Molecular Fountain Of Youth Discovered By University of California Researchers

A recent study published in the journal Cell Reports, in late January this year, reveals a major breakthrough in the understanding of aging and the molecular mechanisms involved in the process. This could be an important stepping stone for future therapy against degenerative diseases that affect the aging process of the patient. The research team from UCB (University of California, Berkeley) managed to reverse the molecular aging clock by infusing a longevity gene in the blood stem cells of aged laboratory mice. Their action caused the stem cells to regain their regenerative capabilities.

The research team found that a certain protein from the sirtuins class, SIRT3, is directly linked to the capabilities of aged stem cells to handle stress. Subsequently to the infusion of the stem cells with SIRT3, the research team observed the formation of new blood cells. This�emphasizes� the fact that the blood stem cells regained a part of their regenerative potential. “We already know that sirtuins regulate aging, but our study is really the first one demonstrating that sirtuins can reverse aging-associated degeneration”, reported assistant professor and main investigator of the study, Danica Chen. According to Chen, in the past couple of decades, scientists have made numerous breakthroughs towards the understanding of the aging process. Aging, once considered a random, uncontrolled process, is now known to be highly regulated.

Precedent studies have shown that as little as a single mutation in a gene can extend the lifespan of a patient. Dr Chen and her research team are investigating whether there is a possibility of reversing the aging process if the aging process is fully understood. The current study was conducted in collaboration with the director of the Center for Regenerative Medicine from the Massachusetts General Hospital. During the past few years, the class of proteins known as sirtuins, has become known to be closely related to the aging process. The most notable protein involved, SIRT3, can be found in the mitochondria of cells. The mitochondria are responsible for the generation of cellular energy,�signaling,�cellular differentiation�and cell death, whilst also playing an important role in the�cellular cycle�and�growth.

Brown Graph Abstract

According to the research team, SIRT3 becomes active during calorie restriction. In order to determine the effects of aging on the organism, the research team investigated the functionality of adult stem cells. These cells start to lose their function with aging. Their main focus was on the hematopoietic stem cells (responsible of blood cells), due to the fact that these cells are capable to completely restore all the blood cells after a successful bone marrow transplant. All research was done on laboratory mice. The research team notes that the absence of SIRT3 in young laboratory mice had no impact on their blood systems. However, with the passing of time and the aging of the mice, the results changed. Tests conducted on 2-year old mice show that the ones where SIRT3 was absent had a lower level of stem cells than the normal mice. Researchers also observed that the regeneration capabilities of the remaining blood stem cells had declined.

Apparently, younger mice weren’t affected by the lack of SIRT3 due to the fact that there is only a small level of oxidative stress in their cells. “When we get older, our system doesn’t work as well, and we either generate more oxidative stress or we can’t remove it as well, so levels build up” reported Chen. Due to this fact, the antioxidative system can no longer cope with the accumulation of oxidative stress, thus needing the help of SIRT3 protein to. Nonetheless, the levels of SIRT3 also decrease with age. In order to see if higher levels of SIRT3 make a difference, scientist injected the mice with SIRT3. According to their report, this experiment managed to rejuvenate the precursors of the blood cells, which further led to an increased production rate of cells.

Further research is needed in order to see if SIRT3 is also capable to extend the lifespan. However, Chen notes that this was not the goal of their study. Researchers concluded that knowing how SIRT3 is involved in the genetic regulation of the aging process could lead to the possibility of new therapies being developed in order to treat age-related disorders such as�cardiovascular disease,�arthritis,�osteoporosis,�Alzheimer’s disease, cancer�and others.

Researchers Reports That Natural Chemicals Can Interrupt Alzheimer’s Progression

The newest study published by a research team from the University of Leeds, reveals the fact that the natural chemicals that are found in both red wine and green tea, could be able to interrupt the progression pathway of Alzheimer’s disease. The results of their study were published in the�Journal of Biological Chemistry. The earliest laboratory tests conducted by the research team have identified the pathway through which proteins form clusters inside the brain cells, thus leading to their apoptosis.

Researchers were able to block this specific pathway through the use of purified extracts of EGCG (Epigallocatechin gallate) –�extracted from green tea, and resveratrol, a natural chemical found in�the skin of red grapes and�wine. Their findings could relate to the development of a new drug against Alzheimer’s disease. Alzheimer’s disease affects almost 1 million people in the UK and approximately 27 million people worldwide. Lead author of the study, professor Nigel Hooper, says that the study further increases the knowledge and understanding of what causes the onset and progression of the disease.

