Neuroscience

Chronic alcohol abuse can severely damage the nervous system, particularly cognitive functions, cerebral metabolism, and brain morphology. Building upon previous findings that alcoholics can experience brain volume recovery with abstinence, this study found that recovery of cerebral gray matter (GM) can take place within the first two weeks of abstinence, but may vary between brain regions.

Results will be published in the January 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

"Shrinkage of brain matter, and an accompanying increase of cerebrospinal fluid, which acts as a cushion or buffer for the brain, are well-known degradations caused by alcohol abuse," explained Gabriele Ende, professor of medical physics in the Department of Neuroimaging at the Central Institute of Mental Health. 
 "This volume loss has previously been associated with neuropsychological deficits such as memory loss, concentration deficits, and increased impulsivity."

"Several processes likely account for changes in brain tissue volume observed through bouts of drinking and abstinence over the course of alcoholism," added Natalie May Zahr, a research scientist in the Department of Psychiatry and Behavioral Sciences at Stanford University School of Medicine. "One process likely reflects true, irreversible neuronal cell death, while another process likely reflects shrinkage, a mechanism that would allow for volume changes in both negative and positive directions, and could account for brain volume recovery with abstinence."

"Gray matter (GM) and white matter (WM) are the main components of the brain that can be distinguished with magnetic resonance imaging (MRI)," explained Ende. "GM consists of neuronal cell bodies, neuropil, glial cells, and capillaries. WM mostly contains myelinated axon tracts."

"Myelin forms an insulating sheath around axons that increases the speed at which they are able to conduct electrical activity," added Zahr. "Because myelin is composed primarily of fat, it gives white matter its color. Cerebrospinal fluid (CSF) is a clear fluid that surrounds and thereby cushions the brain in the skull. Conventional brain structural MRI produces images of protons, with contributions primarily from water and some from fat. Tissue contrast is possible because of the fundamental differences in water content in the primary tissues of the brain: WM consists of about 70 percent water, GM 80 percent, and CSF 99 percent."

Read More →

Decreased activity of a group of genes may explain why in young children the “fear center” of the anxious brain can’t learn to distinguish real threats from the imaginary, according to a new University of Wisconsin study.

The study, published this week in the Proceedings of the National Academy of Sciences (PNAS), lays out evidence that young primates with highly anxious temperaments have decreased activity of specific genes within the amygdala, the brain’s fear center.

The authors hypothesize that this may result in over activity of the brain circuit that leads to higher risk for developing disabling anxiety and depression.

This may be particularly important since the genes involved play a major role in forming the brain connections needed for learning about fears. While all children have fears and anxieties, the authors suggest that children with low levels of activity of these genes develop anxious dispositions because they fail to learn to cope by overcoming their early childhood fears.

“Working with my close collaborator and graduate student, Drew Fox, we focused on understanding the function of genes that promote learning and plasticity in the amygdala,” says Dr. Ned H. Kalin, chair of psychiatry at the University of Wisconsin School of Medicine and Public Health, who led the research. “We found reduced activity in key genes that could impair the ability to sculpt the brain, resulting in a failure to develop the capacity to discriminate between real and imaginary fears.”

Kalin says the study helps support the need for early intervention in children identified as excessively shy and anxious. It may also point a way to better treatments aimed at decreasing the likelihood of children developing more severe psychiatric problems. Anxiety in children is quite common and can lead to anxiety and depression in adolescence and often precedes anxiety disorders, depression and substance abuse in adults.

Most small children go through a phase when they’re frightened of many things, including monsters or new social situations, Kalin says, but their maturing brains soon learn to distinguish real threats from the imaginary. But some children do not adapt, generalize their fears to numerous situations, and may later develop serious anxiety and mood disorders. These children tend to be more sensitive to stress, produce more stress hormones and have heightened nervous-system activity.

Kalin, Fox and co-authors wondered whether some differences in the developing amygdala prevent it from learning how to regulate and adapt to anxiety. Kalin’s earlier work identified a subset of young monkeys, similar to extremely shy children, with an inherited anxious disposition. Using brain imaging, the authors showed that high levels of amygdala activity predicted trait-like anxiety in anxious young primates. Like their stable and enduring anxious dispositions, these individuals also had chronically elevated levels of amygdala activity.

“We believe that this pinpoints a critical region in the brain that determines an individual’s level of trait anxiety,’’ Kalin explains.

