Tips for boosting brain health

Whether you're young or old, it's important to ensure you have a healthy brain. From helping you to enjoy an improved lifestyle to allowing you to concentrate at work, I think looking after your brain is just as important as maintaining your body.

When your brain and overall health is not at its best, it can lead to a number of consequences. Some of these include fatigue, a lack of concentration, depression and having little or no energy. There are a number of ways you can boost your brain health, though, and I've outlined some of my top tips for doing so below.

The first is ensuring you enjoy a healthy diet. People can all too often make the mistake of thinking that if your body appears in a good condition on the outside, everything must be fine on the inside. However, if you're not taking in vital nutrients and vitamins, your brain cannot work at its full capacity.

We all know we should eat at least five portions of fruit and vegetables a day, but we can sometimes be guilty of not doing this. (Give me the choice between a slice of cake and an apple, and I'll certainly choose the dessert!) Try and add lots of vegetables to stirfrys, soups and casseroles to help increase the amount of nutrients you absorb.

brain health

This is especially a good trick if you've got children, as they won't notice they're eating as many greens as they would if you simply piled them on to a plate.

Oily fish is another brain-boosting essential, as this contains omega-3 fatty acids that are one of the best foods to eat when improving your inner health. If you don't like the taste of fish, you can take fish oil in capsule form instead.

Another way to improve your brain health is to avoid experiencing too much stress. While this might seem easier said than done, it's important to make time to wind down and relax if you want to ensure your mind stays healthy.

Modern families often lead busy lives, with long working hours, lots of after-school activities to ferry children to and from and trying to juggle housework. Even if you just take 15 minutes a day to go on a walk with the dog (my favourite activity), soak in the bath or simply lie down and close your eyes, it'll give you a chance to recharge your batteries and put everything into perspective.

My next tip is perhaps not as obvious as having a healthy diet and time to relax, and that is increasing your intake of oxygen. Consider buying a can of oxygen to keep at home. I know this might sound a little extreme, but let me explain the benefits of doing so.

Increasing how much oxygen you breathe in can help eliminate headaches, lead to a better night's sleep, boost your concentration at work and delay the ageing process of your brain cells. With you better able to deal with your employment tasks, you might even find you get to leave the office earlier if it takes you a lot quicker to complete your duties.

Reducing your workload and getting home even just 15 minutes earlier than usual can work wonders for your mental health. I certainly feel a lot more positive with even just these extra minutes to spend relaxing with my family or simply watching TV.

Do you believe in the benefits of oxygen therapy? If so, leave your thoughts below as to what positive results you've seen from this.

Therapeutic target for Fragile X syndrome

According to a new study published in the current issue of Biological Psychiatry, fragile X syndrome could benefit from a new treatment. Researchers at the University of Catania in Italy have discovered a new therapeutic target: serotonin 7 (5-HT7) receptor.

Fragile X syndrome, one of the genetic causes of autism, is one of the most common causes of mental retardation in boys. In addition to intellectual disability, boys with fragile X syndrome have several features in common: elongated face, protruding ears, large testicles, muscle hypotonia, and more. The cause of this syndrome consists of a single gene mutation in the Fragile X Mental Retardation 1 (FMR1) gene, which is found on the X chromosome. Regarding neurological and psychiatric manifestations,  these children have social anxiety, are hyperreactive to visual or auditory stimuli and may have attention deficit hyperactivity disorder. In general their IQ level does not exceed 70. Currently there is no cure for XFS, but medications can be used to improve behavioral problems such as anxiety, hyperactivity etc.

Fragile X syndrome

About a decade ago, Dr. Mark Bear and his colleagues made the first advances in the treatment of fragile X syndrome. They demonstrated that blocking glutamate receptor 5 (mGluR5) could be the basis for the first treatment of XFS. Glutamate receptor 5 (mGluR5) is part of a specific mechanism that mediates a distinct alteration in brain function, that is enhanced long-term depression. Enhanced long-term depression, which was associated with XFS, refers to decreased functionality of neuronal synapses. Recent studies have shown that mGluR5 inhibitors, such as the drug fenobam, have beneficial effects in patients with XFS. It is possible that treatment with mGluR5 become a future therapy for the treatment of patients with fragile X syndrome even if more research should be done about it.

