Circadian Rhythms is  Linked To Weight Problems

Researchers have uncovered the link between body weight and a balanced sleep. It seems that everyone’s metabolism and weight fluctuations are influenced by a gene that regulates internal body clocks, called “Rev-Erb alpha”. It seems that this gene is responsible not only for weight but also the problems that extra pounds can have on ones health. The study was published online in The FASEB Journal.

Rev-Erb alpha gene is a component that adjusts circadian rhythms and plays an important role in determining the metabolic rate. There have been studies that suggested that overexpression of Rev Erb alpha stimulates adipogenesis (creation of fat stores in the body). Metabolism of each person depends on various factors. In principle there genetic and environmental factors are involved. It is a well known fact that the body metabolism influences energy needs. For example, a person with a slow metabolism tends to gain weight. Of course, this weight gain depends not only metabolism, but also on the quantity and quality of food.

Circadian Rhythms

Weight gain occurs when there is an excess of calories (a person consumes more calories than burn). Of course,  lifestyle has direct consequences on the body mass index. It is important to remember that a healthy lifestyle involves not only a healthy diet based on vegetables and fruits, but also includes daily physical activity and restful sleep.

Researchers found that gene “Rev-Erb alpha” is the cause of obesity and hyperglycemia even under a normal diet. Experiments on mice have shown that subjects lacking Rev-Erb alpha gene became obese and hyperglycaemic even if the amount of food consumed was the same compared with a normal group of mice. In addition, scientists have found what differed in two groups of mice. Mice that had a deficit of Rev-Erb alpha genes created more fat than normal mice. Gerald Weissmann, MD, Editor-in-Chief of The FASEB Journal, remarks  that the  finding shows the importance and the influence ‘body clock’ has on body weight.

Etienne Challet, Ph.D., a researcher Involved in the work from the Department of Neurobiology of Rhythms at the Institute of Cellular and Integrative Neurosciences at the University of Strasbourg in Pascal, France, noted that irregular lifestyle,  shift work, exposure to artificial light at night and normal day-night rhythm disturbances may have consequences on metabolism. In other words, a person can find it very hard to lose weight even if  on a normal diet. On the other hand, disorganized lifestyle can lead to less healthy behaviors like eating during the night.

Cocaine Use Ages The Brain Faster

According to a study led by researchers at the University of Cambridge, chronic cocaine consumers present a premature aging of the brain. In other words, chronic cocaine users lose a greater volume of gray matter over time. The central nervous system effects of cocaine are well-known. It is already known that chronic users of cocaine present memory loss, concentration problems and attention deficit disorder. The immediate effect of cocaine is to stimulate the brain. Cocaine interferes with the metabolism of dopamine, binds to dopamine transporter blocking its reuptake. Thus dopamine accumulates in the synaptic gap.

Researchers found that chronic cocaine users lose an average of 3.08 ml brain volume per year, that is double of their nonconsumer peers. In other words, their brain ages faster. The study was conducted on 120 individuals, 60 were consumers and 60 were nonconsumers. Individuals selected had similar age, gender and IQ. Another observation made by researchers was that cerebral atrophy related to cocaine users is predominantly present in the prefrontal cortex and temporal regions, regions with a role in decision-making, attention and memory. It should be noted that there is an inevitable cognitive decline that occurs with age, approximately after 45 years in normal individuals. Moreover, there are studies that  have shown that in  individuals both physically and mentally active, cognitive decline occurs lately.

Studies on psychological changes in cocaine consumer individuals have been also conducted previously. It was found that such changes that occur in cocaine consumers, such as cerebral atrophy, immunodeficiency, are generally associated with age in normal individuals. However, the study conducted by researchers at the University of Cambridge, is the first of its kind that proves gray matter volume loss in cocaine-dependent individuals. Dr Karen Ersche, Behavioural and Clinical Neuroscience of the Institute (BCNI) at the University of Cambridge, said that cocaine users should be warned about the devastating effects of drug on the brain: “Young people taking cocaine today need to be educated about the long-term risk of aging prematurely. “

Cocaine is a drug that stimulates the central nervous system. It has several effects, including inhibition of appetite, local anesthesia etc. Cocaine increases motor activity and causes a state of euphoria. It can also increase performance in athletes. On the other hand, the drug has other effects such as anxiety, paranoia, tremors, convulsions. Long-term cocaine effects are serious and severe. In high doses, cocaine can cause tachyarrhythmias and hypertension. In other words, can lead to death by heart attack or stroke.