In examining a specific part of the amygdala, the central nucleus, the researchers analyzed gene expression, which reflects both environmental and inherited influences. Within the central nucleus of the amygdala the authors found that anxious individuals tended to have decreased expression of a gene called neurotrophic tyrosine kinase, receptor, type 3 (NTRK3). Low levels of this gene that encodes for a brain cell surface receptor may be why the amygdala of an anxious monkey or child is chronically overactive and unable to overcome anxiety and fears.

“This is the first demonstration that the early risk to develop anxiety and depression may be related to the underactivity of particular genes in the developing primate amygdala,’’ Kalin says. “These findings have provided the basis for our hypothesis that can explain the early childhood risk to develop anxiety and depression. It also suggests some creative ways to help children with extreme anxiety by developing new treatments focused on increasing the activity of specific genes involved in facilitating the brain development that underlies fear learning and coping.”

A diverse team of biologists has shown using induced pluripotent stem cells (iPSCs) that a gene mutation that causes malformations in the structure of the nuclear envelope of neural cells, is associated with Parkinson’s disease. In their paper published in the journal Nature, they describe how they found iPSC cells taken from Parkinson’s patients over time demonstrated the same cell disruption found in neural cells taken from other deceased patient’s with the disease. They also found that by introducing a compound known to disrupt the gene mutation, that they could reverse the cell malformation.

Parkinson’s disease is a degenerative disorder of the nervous system characterized by shaking, slowness of movement and difficulty walking. Over time most patients succumb to dementia and eventually die. Much research has centered on the disruption and death of dopamine-generating cells as the root cause of the disorder despite evidence that such a disruption would not result in all of the symptoms Parkinson’s patient’s exhibit. For that reason, researchers have looked to other causes.

In this new effort, the researchers looked at possible reasons for disruption to the nuclear envelope, the thin film that separates the nucleus from the cytoplasm in neural cells. Such disruptions have been associated with Parkinson’s but no definitive correlation has been found, until now.

To gain a better understanding of what might be causing such disruptions, the research team obtained samples of induced iPSCs from Parkinson’s patients and allowed them to grow in an external environment. They noted that the same disruptions occurred as the iPSCs grew into neural cells, suggesting a genetic cause. Prior research had indicated that a mutation of the LRRK2 gene was connected to Parkinson’s disease but no clear indication of the mechanism involved had been found. Testing the cells derived from the iPSCs showed the same mutation, implicating it as a possible cause of the disorder. The researchers also induced the mutation in human embryo stem cells and found that they too developed the same disruption as they grew into neural cells as was found with the iPSCs.

Next the researchers generated a line of iPSCs minus the mutation and found that the cells did not develop the disruptions. They followed that up by adding a chemical compound known to disrupt the mutation to already affected cells and discovered that it prevented them from being disrupted as well.

The researchers don’t know why the mutation occurs but believe a new therapy for treating Parkinson’s patients might be on the horizon as a result of their research.

A study led by researchers at Boston University School of Medicine (BUSM) provides novel insight into the impact that Huntington’s disease has on the brain. The findings, published online in Neurology, pinpoint areas of the brain most affected by the disease and opens the door to examine why some people experience milder forms of the disease than others.

Richard Myers, PhD, professor of neurology at BUSM, is the study’s lead/corresponding author. This study, which is the largest to date of brains specific to Huntington’s disease, is the product of nearly 30 years of collaboration between the lead investigators at BUSM and their colleagues at the McLean Brain Tissue Resource Center, Massachusetts General Hospital and Columbia University.

Huntington’s disease (HD) is an inherited and fatal neurological disorder that typically is diagnosed when a person is approximately 40 years old. The gene responsible for the disease was identified in 1993, but the reason why certain neurons or brain cells die remains unknown.

The investigators examined 664 autopsy brain samples with HD that were donated to the McLean Brain Bank. They evaluated and scored more than 50 areas of the brain for the effects of HD on neurons and other brain cell types. This information was combined with a genetic study to characterize variations in the Huntington gene. They also gathered the clinical neurological information on the patients’ age when HD symptoms presented and how long the patient survived with the disease.

Based on this analysis, the investigators discovered that HD primarily damages the brain in two areas. The striatum, which is located deep within the brain and is involved in motor control and involuntary movement, was the area most severely impacted by HD. The outer cortical regions, which are involved in cognitive function and thought processing, also showed damage from HD, but it was less severe than in the striatum.