Now a team of researchers led by Dr. Lucia Ciranna, discovered new therapeutic targets. Experiments on animals have shown that long-term depression, mediated by mGlu receptors can be reduced by blocking a new therapeutic target: serotonin 7 (5-HT7) receptor. What is interesting is that the researchers found that this effect occurs in the hippocampus, one of the brain structures involved in learning and memory. Dr. Ciranna said the findings open new perspectives for patients with XFS as the selective agonists for 5-HT7 receptors may be useful pharmacological tools. A potential treatment for Fragile X syndrome is the compound LP-211 that acts as an agonist for 5-HT7 receptors, but more research needs to be done before it can be tested on humans.

Gene mutations associated with respiratory distress syndrome in babies

A study conducted by researchers at Washington University School of Medicine in St.. Louis, revealed that ABCA3 gene mutations are responsible for approximately 10% of cases of distress syndrome (RDS). The study was published in the December issue of Pediatrics, and is the first that demonstrates that a single gene is associated with an important number of cases of RDS. Researchers’ findings may provide the basis for new medical therapies to help infants with RDS.

RDS is a life-threatening respiratory disease that occurs especially in premature infants. The disease occurs due to insufficient amount of surfactant, a substance essential in the process of breathing. RDS is the main cause of death in infants in the first month of life. Premature babies and those born to mothers with diabetes are at risk of developing RDS at birth, even though it can occur in children born at term, but these cases are rare. RDS is more severe in new-born with patent dustus arteriosus, a congenital disorder in which the ductus does not close after birth.

Respiratory Distress Syndrome in Babies

Main symptoms and signs of the disease are related to respiratory effort: cyanosis, a bluish skin color, tachycardia, nasal flaring, chest wall recession etc. RDS can be prevented by antenatal glucorticoid adminstration. After birth, oxygen and surfactant are helpful for the management of RDS.  Untreated, the disease progresses to respiratory failure and respiratory arrest, and as complications intracranial hemorrhage can occur.

Jennifer A. Wambach, MD, assistant professor of pediatrics and the study’s lead author, said that ABCA3 gene mutations are responsible for 10% of cases of RDS in premature infants or infants born near term. She added that these children should normally have well-developed lungs and breathe normally. Wambach said she hopes to find other genes associated with RDS that can help identify children at risk.

A team of researchers, including and Aaron Hamvas, MD, and F. Sessions Cole, MD, analyzed five genes involved in surfactant metabolism. DNA samples taken from 500 infants of African and European descent, with and without respiratory distress were assessed. To check the results of the study, researchers analyzed 48 infants with severe RDS plus another 1066 babies to see how common  ABCA3 gene mutations were in the population. In this way it was observed that babies of European descent were more likely to have a single gene mutation ABCA3 than children without RDS. The same was found for babies of African descent or for those with severe RDS, even though for the first the difference was not statistically significant.

Regenerate the heart muscle

A remarkable discovery in heart research was made by scientists at the Fraunhofer Institute for Interfacial Engineering and Biotechnology IGB in Stuttgart: they found the surface markers of cardiovascular functional living progenitor cells (CPCs). This discovery is extremely important for heart research because it demonstrates that the cardiovascular progenitor cells (CPCs) can be derived from induced pluripotent stem cells, (iPS) cells. Investigation results were recently published in the journal PLoS ONE.

Progenitor cells are cells that are normally found only in the fetus and have the ability to develop into all cell types of the heart: cardiomyocytes, etc. The goal of the study  led by Prof. Dr. Katja Schenke-by Layland from the Fraunhofer Institute for Interfacial Engineering and Biotechnology IGB in Stuttgart, was to produce functional cardiomyocytes from progenitor cells. Cardiomyocytes are heart muscle cells that play an essential role in contraction. Myocardial infarction leads to loss of functional cardiomyocytes. As a result of a blockage of a coronary artery, myocardium served by that artery will not be supplied with oxygen anymore, thus it will die. A frequent consequence of patients who suffer a heart attack is heart failure, which means decreased ability of the heart contraction. Myocardial regeneration by stem cells was studied by researchers for a long time and many experiments have been tried over time.

Heart muscle

Of CPCs, cardiomyocytes, smooth muscle cells and endothelial cells develop during embryonic development. Although there were known many things about these cells, the researchers could not use them for therapeutic purposes because  it was difficult to identify the markers that could help isolate them as long as those markers were  found at the nuclear level (Islet1 or Nkx2.5). But a team of researchers Katja Schenke-Layland of Professor from the Fraunhofer IGB in Stuttgart, Prof. Dr. Robb MacLellan and Dr. Ali Nsair of the University of California Los Angeles (UCLA), were able to identify two surface markers: Flt1 ( VEGFR1) and Flt4 (VEGFR3). These surface markers were identified using microarray gene expression profiling. The discovery of these markers is very important because it helps scientists to isolate clinically relevant cardiovascular progenitor cells and use them for therapeutic purposes.