Chronic Myelogenous Leukemia

Chronic myelogenous leukemia (CML) is a neoplastic disease of hematopoietic system characterized by a clonal proliferation of granulocyte precursors, without the loss of their differentiation capability. Therefore in peripheral blood exists an increased number of granulocytes and granulocyte precursors and an increased number of blast cells.

In its evolution, CML is passing through three phases: chronic, accelerated and blast crisis. Chronic phase of disease is characterized by mature cells proliferation. Accelerated phase of CML is characterized by the occurrence of new cytogenetic abnormalities, superimposed over the existing ones. Blast phase or blast crisis is characterized by a rapid proliferation of  immature cells.85% of patients are diagnosed in the chronic phase of the disease and then naturally progress to the accelerated phase and blast crisis in 3 to 5 years from diagnosis. The diagnosis of CML is based on the histopathologic examination of bone marrow and cytogenetic abnormalities in bone marrow cells.

Chronic myelogenous leukemia is a neoplastic disease of hematopoietic system caused by a single, specific genetic mutation. This mutation occurs in 90% of cases  and results from a cytogenetic aberration known as the Philadelphia chromosome (a translocation between chromosomes 9 and 22).

Cytogenetic analysis has a major importance in chronic myelogenous leukemia, because:

• Can confirm the diagnosis of CML;
• Can predict blast crisis;
• Can assess disease prognosis;
• Can assess the degree of remission.

Philadelphia Chromosome

Philadelphia chromosome was the first chromosome described as an aberrant chromosome in a malignant disorder by Nowel and Hungeford in 1960. After 10 years, Rowely found that the Philadelphia chromosome is not the result of a loss of genetic material (deletion of the long arm of chromosome 22), but the result of a reciprocal translocation between chromosomes 9 and 22. After another 10 years, it was demonstrated that after a chromosomal structural modification,  abl gene (Abelson murine leukemia) located on chromosome 9 is translocated on bcr gene (break point cluster region) located on chromosome 22 and form a hybrid gene called bcr / abl which encodes a protein kinase that plays an important role in leukemic cell clonal proliferation.

The breaking point of the bcr gene interests a short portion of the gene, unlike the breaking point of the abl gene that interests a longer portion of the gene and is located in different areas. Indirect evidence of these occurrences are represented by the fact that hybrid gene bcr / abl contains two types of messenger RNA and that this hybrid gene synthesizes two different proteins, P190 and P210.

Philadelphia Chromosome

Due to the fact that Philadelphia chromosome was identified both in chronic myelogenous leukemia and in acute leukemia, some authors propose that in cases where patients presented at the onset of the disease Philadelphia chromosome to be included in acute leukemia than chronic myelogenous leukemia, following that subsequent investigations to decide certainty about the diagnosis.

Although through classical cytogenetic methods, the Philadelphia chromosome is absent in approximately 10% of patients with CML, modern molecular genetic methods, especially polymerase chain reaction (PCR) and Southern blot method highlight this hybrid gene bcr / abl in 30% to 50% of these cases. High proportion of 95% -97% of cases of CML with positive Philadelphia chromosome highlights the major involvement of  bcr/abl gene in clonal proliferation of leukemia cells.

The presence of  Philadelphia chromosome shows a favorable prognosis, respectively patients survive about 3-4 years after diagnosis when conventional therapy is administrated or survival can be extended to 8-9 years if alpha-interferon is administrated. Furthermore, the advent of Gleevec (imatimib) extended survival rate and complete remission to a much longer periods of time.

In some cases of CML were found translocations between chromosome 17 and 22 or more complex translocations involving at least three chromosomes.

In about 5% of cases, besides Philadelphia positive cell population, there are cells with normal karyotype. This mosaicism dose not appear to have prognostic implications.

CML evolution is biphasic, with a chronic phase that has an average duration of 2-4 years, with positive Philadelphia chromosome, followed by an acute phase. Transition to the acute phase may be sudden or gradually through an accelerated phase. The appearance of accelerated phase may be announced by the occurrence of additional chromosomal changes:  Philadelphia chromosome duplications, chromosome 8 trisomy, the occurrence of isochromosome 17 and trisomy 19.