The investigators identified extraordinary variation in the extent of cell death in different brain regions. For example, some individuals had extremely severe outer cortical degeneration while others appeared virtually normal. Also, the extent of involvement for these two regions was remarkably unrelated, where some people demonstrated heavy involvement in the striatum but very little involvement in the cortex, and vice versa.

“There are tremendous differences in how people with Huntington’s disease are affected,” Myers said. “Some people with the disease have more difficulty with motor control than with their cognitive function while others suffer more from cognitive disability than motor control issues.”

When studying these differences, the investigators noted that the cell death in the striatum is heavily driven by the effects of variations in the Huntington gene itself, while effects on the cortex were minimally affected by the HD gene and are thus likely to be a consequence of other unidentified causes. Importantly, the study showed that some people with HD experienced remarkably less neuronal cell death than others.

“While there is just one genetic defect that causes Huntington’s disease, the disease affects different parts of the brain in very different ways in different people,” said Myers. “For the first time, we can measure these differences with a very fine level of detail and hopefully identify what is preventing brain cell death in some individuals with HD.”

The investigators have initiated extensive studies into what genes and other factors are associated with the protection of neurons in HD, and they hope these protective factors will point to possible novel treatments.

At ‘rest,’ right hemisphere of the brain ‘talks’ more than the left hemisphere does

People who like to nap say it helps them focus their minds post a little shut eye. Now, a study from Georgetown University Medical Center may have found evidence to support that notion.

The research, presented at Neuroscience 2012, the annual meeting of the Society for Neuroscience, found that when participants in a study rested, the right hemisphere of their brains talked more to itself and to the left hemisphere than the left hemisphere communicated within itself and to the right hemisphere – no matter which of the participants’ hands was dominant. (Neuroscientists say right-handed people use their left hemisphere to a greater degree, and vice versa.)

Results of this study, the first known to look at activity in the two different hemispheres during rest, suggests that the right hemisphere “is doing important things in the resting state that we don’t yet understand,” says Andrei Medvedev, Ph.D., an assistant professor in the Center for Functional and Molecular Imaging at Georgetown. The activities being processed by the right hemisphere, which is known to be involved in creative tasks, could be daydreaming or processing and storing previously acquired information. “The brain could be doing some helpful housecleaning, classifying data, consolidating memories,” Medvedev says. “That could explain the power of napping. But we just don’t know yet the relative roles of both hemispheres in those processes and whether the power nap might benefit righties more then lefties.”

To find out what happens in the resting state, the research team connected 15 study participants to near-infrared spectroscopy (NIRS) equipment. This technology, which is low cost and portable, uses light to measure changes in oxygenated hemoglobin inside the body.

The study participants wore a cap adorned with optical fibers that delivers infrared light to the outermost layers of the brain and then measures the light that bounces back. In this way, the device can “see” which parts of the brain are most active and communicating at a higher level based on increased use of oxygen in the blood and heightened synchronicity of their activities.

"The device can help delineate global networks inside the brain — how the components all work together," Medvedev says. "The better integrated they are, the better cognitive tasks are performed."

To their surprise, the researchers found that left and right hemispheres behaved differently during the resting state. “That was true no matter which hand a participant used. The right hemisphere was more integrated in right-handed participants, and even stronger in the left-handed,” he says.

Medvedev is exploring the findings for an explanation. And he suggests that brain scientists should start focusing more of their attention on the right hemisphere. “Most brain theories emphasize the dominance of the left hemisphere especially in right handed individuals, and that describes the population of participants in these studies,” Medvedev says. “Our study suggests that looking at only the left hemisphere prevents us from a truer understanding of brain function.”

Changes in the ability to smell and taste can be caused by a simple cold or upper respiratory tract infection, but they may also be among the first signs of neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease. Now, new research from the Perelman School of Medicine at the University of Pennsylvania  has revealed an association between an impaired sense of smell and myasthenia gravis (MG), a chronic autoimmune neuromuscular disease characterized by fluctuating fatigue and muscle weakness. The findings are published in the latest edition of PLOS ONE.

Most humans experience five types of tastes: sweet, salty, sour, bitter, and savory.  The sense of taste is mediated by taste receptor cells which are bundled in our taste buds. “Sour” and “bitter” taste sensations alert the body to harmful foods that have spoiled or are toxic. But based on genetics, up to 25 percent of the population cannot detect certain bitter flavors (non-tasters), 25 percent can detect exceedingly small quantities (super-tasters), and the rest of us fall somewhere between these two extremes.