Green Tea, Red Wine

Alzheimer’s disease is caused by an accumulation of amyloid protein in different regions of the brain. The accumulation of amyloid is toxic to the brain tissue, thus high amounts of clustered-up amyloid can cause the degeneration of brain tissue. Amyloid clusters fuse with the prions (small proteins) found on the surface of the cell membrane and eventually cause cellular death. “We wanted to investigate whether the precise shape of the amyloid balls is essential for them to attach to the prion receptors, like the way a baseball fits snugly into its glove”, said the co-author of the study, Dr Jo Rushworth.

The main target of the study was to investigate whether these clusters of amyloid can be prevented through the alteration of their shape. In order to complete their investigation, the research team created artificial amyloid clusters in a test tube and then added them to brain cells taken from both laboratory animals and humans. The research team used data taken from recent studies, which shows that both EGCG and resveratrol are responsible for altering the shape of amyloid proteins. The results of the study shows that after the two chemicals were added, the amyloid clusters provoked no damage to the brain cells.

Researchers report that nervous cells were protected from the amyloid clusters because the newly developed shape didn’t permit them to bind to the prions on the cellular membrane. Professor Hooper notes that when the amyloid clusters bind to prions, they trigger the production of more amyloid. Further research will be conducted in order to completely understand the effect of amyloid-prion interactions on nervous cells.

Recent Study Shows That Energy Drinks Are Dangerous for Teenagers

A new study sheds light on the potential hazards that energy drinks might have on children, with extra attention given to the mix between energy drinks and alcohol. The paper was published in the journal Pediatrics in Review, in February 2013. The paper consists �of a compilation of already existing research. The conclusion is that caffeine beverages are the cause of obesity, high blood pressure, rapid heartbeat and various other medical issues in teenagers. According to the authors, if these drinks are combined with alcohol, they pose a potential danger for teenagers.

Dr Kwabena Blankson, a specialist in�adolescent�medicine says that there are far better ways to recover energy than drinking energy drinks that contain excessive amounts of caffeine and other additives. He mentions adequate sleep, healthy eating and a good exercise routine as healthy energy regeneration methods. In her opinion, parents and doctors alike should be constantly supervising the behavior of teenagers and inform them about the dangers of energy drinks whilst suggesting healthier alternatives.

Numerous precedent surveys show that approximately 50% of teenagers consume these beverages on a regular basis. Blankson reports that 500 ml cans of Monster Energy, Rockstar or Red Bull contain up to 160 milligrams of caffeine. Another energy drink, Cocaine, which was banned back in 2007, contains 280 milligrams of caffeine in 250 ml cans. These values were then compared to the values of a normal cup of coffee, which only contains around 100 milligrams of caffeine. According to Blankson, excessive amounts of caffeine can have bad side effects. Researchers note that anything over 100 milligrams of caffeine per day is considered to be unhealthy for teenagers. The fact that energy drinks also contain guarana, ginseng, sugar and are most often served cold enhances the effect of caffeine.

Energy Drinks mix with alcohol

“We don’t know what these additives do to the body after periods of extended use”, said Blankson. Furthermore, students from 10 universities in North Carolina were interviewed; almost 25% of them admitted to have consumed energy drinks mixed with alcohol in the past month. Several students from New Jersey and Washington were hospitalized from drinking energy beverages mixed with alcohol. According to SAMHSA�(Substance Abuse and Mental Health Services Administration), the branch of the�U.S. Department of Health and Human Services that is in charge�with improving the quality and availability of prevention, treatment, and rehabilitative services in order to reduce illness, death, disability and cost to society resulting from�substance abuse�and�mental illnesses, the number of hospitalized teenagers due to energy drinks abuse has doubled between 2007 and 2011. Moreover, almost 40% of the cases were also linked to either drugs or alcohol.

The latest report reveals that an unnamed energy drink, that’s sold in 23.5 fl oz cans, contains the same amount of caffeine as 5 coffee cups and the same amount of alcohol as a six-pack of beer. However, ABA (American Beverage Association) responded to the accusations of this study. Regarding this issue, an ABA spokesperson released a statement on Thursday, saying that “This paper contains misinformation about energy drinks and does nothing to address the very serious problem of underage drinking and excessive alcohol consumption among young adults”, whilst adding that the majority of energy drinks on the market only contain around half �the amount of caffeine found in coffee cups from coffeehouses. A�recommendation�has been issued by the ABA regarding the fact that all energy drink companies should have labels that state the exact amount of caffeine contained by their beverages, whilst also informing the buyer that the drink is not recommended for pregnant women, children or caffeine-sensitive people.

