to placing two electrodes, one on the neck and one on the head of the patient, near the motor cortex. Motor cortex is a brain region with a role in controlling voluntary movements. Through these electrodes is sent alternating current stimulation in order to suppress Parkinson tremor. It was found that half the patients had a  reduction in resting tremors using this technique.

Although it is a preliminary study conducted on a sample of 15 patients with Parkinson’s disease, Professor Peter Brown of the Nuffield Department of Clinical Neurosciences, who led the study, says they are optimistic about this research and that they hope this will lead to a successful therapy without medical risks. He also said that in the future may be necessary that the electrodes to be placed under the skin, but it will still remain a minimally invasive procedure.

New Study Breaks Down Link Between Dairy Intake and Bone Health

A new study led by scientists from the IFAR (Institute for Aging Research) reveals that different dairy products have different beneficial effects on bone strength across the body. The research team found out that cream is associated to a lower overall BDM (bone mineral density) while milk and yogurt are associated with a nigher BDM, although only in the hip, without a major impact on the BDM of the spine. The Institute for Aging Research is an affiliate of the Harvard Medical School and has recently published its paper in the journal Archives of Osteoporosis.

Lead author of the study, Shivani Sahni, a member of the IFAR Musculoskeletal Research Team, says that all dairy foods are responsible for providing important nutrients for the health of bones. She adds that cream and products made from cream, such as ice cream, have a lower nutrient level than other dairy products and contain higher levels of sugars and fat. The current study reveals the fact that a daily intake of 2-3 servings of milk and yogurt is linked to an improved bone density. However, scientists say that further research is needed in order to observe whether cheese intake has a beneficial effect on bone density and to see whether the intake of individual dairy foods has an important beneficial effect on bone health and fractures.

Dairy products

More than 3,200 patients were included in the study. Researchers gathered data through a food frequency questionnaire. All patients are also part of the Framingham Offspring study. The data gathered from the patients regarding their daily dairy intake was then compared with their BDM measurement. The comparison shows that milk and yogurt have higher beneficial effects than cream, especially in adult patients. The study also reveals that the nutrient levels differ greatly between different dairy products. For example, the intake of low-fat milk or yogurt is related to higher levels of proteins, vitamin D and calcium, whilst being related to a lower level of saturated fats.

The link between food intake and bone health has only recently become a focus of scientific studies. Precedent studies in this domain reveal that each dairy product contains more than one nutrient that is beneficial to bone health, thus having researchers suggest that some dairy products have a higher beneficial effect on bone health.

The current paper, along with other previous studies in the same domain suggest that a healthy nutrition is able to prevent osteoporosis or even fractures. Osteoporosis is known to be a major health problem in the United States, affecting more than 50% of people aged 50 or above.

Newly approved oral drug is effective in patients with rheumatoid arthritis

The U.S. Food and Drug Administration (FDA) approved a new drug for treating moderate to severe rheumatoid arthritis. The new drug, tofacitinib, which is an oral JAK inhibitor, has been tested in several clinical trials and has been shown to slow the progression of disease in patients who are non-responsive to metrotextat.
The study further confirms previous studies which indicated that tofacitinib is effective in treating symptoms of rheumatoid arthritis. “Our findings provide the first evidence that tofacitinib reduces the progression of structural damage in RA patients with active disease,” said lead investigator Dr. Désirée van der Heijde from Leiden University Medical Center in The Netherlands.

Doctor Consult

Rheumatoid arthritis is a systemic autoimmune disease that mainly affects the joints, but it can affect other organs such as the lungs, heart, kidneys, skin, etc.. The disease usually occurs in adulthood, generally in the range of 40-50 years and affects more women than men. Although it is not known by what mechanism or what causes this illness, it is supposed that it is due to the activation of autoantibodies against the synovium, which is part of the joint. This immune attack against joint structures determines several symptoms such as inflammation, pain, stiffness. Rheumatoid arthritis mainly affects the small joints of the hand, in a symmetrical manner, and leads to specific deformity (ulnar deviation of the hand). Over time, patients begin to have difficulty in  movement, which may go up to stiffness and ankylosis , which seriously affects quality of life.

Rheumatoid arthritis, like many other autoimmune diseases, is treated with immunosuppressive, anti-inflammatory, biological agents, etc.. The problem is that not all patients respond to treatment, so researchers wanted to find other types of drugs to help patients with rheumatoid arthritis. Dr. van der Heijde said that the new drug, tofacitinib, works by inhibiting certain enzymes (Janus kinase – JAK- enzymes)  found in white blood cells and involved in immunity. She said that oral JAK inhibitor tofacitinib is a part of anti-inflammatory disease-modifying drugs (DMARD), that is drugs that regulate the immune system in rheumatoid arthritis.

The study was a phase 3 clinical trial and included 797 patients who were divided into 4 groups to receive either tofacitinib in different doses or placebo. It was demonstrated that patients who received tofacitinib (5 and 10 mg) displayed less disease progression and a joint space narrowing compared with patients receiving placebo. The effect of this drug has been also demonstrated by radiological investigations as there were more patients receiving tofacitinib than those receiving placebo with no radiographic progression of the disease.

Silent stroke may be one of the causes of Parkinson’s disease

In a study published in the journal “Brain Behavior and Immunity”, researchers at The University of Manchester showed for the first time why a seemingly healthy patient may develop Parkinson’s disease. According to new findings, a silent stroke may contribute to the occurrence of this debilitating disease. This explains why some patients with similar health problems in the past begin to have tremors and other neurological symptoms, while others  develop Parkinson’s disease without having major health problems in the past.

A stroke is a medical emergency that usually occurs when a blood vessel in the brain is obstructed. Stroke can result in strong headache, blurred vision, intense weakness, fatigue, malaise. There are also other symptoms that occur due to  brain damage, such as paralysis, blindness, etc.. Common causes of stroke are high blood pressure and atherosclerosis, cardiovascular disease being one of the main risk factors for stroke.

Parkinson’s disease

There are situations when the stroke is silent, that is it occurs without the patient realizing that he went through such a condition. So it happens when ischemia that is causing stroke is transient, in other words the blood vessel is blocked for a short time. However, even silent stroke may have long-term consequences. One of them is the death of dopaminergic neurons in the substantia nigra in the brain. Substantia nigra is a brain region with an important role in coordinating movement.

Dr. Emmanuel Pinteaux, who led the research, said they did not know at basaline why dopaminergic neurons die and why Parkinson’s disease develops. Several theories have been launched in this regard: oxidative stress and aging seem to be responsible for the disease. Therefore, researchers wanted to see which are the immediate consequences of silent stroke and if these changes have anything to do with Parkinson’s disease.

Results of experiments on laboratory animals were those expected by researchers. After they induced a mild stroke in the striatum area, a specific region of the brain, in mice, the researchers found that, besides affecting that specific area, the stroke also damaged  the substantia nigra. It was observed that the striatum area suffered a significant reduction of substance P along with a process of inflammation. In addition, 6 days later, the researchers noted an important process of neurodegeneration in the substantia nigra, that is death of dopaminergic neurons.

Dr Pinteaux said that the study points out the importance of maintaining a healthy lifestyle, which includes a healthy eating along with physical activity, so as to reduce the risk of stroke and possibly Parkinson’s disease.