So what exactly does drinking a cup of bitter coffee have to do with chronic sinus infections, which account for approximately 18-22 million physician visits in the U.S. each year?  Recent investigations have shown that these taste receptors (T2Rs) are also found in both upper and lower human respiratory tissue, likely signaling a connection between activation of bitter tastes and the need to launch an immune response in these areas when they are exposed to potentially harmful bacteria and viruses.

“With this information in mind, we wanted to better understand the exact role that bitter taste receptors play in the upper airway, especially between these super and non-tasters,” says Noam Cohen, MD, PhD, assistant professor of Otorhinolaryngology: Head and Neck Surgery, staff physician at the Philadelphia VAMC, and senior author of the new study.

If only there were a way to forget that humiliating faux pas at last night’s dinner party. It turns out there’s not one, but two opposite ways in which the brain allows us to voluntarily forget unwanted memories, according to a study published by Cell Press October 17 in the journal Neuron. The findings may explain how individuals can cope with undesirable experiences and could lead to the development of treatments to improve disorders of memory control.

"This study is the first demonstration of two distinct mechanisms that cause such forgetting: one by shutting down the remembering system, and the other by facilitating the remembering system to occupy awareness with a substitute memory," says lead study author Roland Benoit of the MRC Cognition and Brain Sciences Unit at the University of Cambridge.

Previous studies have shown that individuals can voluntarily block memories from awareness. Although several neuroimaging studies have examined the brain systems involved in intentional forgetting, they have not revealed the cognitive tactics that people use or the precise neural underpinnings. Two possible ways to forget unwanted memories are to suppress them or to substitute them with more desirable memories, and these tactics could engage distinct neural pathways.

Research has found that prion helps our brains to absorb zinc, which is believed to be crucial to our ability to learn and the wellbeing of our memory.

The findings published in Nature Communications show that prion protein regulates the amount of zinc in the brain by helping cells absorb it through channels in the cell surface. It is already known that high levels of zinc between brain cells are linked with diseases such as Alzheimer’s and Parkinson’s.

Professor Nigel Hooper from the University’s Faculty of Biological Sciences explains: “With ageing, the level of prion protein in our brains falls and less zinc is absorbed by brain cells, which could explain why our memory and learning capabilities change as we get older. By studying both their roles in the body, we hope to uncover exactly how prion and zinc affect memory and learning. This could help us better understand how to maintain healthy brain cells and limit the effects of ageing on the brain.”

Whilst the abnormal infectious form of prion - which causes Creutzfeldt-Jakob disease (CJD) in humans and bovine spongiform encephalopathy (BSE) in cattle - has been extensively studied, the Leeds team is among the first to investigate the role of the ‘normal’ form of the protein.

Lead researcher, Dr Nicole Watts, says: “Zinc is thought to aid signalling in the brain as it’s released into the space between brain cells. However, when there’s too much zinc between the brain cells it can become toxic.  High levels of zinc in this area between the brain cells are known to be a factor in neurodegenerative diseases, so regulating the amount of absorption by the cells is crucial.”

The research, funded by the Medical Research Council, Wellcome Trust and Alzheimer’s Research UK, may have implications for how we treat - and possibly prevent - neurodegenerative diseases in the future.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said: “We’re pleased to have helped support this study, which has uncovered new information that could one day aid the development of new treatments for Alzheimer’s. One next step would be to understand how regulating zinc levels may affect the progress of the disease. Results like these have the potential to lead to new and effective treatments - but for that to happen, we must build on these results and continue investing in research.”

People in creative professions are treated more often for mental illness than the general population, there being a particularly salient connection between writing and schizophrenia. This according to researchers at Karolinska Institutet, whose large-scale Swedish registry study is the most comprehensive ever in its field.

Last year, the team showed that artists and scientists were more common amongst families where bipolar disorder and schizophrenia is present, compared to the population at large. They subsequently expanded their study to many more psychiatric diagnoses - such as schizoaffective disorder, depression, anxiety syndrome, alcohol abuse, drug abuse, autism, ADHD, anorexia nervosa and suicide - and to include people in outpatient care rather than exclusively hospital patients.