According to Dr Sean Patrick Nordt, who is the director of the toxicology section of USC (University of South California), these drinks appear to be “relatively safe”, if consumed only�occasionally. However, he states that these beverages should be better viewed as medication, and they should never be combined with illegal drugs or alcohol.

Lymphoma

According to a study which appears online in the Journal of Clinical Investigation and will be published in the December 2012 issue, scientists lead by Lori Hart, Ph.D., research associate and Constantinos Koumenis, Ph.D., associate professor,and research division director in the Department of Radiation Oncology, both from the Perelman School of Medicine, University of Pennsylvania, and Davide Ruggero, Ph.D., associate professor, Department of Urology, University of California, San Francisco, discovered a new pathway that helps cancerous cells to escape apoptosis (programmed cell death) during the development of lymphomas. This new pathway, called Unfolded Protein Response or UPR, a cell’s way of responding to unfolded and misfolded proteins, is activated in patients with lymphomas and in mice genetically bread to develop human lymphomas. In the moment when UPR pathway was inactivated, malignant cells undergo apoptosis.

The general implications of our work are that components of this pathway may be attractive anti-tumor targets, especially in lymphomas. Indeed, an enzyme called PERK, a kinase that we found to play a central role in UPR, is already being targeted by several groups, in academia and pharmaceutical companies with specific inhibitors.�, says�Constantinos Koumenis, Ph.D.

c-Myc, a gene that has the potential to cause cancer (oncogene) activates both cell proliferation and death. When a cell becomes malignant, c-Myc gene fails to induce cellular death, instead promoting tumor formation by cancerous cell proliferation. Scientists observed that in the moment when a cell is overexpressing c-Myc gene, an increased protein synthesis appears which is essential for c-Myc to cause cancer. To promote malignant cell proliferation, c-Myc gene use this aberrant production of proteins in order to block programmed cell death and to activate the UPR pathway. In conclusion, this malignant cells in order to survive need an increased protein synthesis induced by c-Myc gene. Researchers believe that targeting aberrant protein synthesis by inhibiting c-Myc gene activity may represent a promising therapeutic option for cancer treatment.

Malignant Cell

Increased synthesis of proteins induced by c-Myc gene leads to an accumulation of unfolded proteins in the endoplasmic reticulum (organelle that�is involved in the synthesis of proteins) where this proteins must be folded to be used in metabolic processes. The accumulation of this unfolded protein initiates a stress in endoplasmic reticulum which activates UPR and lead to the promotion of malignant cells proliferation. Normally, UPR is activated when in endoplasmic reticulum exists an imbalance between the number of unfolded proteins that need to be folded and chaperones, specialized proteins that have the function to fold them.� By analyzing lymphoma cells, researchers observed that this abnormal cells express higher levels of UPR activation, compared with normal cells and c-Myc gene activates only one arm of the UPR pathway, which increase cells survival by autophagy.

Autophagy is a catabolic mechanism that involves cell degradation of unnecessary or dysfunctional cellular components through the lysosomes, which can ensure cellular survival during starvation or stress by maintaining cellular energy levels. Scientists believe that malignant cells might be addicted to this mechanism, because cancerous cells can survive and proliferate if are deprived of nutrients and oxygen.

It was observed that inhibition of a protein called PERK, which has a very important role in UPR pathway reduced autophagy induced by c-Myc expression and tumor formation. It was also noted that drug and genetic inhibition of autophagy increased cellular death mediated by c-Myc genes.

Our findings establish a role for UPR as an enhancer of c-Myc�induced lymphomas and suggest that inhibiting UPR may be particularly effective against cancers characterized by c-Myc overexpression. In this context the UPR essentially acts as one of the cell's rheostats to counterbalance Myc's runaway cell replication nature and its pro-cell-death tendencies.�, says Koumenis.

However, researchers indicate that further studies are needed in order to explore the potential effects of PERK inhibition on normal tissues, because data from their labs suggest that PERK inhibition in lymphomas grown in animals is feasible, while other studies suggest that PERK has an important role in the function of secretory tissues such as the pancreas.