In the acute phase (blast crisis) can be seen diverse cell clones with different chromosomal abnormalities, characterized mainly by aneuploidy (changes in the number of cell chromosomes, there are normally 46 chromosomes).

The existence of correlations between chromosomal changes and their effect on phenotype provides indications regarding prognosis.

Mesothelioma Diagnosis

New findings regarding the treatment and diagnosis of malignant pleural mesothelioma were presented at the 3rd European Lung Cancer Conference  in Geneva. Malignant pleural mesothelioma is a rare form of tumor associated with asbestos exposure.

Currently, the diagnosis is set by analyzing the patient’s symptoms, imaging investigations, but it is only confirmed by pleural biopsy and histopathology. Patients go to the doctor due to dyspnea caused by pleural effusion or chest pain. In order to confirm the diagnosis of mesothelioma, the patient must be the subject of a biopsy. Histopathological examination can determine the type of  mesothelioma (epithelial, most commonly, sarcomas and mixed). However the result is sometimes ambiguous. Tumor markers found in the bloodstream are currently able to aid the diagnosis of mesothelioma (serum proteins  related with mezotelina or osteopontin). However, sometimes the results are not clear and the diagnosis is much delayed making life expectancy drop even more. So researchers focused on finding more rapid diagnostic methods.

Mesothelioma Diagnosis

Researchers tried to find a quick test, specific and sensitive in order to detect mesothelioma. The researchers analyzed small molecules called microRNAs in blood samples from patients with mesothelioma and healthy patients. They found that in the blood of patients with mesothelioma, the level of  a particular type of microRNAs named miR-625-3p was 4 times higher than normal. Although the test accuracy is about 82%, Dr. Kirschner said that in order to microRNA to become a routine test, further studies must be conducted to confirm this accuracy. If results are still promising, this test could play a key role in the early detection of mesothelioma.

Furthermore, studies on biomarkers of mesothelioma have also been made by  Swiss, Italian and U.S. researchers. They reported the discovery of peptides found in serum of patients with mesothelioma. However, this discovery is still under research. Also, Australian Researchers believe that high-dose radiotherapy in patients with mesothelioma has a good response rate. The study conducted between 2003 and 2011 on 45 patients with stage III-IV mesothelioma,  showed that the average survival period was about 12 months. “Many believe mesothelioma to be radioresistant and toxicity that is prohibitive if high doses is given with the long affected in situ,” said Dr Feigen from Austin Health Radiation Oncology Center in Melbourne.

Another finding reported by British researchers is that sorafenib is well tolerated in patients with mesothelioma. Sorafenib is an inhibitor of protein tyrosine kinases Several (VEGFR and PDGFR) and Raf kinases. Since the discovery, there were reported more side effects like rash, hypertension, diarrhea and others. However, it seems to be well tolerated in patients with mesothelioma.

Chromosomal Abnormalities In Lymphoproliferative Disorders

Leukemias are clonal hematopoietic neoplastic diseases, originate from an abnormal stem cell. In the course of biological evolution, cancer cells undergo a gradual change of genotype, resulting in mutant cells. Cytogenetic analysis represents a major tool for investigating the biology of cancer because it offers the most valuable information. Karyotype is a useful tool for monitoring patients with leukemia.

Acute Lymphoblastic Leukemia (ALL)

It is the most common type of leukemia that occurs in childhood. Chromosomal abnormalities are present in most patients with acute lymphoblastic leukemia (ALL).

One of the features of ALL in children is increased incidence of hyperdiploidy, which usually includes trisomies of chromosomes 4, 6, 10, 17, 18, 20, 21. Hyperdiploidy with more than 50 chromosomes is associated with a favorable outcome (cure up to 90% by conventional therapy), while a modal number below 50 chromosomes confers a poor prognosis.

Hypodiploidy in acute lymphoblastic leukemia is rare, however, a massive loss of chromosomes that is leading to modal number of maximum 24 chromosomes is almost exclusively found in ALL and in lymphoid form of blast crisis of chronic myeloid leukemia.