The researchers then wanted to derive the cells from induced-pluripotent cells stem (iPS) cells using a technique discovered by a Japanese scientist Shinya Yamanaka, Nobel laureate for Medicine in 2012. By manipulating the genes responsible for of the state of the cells, scientists were able to reprogram them into embryo cells (induced pluripotent stem cells), that is cells that can developed in all cells of the body.

Then the researchers investigated this finding in mouse model. “When we cultured the isolated mouse CPCs then in vitro, they actually developed “ as well as the embryonic stem cell-derived progenitor cells “ into endothelial cells, smooth muscle cells and more interestingly into functional heart muscle cells.”Schenke-Layland said.
The experiment is extremely valuable in heart research because it can potentially regenerate heart muscle and because it  is a step forward in the treatment of heart disease.

Vitamin D can potentially prevent cancer

A team of researchers led by McGill Professors John White and David Goltzman, of the Faculty of Medicine’s Department of Physiology, discovered the molecular mechanisms underlying vitamin D potential to prevent cancer. According to study results published in the latest edition of Proceedings of the National Academy of Sciences, the active form of vitamin D inhibits both production and function of a protein called cMYC. cMYC protein is elevated in most tumors and is correlated with growth and cell proliferation in cancer.

Vitamin D is a fat-soluble vitamin that has two sources: endogenous and exogenous. Endogenous source is represented  by synthesis of this vitamin in the skin by ultraviolet rays. It is important to remember that sun exposure is essential for vitamin D synthesis in the skin, so it is recommended taking vitamin D supplements in winter. Transforming 7-dehydrocholesterol in cholecalciferol is made in the skin through a non-enzymatic reaction. Then, cholecalciferol is converted in the liver to 25-hydroxycholecalciferol, but this compound has low enzymatic activity. Therefore, in kidneys it will undergo another transformation and thus the active vitamin D 3 (1, 25 dihydroxycholecalciferol) is formed. Exogenous vitamin D intake comes from foods like salmon, catfish, sardines, tuna etc.

Vitamin D

Vitamin D has many effects in the body, although the most popular are on the phosphocalcic metabolism. Vitamin D promotes absorption of calcium and phosphate in the intestine as well as  mobilization of calcium from bone. In addition to these actions, the effects of vitamin D have been extensively studied in recent years. Thus, it appears that vitamin D is involved in immune stimulation in preventing or protecting cardiovascular disease, cancer prevention etc. There have been studies that have shown that vitamin D is correlated with certain cancers such as cancers of the digestive tract, colon cancer and certain forms of leukemia.

Professor White said that his team of researchers studied the molecular mechanisms of vitamin D in human cancer cells, especially the role to stop proliferation. After numerous studies, it was found that vitamin D not only can control the production rate but also the cMYC degradation rate. What is interesting is that it was discovered that this vitamin stimulates the production of a natural antagonist of cMYC Called MXD1, which stops cMYC function.

To check the effects of vitamin D on protein cMYC, researchers have made some experiments on laboratory animals. They found that if vitamin D is administered to mice, there is a decrease in the level of cMYC and a reduction in its activity. Conversely, in mice that lacked the specific receptor for vitamin D, so those who could not absorb vitamin D, cMYC level was high.

Genetic Cause For Hypertension

According to a multinational research project conducted by the Universities of Dundee and Glasgow, scientists were able to identify a genetic determinant factor which can led to hypertension. This finding is very important because in the future scientists will be able to determine patient’s susceptibility to develop high blood pressure.

It is known that hypertension or high blood pressure  is an inherited condition which appears as a result of interaction between genetic factors and environmental factors. To date, genes that are involved in the arising of this condition have proven difficult to be identified, but with this research project, researchers were able to identify a common mutation which is located on the genes that regulate the production of aldosterone and cortisol (important hormones secreted by adrenal glands) as being influential in high blood pressure development. This genes are represented by the corticosteroidogenic genes CYP11B2 and CYP11B1.