Ipilimumab brings benefit in advanced melanoma patients, according to study

German Institute for Quality and Efficiency in Health Care (IQWiG) compared the benefit of ipilimumab, a drug used in treating patients with metastatic melanoma, �compared with so-called “best supportive care”.

The study included patients who were divided into 3 groups: the first group was treated with ipilimumab, the second group was treated with ipilimumab�and�an experimental tumor vaccine (gp100) which has not yet been approved, and the third group received placebo and the tumor vaccine. The researchers conducted a randomized trial to see if�ipilimumab has an added benefit than other therapies.

Ipilimumab

Ipilimumab�is a humanized monoclonal antibody that was approved in 2011 to treat advanced melanoma. Melanoma is a skin cancer with very poor prognosis. Although it represents only 5% of all skin cancers, melanoma is responsible for 80% of skin cancer deaths. Basic treatment consists of surgical excision with oncological safety limits, but if the disease is advanced, that is if there are�many metastases, surgical excision does not bring any benefit to the patient. If the number of metastases is limited��( 1-5), they can be excised.

The risk of melanoma increases if the patient has relatives who have had melanoma or if the patient has melanocytic�nevi. In addition, it appears that exposure to ultraviolet radiation plays a role in melanoma occurrence. It should be noted that melanoma can occur both in healthy skin and in�underlying lesions. There is a mnemonic formula for signs of malignant degeneration of a melanocytic�nevus. ABCDE�means asymmetry, irregular borders, color change, diameter grater than 6 mm and�enlargement.�Any melanocytic�nevus� that begins to grow in size, changes color or bleeds should be evaluated by a physician.

IQWiG researchers wanted to assess whether ipilimumab�brings any benefit to patients with advanced disease. They focused on evaluating several aspects such as survival time,�symptoms complaints and quality of life. The conclusion was that ipilimumab brings benefit�because it�prolongs survival. Patients who did not receive ipilimumab�died after 6.5 months while patients who received the drug lived 10 months. It was also found that there was no difference in terms of quality of life between ipilimumab�and placebo. Patients had the same health status and symptoms: nausea, vomiting, digestive disorders, fatigue, pain.

Regarding discontinuation of treatment, it was observed that more patients who received ipilimumab�discontinued the therapy due to adverse reactions. However, it has not been�proven that ipilimumab is�more harmful�even though there is an indication of greater harm.

Researchers discover protein that indicates diabetes risk

Researchers at Lund University have discovered a new way to diagnose type 2 diabetes. According to a study published in the journal Cell Metabolism, a protein called SFRP4 can predict risk of diabetes many years before it is clinically manifest.

Diabetes mellitus is a metabolic disease characterized by high levels of glucose in the blood. Diabetes is asymptomatic for a long time, but after several years of development, diabetes can result in polyuria, polydipsia and polyphagia. These manifestations are due to increased levels of glucose that accumulate in the blood instead of�entering the cells. Normally after food intake, glucose passes into the bloodstream�from intestinal tract and then, passes into cells using insulin as transporter. If insulin is insufficient or if there is insulin resistance (obesity), glucose remains in the blood and so hyperglycemia occurs.

Blood samples

Hyperglycemia leads to serious complications. It can affect blood vessels, leading to kidney complications (diabetic nephropathy) and eye complications (diabetic blindness), or even diabetic acidosis. Finally diabetic coma occurs. Although diabetes is a disease that does not hurt, it is very important that this condition be diagnosed and treated properly.

Currently, type 2 diabetes is diagnosed using blood tests: measurement of blood glucose levels and glycosylated hemoglobin. But these tests diagnose diabetes when it is already installed.

The new test consists of measuring the SFRP4�that can predict diabetes several years before. Anders Rosengren, a researcher at the Lund University Diabetes Centre (LUDC), who has led the work on the risk marker, said the study showed that individuals with high levels of SFRP4 have a 5 times higher risk to develop diabetes in coming years.
SFRP4�is a protein with a role in inflammatory processes in the body. Researchers have realized the importance of this protein when they noticed that diabetic patients had increased levels of blood SFRP4. In diabetes pancreatic beta cells that secrete insulin�have a chronic inflammatory process, which prevents them from producing insulin.