About 30% of leukaemic cells in adults with ALL have a pseudodiploid constitution (46 chromosomes but with structural rearrangements).

Karyotype instability is a phenomenon that occurs frequently in acute lymphoblastic leukemia. During relapses, 30% -80% of patients present a variety of additional or structural modifications superimposed or derived from the original  modifications. The most common structural rearrangements are the translocations.

Acute Lymphoblastic Leukemia Karyotype

In B-cell acute lymphoblastic leukemia are more common translocations between chromosomes 9 and 22 (Philadelphia chromosome), translocations between chromosomes 4 and 11 and translocations between chromosomes 1 and 19.

Philadelphia chromosome (translocation between chromosomes 9 and 22) occurs in 17% of ALL cases in adults and only 5% of ALL in children and has the same morphological aspects as in chronic myelogenous leukemia. Molecular analysis revealed that Philadelphia chromosome break point on chromosome 22 is located more proximally than that involved in the formation of Philadelphia chromosome in chronic myelogenous leukemia. By molecular analysis were revealed fusions between  BCR gene (breakpoint cluster region, located on chromosome 22) and ABL gene (abelson murine leukemia, located on chromosome 9) in about 30% of patients with ALL. Translocations between chromosomes 9 and 22 are associated with hyperleukocytosis and is a factor of poor prognosis (life expectancy is 15 months).

In patients with T cell acute lymphoblastic leukemia were observed chromosomal rearrangements involving the genes that encode T cell receptors:

• TCRA and TCRD on chromosome 14;
• TCRB and TCRG on chromosome 7.

So far, these translocations have been described as specific for T-cell acute lymphoblastic leukemia:

• Translocations between chromosomes 8 and 14;
• Translocations between chromosomes 11 and 14;
• Translocations between chromosomes 10 and 14;
• Translocations between chromosomes 1 and 14;
• Translocations between chromosomes 7 and 19.

Chronic Lymphocytic Leukemia (CLL)

Chronic lymphocytic leukemia is the most common type of leukemia, accounting for 30% of all leukemias. Is more common in men aged over 60 years.

Although the etiology is unknown, the involvement of genetic factors is evidenced by:

• High familial incidence;
• Coexistence of CLL with autoimmune diseases or malignant tumors;
• Certain areas of the world are endemic for leukemia / lymphoma with T cells produced by infection with a lymphotropic retrovirus ( RNA virus), HTLV 1 (Human T Leukemia / Lymphoma Virus 1).

In chronic lymphatic leukemia, in over 95% of the cases appear a clonal expansion of B cell line and in less than 5% of the cases appear a clonal expansion of malignant cells with T phenotype.

Chronic Lymphocytic Leukemia

In 50% of patients with CLL are identified chromosomal abnormalities. At the onset, the most common chromosomal abnormality is trisomy 12, this situation represents a factor of good prognostic, patients having a longer disease-free survival.

In advanced stages appear other chromosomal abnormalities, the most common being  rearrangements of chromosome 14 or translocations between chromosomes 11 and 14. On chromosome 14 are localized the gene responsible  for immunoglobulin heavy chain synthesis and the gene responsible for synthesis of alpha chain T cells receptor. Translocation between chromosomes 11 and 14 activate bcl1 oncogene (B cell lymphoma / leukemia 1), located on chromosome 14, gene that encodes BCGF protein (a protein that acts as a B cell growth factor). Patients with chronic lymphocytic leukemia who have chromosomal abnormalities have a lower survival rate.

A special type of chronic lymphocytic leukemia is the type associated with ataxia-telangiectasia (a genetic disorder characterized by progressive cerebellar degeneration), in which translocations occur between chromosomes 14.

Prenatal Diagnosis

Prenatal screening is performed during pregnancy by specific investigations.

Indications for prenatal diagnosis:

• Maternal age over 35 years;
• A child with chromosomal abnormality in history;
• One parent carrier of genetic structural abnormalities;
• Mother carrying a recessive X-linked disease;
• Monogenic diseases in history;
• Parents are carriers of recessive genes, which can be detected by prenatal diagnosis;
• Family history of neural tube defect;
• Screening tests at risk;
• Abnormal fetal ultrasound;
• After in vitro fertilization procedures or intracytoplasmic injection of spermatozoon in egg, which can predispose to chromosomal abnormalities.