“It has proved very difficult to identify genetic causes of hypertension but this research shows that a gene variation that is present in around 40% of the population is a significant factor. Drugs targeting aldosterone are already used in the treatment of hypertension, so this study emphasises that these should be more widely used. It will also inform the development of other therapies that could affect the way that aldosterone is produced. We know that the effects of aldosterone are amplified by a high salt diet, so this could give an important clue to an interaction between a common genetic variation and the environment.”, said Professor John Connell, Vice-Principal of the University of Dundee, who led the project.

Hypertension

The research project, led by Professor Connell (University of Dundee) and Professor Eleanor Davies (University of Glasgow), in collaboration with partners across the UK and Europe including the Universities of Cambridge, Aberdeen, Queen Mary London, Oxford and Leicester, was funded by the Medical Research Council and the results of this study by Hypertension, the journal of American Heart Association.

In this study were processed data on more than 3000 patients that were included in the MRC BRIGHT (British Genetics of Hypertension) study and on 2900 patients included in the NORDIL (Nordic Diltiazem) study and the Malmo Cancer and Diet Study. Scientists are satisfied with the results of this study, because this research project was built on theoretical models according to which gene variations that control aldosterone and cortisol synthesis could represent a risk for hypertension, theory which was confirmed by laboratory findings.

“We will now look to carry out further research, particularly with regard to the importance of genetically determined variation in aldosterone in other forms of cardiovascular disease.”, professor Connell added.

Myelin Formation In The Central Nervous System

According to a study, which was recently published in the journal EMBO reports, researchers at the Mainz University Medical Center of Johannes Gutenberg University have discovered a new molecule the possess an important regulating role in the process of myelin formation in the central nervous system. Myelin is a sheath around dendrites (nerve cell axonal projections) that has an important role in promoting the conduction of nerve cell impulses at specific locations, acting like the plastic insulation around a power cord.

Human nervous system poses a very effective method that confers a feature to nerve cells to transmit information over large distances more efficiently, method known as saltatory conduction of impulses. This technique is possible due to the fact that dendrites involved in impulses transmission are coated at specific intervals with myelin, which has the role to act like an insulating layer. The process of myelin formation begins in the central nervous system when oligodendrocytes, a type of brain cells, wrap their cellular processes around the axons of neurons and form a compact membrane called myelin sheath. Besides a high lipid content, myelin sheath also contains two proteins with a very important function, which synthesis have a very precise regulation process.

In this research, scientists analyzed the synthesis of myelin basic protein (MBP), a compound which posses an essential role in the formation and stabilization of myelin sheath. As all proteins, MBP synthesis is a two-stage process which begins with the synthesis of DNA, the basic genetic material. First step is represented by the conversion of DNA into messenger RNA (mRNA), which serves as a template for the synthesis of MBP. At one specific point, during the process of myelin formation, the synthesis of MBP in olygodendrocytes is stopped until certain molecular signals from nerve cells initiate myelination at specific sites. Until now, the mechanism that inhibit the synthesis of MBP have not been understood but, the current study demonstrates that in this process of suppression a certain molecule is responsible for the inhibition of MBP.

Myelin Sheath

“This molecule, called sncRNA715, binds to MBP mRNA, thus preventing MBP synthesis. Our research findings show that levels of sncRNA715 and MBP inversely correlate during myelin formation and that it is possible to influence the extent of MBP production in oligodendrocytes by artificially modifying levels of sncRNA715. This indicates that the recently discovered molecule is a significant factor in the regulation of MBP synthesis.”, explains Dr. Robin White, the head of the Institute of Physiology and Pathophysiology at the University Medical Center of Johannes Gutenberg University Mainz.

For scientists is very important to understand the molecular basis for the process of myelin formation, because various neurological disorders are the result of the loss of myelin sheath. To date, researchers have not found an explanation why olygodendrocytes lose their propriety to repair damaged myelin as multiple sclerosis (MS) progresses. “Interestingly, in collaboration with our Dutch colleagues, we have been able to identify a correlation between levels of sncRNA715 and MBP in the brain tissue of MS patients.

In contrast with unaffected areas of the brain in which the myelin structure appears normal, there are higher levels of sncRNA715 in affected areas in which myelin formation is impaired. Our findings may help to provide a molecular explanation for myelination failures in illnesses such as multiple sclerosis.”, Dr. Robin White added.

Insomnia increases the risk of stroke, according to study

According to a study, insomnia increases the risk of stroke and heart attack. Researchers in Taiwan have found that sleep disorders can lead to serious health problems. The study, led by Dr. Chien-Yi Hsu at the Taipei Veterans General Hospital, found that people who have insomnia have an increased risk of cardiovascular events such as heart attack or stroke.