Taman�Mahdi, main author of the study and one of the Researchers in Anders Rosengren’s�group, said the SFRP�4 explains the link between inflammation and diabetes. SFRP�Level 4 was measured in diabetics and non-diabetics every 3 years. It was found that 37% of those who initially had high levels of SFRP4�developed diabetes while only 9% of those with low levels of SFRP4�made diabetes. Researchers are now confident that they can develop a new treatment for diabetes by blocking protein SFRP4.

Researchers Reveal the Key Element Related to the Activation of Brown Adipocytes

A new study reveals the key element related to the activation of brown adipocytes. The cellular activation results in the burning of the fat molecules, instead of storage. This new discovery allows pharmaceutical companies to start research on new drugs against obesity. Brown adipocytes are responsible for burning calories in order to generate heat. This is a distinct feature, compared to other mammals. Researchers have only recently discovered that brown adipocytes are present in adult humans, contrary to the belief that brown fat is only present in infants. According to recent studies, adult humans possess significant amounts of brown fat along with white fat.

Results of precedent studies have shown that brown adipocytes are mainly activated by low temperatures. However, there’s data suggesting that ingesting high amounts of food also activates the brown fat cells. Activated brown adipocytes are responsible for converting fat molecules to heat.

Brown Adipocyte

�The research team from the UCSF (University of California, San Francisco) published their results in the journal Cell, on the 12th of October. The main authors of the study are associate professor Yuriy Kirichok, research specialist Polina Lishko and Andriy Federenko, who is now an assistant professor at UCB (University of California, Berkeley).

Their new discovery, regarding the action mechanism of a protein that triggers the biochemical reaction that is involved in the fat burning process, suggest that the possibility to create a drug that would keep this mechanism active is possible. This would increase the fat burning process and thus help patients to lose more weight. However, researchers aren’t yet convinced that this is a valid strategy for weight control.

The relationship between the protein, called UCP1 (uncoupling protein 1) and the heat-generating process has been long known. According to professor Kirichok, even if the protein has high specificity for this process, artificial drugs could prove to be ineffective due to a different cellular response.

“Low levels of brown fat correlate with obesity. We have shown how fatty acids attach directly to UCP1 and help it to break down an electrical potential across the mitochondrial membranes, causing the cell to burn more fat and to generate heat in order to regenerate this potential”, noted professor Kirichok.

Every cell contains mitochondria, which are small organelles that generate energy. This energy is created through oxidative phosphorylation, a metabolic process that converts energy taken from food, into ATP (Adenosine triphosphate). Through this process, the mitochondrial membrane gains a voltage gradient which further helps make ATP.

Compared to other cellular types, the brown adipocytes are packed with mitochondria. This plenitude of mitochondria is responsible for the brown color of the adipocyte. However, unlike in other cells, where mitochondria produces ATP, in the brown adipocytes, it produces heat, with the help of UCP1.

The research team used a technique called “patch clamping” in order to track down the electrical currents and reveal the connection between UCP1 and fatty acids. Through this technique, the researchers were able to track down the electrical activity of each mitochondria in particular.

Professor Kirichok notes that the role of UCP1 has been known for almost 20 years. The connection between fatty-acids and the activation of UCP1 has also been known. However, there were certain doubts regarding the actual mechanism which links the fatty acids to UCP1.

The research team was able to track every change that appears in the electrical currents that move across the mitochondrial membranes. This technique allowed researchers to make suppositions about the biochemical reaction that takes place. Their conclusion was that UCP1 captures the fatty acids and further directs them to transport protons into the mitochondria. With the proton numbers inside the mitochondria rising, the inner electrical membrane potential dissipates. In order to restore and maintain this electrical potential, supplementary cycles of oxidative phosphorylation are needed and thus heat is generated.

Abstract here

New imaging tehnique improves COPD diagnosis and treatment

A team of researchers from the University of Michigan Medical School have developed a new imaging technique that improves diagnosis of COPD. The new technique, called parametric response mapping, or PRM, uses CT scans of patients with COPD�and allows to distinguish different types of lung damage. Co-author Meilan�Han, M.D. MS, a pulmonologist�and COPDGene�UM investigator, said that PRM�is a step forward that allows the sub-classification of patients with COPD. In addition, he added that�better�understanding of the patient’s characteristics�allows more targeted therapies.