The purpose of prenatal diagnosis is to detect birth defects with chromosomal, monogenic, genomic and multifactorial etilogy.

In practice, prenatal screening is used to determine biochemical markers, ultrasound measurements and signs which can highlight genetic abnormalities.

Methods Of Prenatal Diagnosis

• Non-invasive: ultrasound, Doppler ultrasound, biochemical screening, analysis of fetal cells from maternal blood.
• Invasive: chorionic villi biopsy, amniocentesis, cordocentesis.

Prenantal Diagnosis

Chorionic Villi Sampling (CVS)

An early diagnosis (between 10-12 weeks of gestation) is possible using chorionic villi sampling (CVS). This is done under ultrasound control, transabdominal or transcervical and allows the study of biopsied material.

Cells taken from CVS can be subjected to:

• Molecular genetic testing – allows diagnosis of monogenic genetic disorders;
• Biochemical tests – allows diagnosis of metabolic disorders;
• Fetal karyotype – allows diagnosis of chromosomal abnormalities;

Disadvantages of the technique: the possibility of contamination with maternal cells, leading to false positive results of mosaicism, reason why amniocentesis is often necessary for diagnosis.

CVS complications:

• Abortion: 1/50-1/100;
• Infections;
• Bleeding;
• Abnormalities of limbs due to amputations of embryonic buds by vacuuming.

Chorionic Villi Sampling

Amniocentesis

Amniocentesis consists of transabdominal aspiration of amniotic fluid (10-20 ml) under ultrasound guidance.

Depending on the moment when is performed, amniocentesis is:

• Standard (15-18 weeks gestation);
• Early (11-14 weeks of gestation) as an alternative to CVS;
• Late (in the last trimester of pregnancy) used to diagnose Rh isoimmunization diseases. Can also be used as a treatment in case of polihidroamnios.

Analyses performed from amniotic fluid:

• Cytogenetic examination- fetal karyotype;
• Polymerase chain reaction (PCR), Fluorescence in situ hybridization (FISH) – for a rapid diagnosis of numeric chromosomal abnormalities;
• Alpha-fetoprotein dosage – in suspicion of neural tube defects;
• Acetylcholinesterase dosage (elevated in neural tube defects);
• Biochemical tests – to diagnose metabolic diseases;
• Molecular genetic testing – to diagnose monogenic diseases.

Indications for amniocentesis:

• Establishing the genetic sex, in case of a family history of X-linked disease;
• Karyotype for diagnosis of a aneuploidy;
• Diagnosis of metabolic diseases: errors in lipid metabolism, familial hypercholesterolemia, mucopolysaccharidosis, homocystinuria, galactosemia, glicogenoze, Lesh-Nyhan disease;
• Molecular diagnosis for monogenic diseases: thalassemia, hemophilia, phenylketonuria, Duchenne disease, fragile X syndrome, osteogenesis imperfecta;

Amniocentesis

Amniocentesis complication:

• Abortion: 1/100-1/400;
• Infections;
• Bleeding;
• Rh immunization.

Cordocentesis

Analysis is made from fetal umbilical cord blood collected after week 18 of gestation. Can be determined:

• Accurate diagnosis in case of mosaicism detected by amniocentesis;
• Diagnosis of hematologic diseases: haemoglobinopathies (thalassemia, sickle cell anemia), hemophilia;
• Diagnosis of fetal infection;
• Diagnosis of chromosomal abnormalities with instability;
• Blood group incompatibility (in case of confirmation blood transfusion is possible);
• Fetal hydrops.

Condrocentesis complications:

• Bleeding;
• Infections;
• Rh immunization;
• Abortion: 3% -5% of cases;
• Fetal death;
• Premature birth.

Diagnosing Breast Cancer

Researchers at the Departament of Biomedical Engineering at McGill University’s Faculty of Medicine have discovered a new method of detecting breast cancer using a simple blood sample. The discovery that can totally change the future diagnostic methods was published in the journal Molecular & Cellular Proteomics.