The present study tracked almost 1.2 million patients and their relatives, identified down to second-cousin level. Since all were matched with healthy controls, the study incorporated much of the Swedish population from the most recent decades. All data was anonymized and cannot be linked to any individuals.

The results confirmed those of their previous study: certain mental illness - bipolar disorder - is more prevalent in the entire group of people with artistic or scientific professions, such as dancers, researchers, photographers and authors. Authors specifically also were more common among most of the other psychiatric diseases (including schizophrenia, depression, anxiety syndrome and substance abuse) and were almost 50 per cent more likely to commit suicide than the general population.

The researchers also observed that creative professions were more common in the relatives of patients with schizophrenia, bipolar disorder, anorexia nervosa and, to some extent, autism. According to Simon Kyaga, consultant in psychiatry and doctoral student at the Department of Medical Epidemiology and Biostatistics, the results give cause to reconsider approaches to mental illness.

"If one takes the view that certain phenomena associated with the patient’s illness are beneficial, it opens the way for a new approach to treatment," he says. "In that case, the doctor and patient must come to an agreement on what is to be treated, and at what cost. In psychiatry and medicine generally there has been a tradition to see the disease in black-and-white terms and to endeavour to treat the patient by removing everything regarded as morbid."

Cigarettes have already been linked to a plethora of different diseases and adverse health conditions, and now a new study has found that the smoking could also increase the risk of developing cataracts in some individuals.

Dr. Juan Ye of the Zhejiang University Institute of Ophthalmology and colleagues conducted a meta-analysis, reviewing a dozen cohorts and eight case-control studies from five continents (Africa, Asia, Australia, Europe and North America) to determine smoking’s impact on the development of age-related cataracts, the leading cause of vision loss and blindness in the world.

They looked at the occurrence of age-related cataract in individuals who had smoked cigarettes versus those who had never lit up. They also looked at the differences between former and current smokers, as well as each of the three different types of cataract that can develop in older individuals, the Association for Research and Vision in Ophthalmology (ARVO) explained in an October 12 press release.

“The results showed that every individual that ever smoked cigarettes was associated with an increased risk of age-related cataract, with a higher risk of incidence in current smokers,” they said, adding that “former and current smokers showed a positive association with two of the subtypes: nuclear cataract, when the clouding is in the central nucleus of the eye, and subscapular cataract, when the clouding is in the rear of the lens capsule.”

The study did not find a link between smoking and cortical cataract, a type of cataract in which the cortex of the lens is affected by cloudiness. Their findings have been published in the journal Investigative Ophthalmology & Visual Science (IOVS).

“Although cataracts can be removed surgically to restore sight, many people remain blind from cataracts due to inadequate surgical services and high surgery expenses,” Ye said. “Identifying modifiable risk factors for cataracts may help establish preventive measures and reduce the financial as well as clinical burden caused by the disease.”

“We think our analysis may inspire more high-quality epidemiological studies” the study author added. “Our analysis shows that association between smoking and the risk of age-related cataract differ by subtypes, suggesting that pathophysiologic processes may differ in the different cataract types.”

In a study that challenges the long-held notion that the primary function of sleep is to give rest to the brain, researchers have found that not getting enough shut-eye has a harmful impact on fat cells, reducing by 30 percent their ability to respond to insulin, a hormone that regulates energy.

Sleep deprivation has long been associated with impaired brain function, causing decreased alertness and reduced cognitive ability. The latest finding—published by University of Chicago Medicine researchers in the Oct. 16 issue of the Annals of Internal Medicine—is the first description of a molecular mechanism directly connecting sleep loss to the disruption of energy regulation in humans, a process that can lead over time to weight gain, diabetes and other health problems. The study suggests that sleep’s role in energy metabolism is at least as important as it is in brain function.

"We found that fat cells need sleep to function properly," said study author Matthew Brady, PhD, associate professor of medicine and vice-chair of the Committee on Molecular Metabolism and Nutrition at the University of Chicago.

Read more

Assessing consciousness may seem like the ultimate exercise in subjectivity, but some researchers are moving closer to what they call an objective measure.

The goal is to provide clearer information for families with loved ones living in vegetative or minimally conscious states — conditions that are often caused by brain trauma or cardiac arrest.

“We really need to find a way to be able to measure consciousness reliably,” says Melanie Boly, a postdoctoral fellow at the Belgian National Fund for Research in Liege, Belgium. “For the family, this changes everything,” says Boly, who presented her team’s research on 14 October at the Society for Neuroscience meeting in New Orleans, Louisiana.