COPD Diagnosis And Treatment

COPD�is a chronic respiratory disease characterized by chronic bronchitis and emphysema occurring due to lung tissue damage. In other words, COPD�refers to narrowed airways which means that gas exchanges do not occur as it should. Patients with COPD�often suffer from dyspnea. Of course, the symptoms vary depending on the type of COPD: in those with chronic bronchitis (blue boaters),� the�main symptom is cough while in those with emphysema (pink puffers),� the main symptom is dyspnea. These symptoms are due, on the one hand, to the fact that��the bronchi are filled with mucus(cough) and, on the other hand, due to�destruction of septa between alveoli (dyspnea). COPD�can be kept under control with drugs: bronchodilators�(beta2�adrenergic�receptor agonists) such as salbutamol, corticosteroids (budesonide), anticholinergic�(ipratropium), theophylline etc.

COPD is most commonly associated with smoking, but there are also other factors involved, such as exposure to pollutants,�etc.�It must be said that COPD �is diagnosed using spirometry tests . But spirometry has several limitations because it can not distinguish between different types of lung damage that patient has. In addition, spirometry results are highly dependent on patient cooperation. Spirometry requires the patient to blow several times through�a device called spirometer. Therefore, the results can sometimes be underestimated.

Diagnostic imaging methods such as CT scans, help locate�the emphysema and excludes other lung diseases. PRM�was originally developed to assess the response to treatment of brain tumors but researchers thought to extend the application of this technique�to the lungs. Now with PRM, patients with COPD�may benefit from a more precise diagnosis that carefully examines the small airways. Researchers can create a three-dimensional map of the patient’s lung tissue. This� three-dimensional map tissue reflect the extension of impaired lung tissue: red means very low lung capacity to give off the air of small airways, yellow means low capacity and green means healthy tissue. Lead author Craig Gabana, assistant professor of radiology, said that PRM�is useful in evaluating COPD progression and response to treatment.

Researchers Identify Mechanism Related to Sporadic Parkinson’s Disease

A research team from the Taub Institute at CUMC (Columbia University Medical Center) managed to identify the main mechanism that causes the progressive movement disorder in sporadic Parkinson’s disease patients. This new discovery could bring new therapeutic targets for patients that have Parkinson’s disease. Researchers analyzed tissue from the human brain. The study was published in the journal Nature Communications.

Precedent studies on heritable forms of Parkinson’s disease have shown that a very important role in the onset and development of the disease is played by a protein called alpha-synuclein. Patients that have a higher number of alpha-synuclein gene copies will produce a higher quantity of this protein, thus damaging their neurons. The effect of the protein can be best seen in dopamine neurons. These neurons are located in the substantia nigra (in the mesencephalon, or midbrain) and are responsible for the control of normal movement. Parkinson’s patients also show an excess of alpha-synuclein aggregates in the brain.

Due to the fact that the majority of Parkinson’s disease patients do not have a rare familial mutation, the question about why these patients have an excess of alpha-synuclein protein arises. The loss of dopamine neurons caused by the excess of this proteins is responsible for the onset of the disease.

Parkinson disease

�Through the use of multiple techniques that include gene-network mapping and gene-expression analysis, the researchers from the CUMC, managed to reveal the way alpha-synuclein contributes to the onset of sporadic Parkinson’s disease. “It turns out multiple different alpha-synuclein transcript forms are generated during the initial step in making the disease protein; our study implicates the longer transcript forms as the major culprits”, said professor Asa Abeliovich, who is also the lead author of the study. She added that some particular variants of these alpha-synuclein genes were discovered to increase the risk of sporadic Parkinson’s disease onset.

Dr Abeliovich adds that the study wasn’t based on animal models, instead it was based on a detailed analysis of tissue taken from human patients. The longer forms of the alpha-synuclein gene were found to be specific to human patients, as well as some of the genetic variants that are in close connection to the onset of the disease. The research team also showed that if patients are exposed to environmental toxins that are related to Parkinson’s disease, there is an increase in alpha-synuclein.

The results of the study show that if a drug is capable of reducing the amount of alpha-synuclein transcripts, it could have a major impact in the future treatment of the disease. The research team is currently studying several drug candidates with this property.

Another finding of the study was that of high levels on alpha-synuclein in the blood samples taken from patients that were suffering from sporadic Parkinson’s disease. The blood samples from the control group were did not show the same high levels. Dr Abeliovich concludes that this could lead to using alpha-synuclein as a biomarker for Parkinson’s in the near future.