Breast cancer is one of the most common cancers found in women. Current detection methods rely mainly on imaging, that is mammography or ultrasonography. Diagnosis should be confirmed by biopsy with histology of the sample. Mammography is also the screening method, as recommended to every women of 40-45 years. However, many cancers go undetected and are found in a late stage when treatment options are limited. In principle,  if  cancer is discovered sooner  chances of cure are higher.

Droplet Of Blood

Useful in detecting and monitoring breast cancer are the laboratory findings. There are specific proteins in the blood that detect the  presence of breast cancer, such carcinoembryonic antigen, CEA. However, this antigen is not  very specific for breast cancer because it  can occur in other situations. Moreover, CEA can be found even in healthy people,  its present in the blood being dependent on genetic structure and lifestyle of each person. Therefore, scientists have tried to discover what is the limit and how to distinguish between people with cancer and those without cancer. Dr. David Juncker, the team’s principal investigator, said that researchers are focusing on building a profile of cancer based on the presence of certain markers present in cancer. “However, no reliable set of biomarkers has been found, and no such test is available today. Our goal is to find a way around this,” said Dr. David Juncker.

Researchers were able to develop a technology that detects the presence of these biomarkers in the blood without analysis to give false positive results. The team have developed a novel microfluidics-based microarray technology, which is more specific for detecting cancer. Scientists analyzed 32 proteins present in the blood of healthy individuals and that of individuals with cancer (breast cancer estrogen receptor). Based on blood tests, researchers were able to make a profile of the patient with cancer. Dr. Juncker said that in addition to these investigations, there  are required others to confirm the diagnosis of cancer. However, this new technology is promising and may be the way to new advances in cancer diagnosis. Also, Dr. Juncker also said the researchers intend to put up a hand-held version of the test in order to be  widely available to patients.

Rapamycin Diabetic

Researchers have discovered what is the mechanism underlying the symptoms of diabetes in patients treated with rapamycin. Researchers at Dana-Farber Cancer Institute have found that the link between Yin Yang 1 (YY1), a transcription factor, and rapamycin. Rapamycin is an immunosuppressive drug used initially in kidney transplantation, but gradually it  has been found that it has cancer and anti-aging effects.

Rapamycin or sirolimus is actually a macrolide for the first time extracted from the bacterium Streptomyces hygroscopicus present in soil from Easter Island. Originally, rapamycin was used as antifungal, but scientists found it more useful as immunosuppressive and antiproliferative agent. As an immunosuppressant, rapamycin prevents T and B cell activation by inhibiting the response of these cells to interleukin-2. Therefore, rapamycin  was approved in 1999 by the FDA as immunosuppressive organ transplantation.

Rapamycin

Regarding the anticancer properties, rapamycin inhibits mTOR signaling pathway (mTOR stands for “mammalian target of rapamycin”). mTOR is involved in regulating growth, proliferation and cell life. Moreover, mTOR is also one of the markers of cancer. Due to this property, rapamycin is being evaluated as a cancer treatment in several clinical trials. This drug is in clinical trials as a treatment for kidney cancer, brain tumors, lymphomas, etc. However, it was found that 15% of patients treated with rapamycin develop insulin resistance and glucose intolerance. So far, researchers have not found an answer to these effects, but study led by researchers at Dana-Farber Cancer Institute could elucidate the mechanism by which rapamycin induces diabetes.

Studies on rats showed that those treated with rapamycin had problems with regulating blood sugar,  the insulin resistance being caused by the activity of a protein Yin Yang 1, or YY1. Researchers have found that YY1 is the target of rapamycin as rats without this protein have not developed problems with blood sugar regulation. “”We thought that maybe YY1 was responsible for the diabetic effects,” says Puigserver PhD, senior author of the report published in Cell Metabolism.
Although study results are promising, researchers still have to investigate why only some patients develop diabetes after treatment with rapamycin.

Another property of rapamycin exploited more recently is related to extending the life of cells. In fact, many studies are focused precisely on these anti-aging. The first studies which showed that rapamycin increases lifespan in eukaryotes have been completed in 2006. Later studies in rats had positive results, that is  lifespan of rats was increased by 28-38%. However, it is unknown whether the same people might have given promising results as rapamycin suppress immunity.