Vegetative patients make only reflexive movements and appear insensitive to their surroundings, while minimally conscious patients can make some purposeful movements and even feel pain. Clinically, the differences between these patients can be difficult even for experienced physicians to discern. But legally, the differences are clear.

In 2011, the UK court system denied a family’s request to end life support for their daughter after additional tests revised her initial diagnosis from ‘vegetative’ to ‘minimally conscious’.

To derive a numerical measure of consciousness, Boly and her colleagues pulsed subjects’ heads with a brief electromagnetic wave, then measured neural responses using electrodes stuck to the scalp.

In 32 healthy, awake people, the electromagnetic impulse sent complex patterns of electrical activity reverberating throughout the brain. In healthy sleeping people, or people under general anaesthesia, the brain displayed shorter, simpler responses that stayed closer to the site of the initial stimulation. The researchers quantified these differences in a measure of response complexity.

In six patients diagnosed as vegetative, the electromagnetic pulse elicited responses with complexity indices similar to those in sleeping or anaesthetized healthy subjects. Twelve minimally conscious patients showed slightly more complex responses. And two ‘locked-in’ patients — people who are fully conscious but unable to move or communicate — showed complexity indices similar to healthy, awake subjects.

Boly and her colleagues have previously noted some of these differences across patient groups but with poor reliability for individual patients. With the complexity index, which combines several aspects of the brain’s response, she says, “this is the first time we really have a measure that works at a single-subject level.”

“It’s not going to supplant a clinical assessment,” says Nicholas Schiff, a neurologist at the Weill Cornell Medical College in New York. But he says the complexity index could become a valuable tool for adding some certainty to the subjective process of evaluating patient consciousness.

“I personally would welcome a test that could provide us with objective measurements,” says David Okonkwo, clinical director of the Brain Trauma Research Center at the University of Pittsburgh in Pennsylvania. However, he said much more testing is needed to tell whether the complexity index meets that standard.

“We need more patients,” agrees Boly, “but it’s extremely promising.”

Rapamycin, a drug used to prevent rejection in transplants, could delay the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. This is the main conclusion of a study published in the Nature in which has collaborated the researcher Isidro Ferrer, head of the group of Neuropathology at the Bellvitge Biomedical Research Institute (IDIBELL) and the Bellvitge University Hospital and Full Professor of Pathological Anatomy at the University of Barcelona. The research was led by researchers from the International School for Advanced Studies (SISSA) in Trieste (Italy).

The collaboration of the research group led by Dr. Ferrer with SISSA researchers began five years ago when they observed that Parkinson’s patients showed a deficit in UCHL1 protein. At that time, researchers didn’t know what mechanism produced this deficit. To discover it a European project was launched. It was coordinated by the Italian researchers and participated by other European research groups, including the group led by Dr. Ferrer. The project, called Dopaminet, focused on how dopaminergic neurons (brain cells whose neurotransmitter is dopamine) are involved in Parkinson’s disease.

Contrary to most common hypothesis that a DNA fragment encodes a protein through a messenger RNA molecule, the researchers found that it also works in reverse. They found a balance between the protein and its mirror protein, which is configured in reverse, and they are mutually controlled. If the protein mirror is located in the nucleus of the cell, it does not interact with the protein, while if it is in the cytoplasm, then both of them interact.

In the case of Parkinson’s disease the protein UCHL1 appears reduced and also its mirror protein is localized in the nucleus, and in the cytoplasm. Thus, the researchers sought a method to extract the mirror protein from the nucleus and made it interact with the original UCHL1 protein. The authors found that rapamycin was able to extract them from the nucleus. The drug allows the two proteins, the UCHL1 and its mirror, hold together in the cytoplasm, which would correct the mistakes that occur in Parkinson’s disease.

This in vitro research has allowed describing a new unknown mechanism. It is necessary that the UCHL1 mirror protein should accumulate in the nucleus and escape from the cytoplasm and join the UCLH1 protein. The combination of both makes the system work.

"The rapamycin can not cure Parkinson’s disease, but it may delay the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s itself. Rapamycin can protect and delay the beginning of these diseases. It can complete the treatment, but it should be combined with other existing treatments", explains Isidro Ferrer.

Anyway, it is still far its application in patients. The next step is to validate these results in animal models and study the effects of rapamycin in combination with other drugs.