It seems that, compared to people who sleep well, people with insomnia have a higher risk of developing stroke or heart attack. Dr. Gregg Fonarow, professor of cardiovascular medicine at the UCLA David Geffen School of Medicine, Los Angeles, added that factors such as stress or diabetes that cause insomnia can affect health. He said that there are studies showing that circadian rhythms are correlated with insulin sensitivity,  that is with metabolic changes.

Stroke

That sleep has serious implications on health is not new thing. We already know that sleep disorders can lead to hypertension, obesity, diabetes, depression, lack of attention and concentration during the day. On the other hand there are many diseases that can cause insomnia, such as thyroid disease (hyperthyroidism), anxiety,  chronic pain, and others.

To conduct the study, researchers used nationwide database heath from which they excluded people with depression, anxiety, sleep apnea, seizures, etc.. Finally there were analyzed 11,000 people aged 45 or older who suffered from insomnia, and more than 32,000 people who have not had trouble sleeping.

Participants were followed for 4 years and it was found that 1.6% of those who had insomnia had a heart attack. Of those who did not have trouble sleeping, only 0.76% had heart attack. Regarding stroke, the percentages were higher. It was found that over 11% of those with insomnia had stroke while only 6.5% of those who slept well had stroke.

Although the link between insomnia and cardiovascular accidents is obvious, scientists believe that clinicians should not aggressively treat insomnia. Fonarow said it is too early to say that the treatment of insomnia would decrease the incidence of these accidents (stroke and myocardial infarction).

In addition, the study did not show what kind of insomnia participants had. Dr. Aparajitha Verma, medical director of the Comprehensive Sleep Disorders Program Methodist Hospital in Houston, says it is essential to know the type of insomnia in order to make correlations with cardiovascular disease. Insomnia can manifest in several ways: fragmented sleep, difficulty in inducing sleep, insufficient number of hours of sleep etc. It is however highly recommended to rest at least 6-7 hours per night.

New Discoveries On Celiac Disease Could Lead To New Treatment Options

Researchers made new discoveries regarding celiac disease that could lead to new treatments. Although it was known that celiac disease is caused by hyperactivity of the immune system, it is the first time when researchers were able to visualize the interaction between T lymphocytes and gluten, the protein that triggers the disease. Celiac disease can affect both young children and adults and the prevalence of the disease is about 1 in 300 (not certain data). It should be noted however that celiac disease may be clinically latent so the number of people affected may be higher than currently reported. Celiac disease is associated with autoimmune diseases such as dermatitis herpetiformis, thyroid disease (Basedow’s disease) etc.

Greain

Celiac disease is a chronic intestinal disorder characterized by intolerance to certain proteins in wheat, rye, barley. There are some toxic protein fragments responsible for manifestations of celiac disease, which differs depending on the type of grain: gliadin in wheat, secalina in rye and others. Manifestations of celiac disease are diarrhea, abdominal pain, flatulence, etc. The exact celiac disease prevalence remains unknown. The positive aspect is that the symptoms subside on withdrawal of gluten from the diet. Moreover, clinical improvement after removing gluten from the diet is a diagnostic criterion.

Symptoms are caused by an abnormal immune response against gluten from the diet. Immune system cells attack the intestinal mucosa and in this way appears atrophy and intestinal malabsorption. Therefore, in addition to gastrointestinal symptoms (diarrhea, abdominal pain, flatulence) also there are many symptoms caused by malabsorption: vitamin D, iron, vitamin K, protein deficiency which can lead to fatigue, anemia, fractures , bleeding etc. Celiac disease is diagnosed by symptoms, serological tests (antigliadin antibodies, etc) and intestinal biopsy.

Now a team of researchers led by Dr Hugh Reid and Professor Jamie Rossjohn of Monash University, were able to visualize how  T lymphocytes, involved in the immune response of celiac disease, interacts with gluten. Dr. Reid, a senior research fellow at Monash University, said that this finding is a step forward not only in the study of celiac disease but also in the study of autoimmune diseases. This discovery is the starting point for the blood test and a therapeutic vaccine, Nexvax2 ®. However it should be mentioned that this vaccine will be available only if the patient with celiac disease carries the gene HLA-DQ2. There is a genetic susceptibility in the population that favors the development of celiac disease. People who carry HLA-DQ2 or HLA-DQ8 are more prone to celiac disease. But now researchers believe the vaccine can restore immune tolerance to gluten. This would mean that patients can eat gluten again without having intestinal symptoms.