New SAD Treatment

The winter season sometimes comes along with depression and lack of energy and this is called seasonal-affective disorder (SAD). It is thought that the reason why people develop this disorder is shortage of natural light and so the obvious treatment for these patients is light therapy. This consists of exposing the patient to a bright, full-spectrum light at certain times of the day. The effectiveness and exact mechanism of this light-treatment was not fully understood until now, until researchers from Oulu, Finland, found that the central role was not played by the retina. Instead the light acts on light-sensitive proteins on the brain’s surface. Special earphones were designed that shine a beam of light through the ear canal to a light-sensitive area in the brain, this being an efficient alternative to light therapy.

SAD Treatment

Juuso Nissilä, a physiologist at Oulu University, found that 18 separate regions of the brain express opsin-3, a light-sensitive protein that is also found in the human retina. There regions include areas that are involved in the production and storage of neurotransmitters like melatonin (which plays an important role in sleep activity) and serotonin and dopamine. The light-sensitive proteins in these areas may have a greater impact on the mood than proteins normally found in the retina. Nissilä considers that during daylight these proteins react to light transmitted through the skull: “Bone is actually quite a good transmitter of light – put a torch inside a skull and you'll see the beam very clearly – so I now think that it's the light reaching your brain surface through your skull which is the important factor.”

Alzheimer’s Disease

Scientists have discovered the mechanisms located inside the cells that are influenced and regulated by vitamin D3 according to a study published on the 6th of March in the Journal of Alzheimer’s Disease. This new research could probably solve the problem of amyloid plaques associated with Alzheimer’s disease. The study currently suggests that vitamin D3 could be responsible for the activation of genes and signaling networks that could influence the immune system to clear the amyloid proteins.

There have been earlier studies that suggested a link between vitamin D3, curcumin (also known as E100, a chemical substance found in Indian spices) and the stimulation of the immune system that led to clearing the amyloid proteins.

Alzheimer Patient

“This new study helped clarify the key mechanisms involved, which will help us better understand the usefulness of vitamin D3 and curcumin as possible therapies for Alzheimer’s disease”, said Dr. Milan Fiala, lead author of the study and researcher at University of California, Los Angeles (UCLA).

Scientists used the blood of healthy patients from the control group and patients that suffer from Alzheimer’s disease and isolated the immune cells that deal with the destruction of amyloid proteins. These cells are called macrophages and are in charge of clearing residual cells and other non-self particles from the body.

After the macrophages were isolated the team stored them in an enclosed space along with a quantity of amyloid.  1a,25“dihydroxyvitamin D3, which is one of the active forms of vitamin D3 was added to the mixture in order to see what effect it had on the consumption of amyloid.

Earlier research conducted by scientists has shown that patients with Alzheimer’s have two types of macrophages. The first type (called Type I macrophages) show an improved rate of consumption after adding curcuminoids along with 1a,25“dihydroxyvitamin D3, whilst the second type of macrophages (Type II macrophages) show an improved rate of consumption after adding only 1a,25“dihydroxyvitamin D3.

However, researchers have found that 1a,25“dihydroxyvitamin D3 has the important role of opening the chloride channel 3 (an important channel that supports the phagocytosis done by the macrophages. The addition of curcuminoids only affected the opening of this particular chloride channel in the Type I macrophages. Research also shows that 1a,25“dihydroxyvitamin D3 plays a very important role in the triggering of the transcription (the first stage of gene expression) of these particular chloride channels.

There are very complex mechanisms that stand behind the effects of 1a,25“dihydroxyvitamin D3 on phagocytosis, being dependent on calcium. With the help of Dr. Patrick R. Griffin and Dr. Mathew T. Mizwicki, the team of scientists have shown that 1a,25“dihydroxyvitamin D3 has a crucial effect, by using a method called mass spectrometry. They have shown that 1a,25“dihydroxyvitamin D3 has a greater effect than curcuminoids.

“Our findings demonstrate that active forms of vitamin D3 may be an important regulator of immune activities of macrophages in helping to clear amyloid plaques by directly regulating the expression of genes, as well as the structural physical workings of the cells”, said Dr. Mizwicki.

The team of scientists suggests that the next important step in the research would be to assess the impact of vitamin D3 on Alzheimer’s disease patients through a clinical trial. The also add that ongoing studies already show that vitamin D3 could also be beneficial in the case reduction of other diseases as well, not just Alzheimer’s disease.