Researchers Explain How Ketamine Improves Depression Within Minutes After The First Dose

Numerous precedent studies have shown that the drug called ketamine, if taken in small doses, is very effective for patients suffering from chronic depression. The studies have shown that the effect of the drug is immediate in relieving patient’s symptoms. For the past 10 years, researchers tried to explain this discovery, which was firstly made at the Yale University, in the United States of America.

Current evidence shows that ketamine, which is a known pediatric anesthetic, aids the regeneration of the synapses found between the brain cells. These damaged synapses are the result of chronic depression and stress. Researchers from the Yale School of Medicine  reported their results in the journal Science, on the 5th of October.

The antidepressants that are currently used in treating chronic depression take a few months until visible results are shown. Furthermore, these therapies are completely ineffective for almost one third of the patients. Ketamine, however, targets a different type of neurotransmitter, thus being able to aid a larger number of patients. If researchers were able to understand the mechanisms through which ketamine aids the synaptic regeneration, a novel class of antidepressants could be synthesized.

Ketamine Drug

“The rapid therapeutic response of ketamine in treatment-resistant patients is the biggest breakthrough in depression research in a half century”, said the co-authors of the study, Ronald Duman, Elizabeth Mears and House Jameson. The authors of the study are also professors at the Yale University. The authors added that because the drug has many usage limitations, the understanding of its working mechanism is crucial for further drug development. If administered in small doses, the effects of ketamine are only visible for 7 to 10 days. However, if used in large doses, a major side effect is psychosis.

In previous research, professor Duman and his team showed that ketamine triggers the release of glutamate, which is a neurotransmitter that stimulates the growth of damaged synapses. This triggered release happens over a series of steps. Also, the team showed that chronic stress and depression are responsible for damaging the synapses. A single small dose of ketamine can rapidly reverse this damage, said the authors.

The first study that showed that ketamine is linked to relieving depression symptoms was published by John Krystal and Dennis Charney. Krystal is the chairman of the psychiatry department from the Yale University, whilst Charney is the dean of the Mount Sinai School of Medicine. The results of their several clinical trials that suggested the effect of ketamine on chronic depression.

Researchers have managed to reproduce the effects of ketamine in newly developed drugs, however, the action of the new drugs is slower than that of ketamine. Researchers are currently trying to identify alternative ways to duplicate the effectiveness of ketamine.

The study abstract can be found here: Science Magazine

The time-line of ketamine being developed as a new rapid, effective antidepressant

The first evidence of that glutamate and NMDA (N–methyl-D–aspartate), both neurotransmitters, have an important role in the cortical functions originated in the 1980’s.

Ketamin was first used to explore the mechanisms of ordinary psychiatric disorders in the 1990’s by researchers from the Yale University. The psychiatric disorders studied included alcoholism and schizophrenia. Based on the results of the trials, it was suggested that ketamine is very effective against these disorders. Scientists observed the rapid effect and high effectiveness of ketamine in patients. The symptoms ameliorated within a few hours and lasted for more than a day.

In they year 2000, the first double-blinded clinical trial that assessed the effect of ketamine on patients suffering from chronic depression was conducted. The results were published in the journal Biological Psychiatry. Researchers reported that ketamine has a rapid antidepressant effect, thus suggesting that it could be used for treating depression.

In 2006 the results of the clinical trial that took place in 2000 were replicated by a team from the NIMH (National Institute of Mental Health). One of the co-authors of the study also took part in the first clinical trial from 2000.

Another research coming from Yale, in 2010, suggested that the rapid antidepressants of ketamine is linked to the fact that a small dose increases the function and numbers of new synapses. This is a process called synaptogenesis and is reported to be a much faster process than the process of forming new neurons.

A more recent study, published in 2011 in the journal Biological Psychiatry, revealed that the administration of  a small dose of ketamine can reverse the dendrites atrophy caused by chronic stress. The study was conducted on rodents.

Timeline References:

www.ncbi.nlm.nih.gov/pubmed/8122957

www.ncbi.nlm.nih.gov/pubmed/9554431

www.ncbi.nlm.nih.gov/pubmed/10686270

www.ncbi.nlm.nih.gov/pubmed/16894061

www.ncbi.nlm.nih.gov/pubmed/20724638

www.ncbi.nlm.nih.gov/pubmed/21292242