“It appears from our research that administering Vitamin K2 could possibly help patients with Parkinson’s. However, more work needs to be done to understand this better,” said Patrik Verstreken, who is associated with The Flanders Institute for Biotechnology and KU Leuven. He also worked with colleagues at Northern Illinois University on the research, which has been published online in the journal Science.

Verstreken uses a factory to explain what happens with Parkinson’s patients: “If we looked at cells as small factories, then mitochondria would be the power plants responsible for supplying the energy for their operation. In Parkinson’s patients, the activity of mitochondria and the transport of electrons have been disrupted, resulting in the mitochondria no longer producing sufficient energy for the cell. This has major consequences as the cells in certain parts of the brain will start dying off, disrupting communication between neurons. The results are the typical symptoms of Parkinson’s: Lack of movement (akinesia), tremors and muscle stiffness.

While the exact cause of Parkinson’s is not known, scientists have been able to pinpoint several genetic defects found in Parkinson’s patients, including the so-called PINK1 and Parkin mutations, which both lead to reduced mitochondrial activity, the researcher said.

For their research, Verstreken and his team used fruit flies with a genetic defect in PINK1 or Parkin that is similar to the one associated with Parkinson’s. They found that the flies with a PINK1 or Parkin mutation lost their ability to fly.

Upon closer examination, they discovered that the mitochondria in these flies were defective, just as in Parkinson’s patients. Because of this they generated less intracellular energy – energy the insects needed to fly. When the flies were given Vitamin K2, the energy production in their mitochondria was restored and the insects’ ability to fly improved. The researchers determined that the energy production was restored because the Vitamin K2 had improved electron transport in the mitochondria.

Because defective mitochondria are also found in Parkinson’s patients with a PINK1 or Parkin mutation, Vitamin K2 potentially offers hope for a new treatment for Parkinson’s, the researcher concludes.

Source: The Flanders Institute for Biotechnology

A pilot study on a handful of people suggests that deep brain stimulation, a therapy already used in some patients with Parkinson’s disease and depression, may offer hope for at least some with Alzheimer’s.

Alzheimer’s disease is a progressive and lethal dementia that mostly strikes the elderly, affecting memory, thinking and behavior. Experts estimate that as many as 5.1 million Americans may have Alzheimer’s — and that number is expected to skyrocket as baby boomers age.

The study was designed to establish the safety of the brain pacemaker and involved just six people, said the study’s first author, Gwenn Smith, Ph.D., a professor in the department of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine.

The research, published in the Archives of Neurology, was conducted while Smith was on the faculty at the University of Toronto, and will be continuing at Toronto, Hopkins and other U.S. sites in the future. The study was led by Andres M. Lozano, M.D., chairman of the department of neurosurgery at the University of Toronto.

Smith notes that while the study needs to be replicated on a larger scale, there is not another treatment for Alzheimer’s “that shows such promising effects on brain function.”

One month and one year after implanting a device that allows for continuous electrical impulses to the brain, Smith and her colleagues performed PET scans that detect changes in the metabolism of glucose in the brain’s cells. The scans showed that patients with mild forms of Alzheimer’s showed sustained increases in glucose metabolism, an indicator of neuronal activity. The increases were larger than those found in patients who have taken the drugs currently marketed to fight the progression of Alzheimer’s, the researchers note.

Other imaging studies have shown that a decrease in glucose metabolism over the course of a year is typical in the disease.

The researchers observed roughly 15 percent to 20 percent increases in glucose metabolism after one year of continuous stimulation. The increases were observed in patients with better outcomes in cognition, memory and quality of life. In addition, the stimulation increased connectivity in brain circuits associated with memory.

Deep brain stimulation (DBS) requires surgical implantation of a brain pacemaker, which sends electrical impulses to specific parts of the brain. For the study, surgeons implanted a tiny electrode able to deliver a low-grade electrical pulse close to the fornix, a key nerve tract in brain memory circuits.

The trial came about when Lozano used DBS on the fornix to treat an obese man. The procedure, designed to target the regions of the brain involved in appetite suppression, unexpectedly brought about significant increases in his memory, according to Smith.

Smith, who also is director of the Division of Geriatric Psychiatry and Neuropsychiatry at Johns Hopkins Bayview Medical Center, is an authority on mapping the brain’s glucose metabolism in aging and psychiatric disease. It was her earlier analysis of Alzheimer’s patients’ PET scans that revealed their pattern of lowered brain metabolism. She determined that specific parts of the temporal and parietal cerebral cortex — memory network areas of the brain where Alzheimer’s earliest pathology surfaces— became increasingly sluggish with time.

The new study was supported by grants from the Neurosurgical Research and Education Foundation, the Dana Foundation and the Krembil Neuroscience Discovery Fund.

Source: Johns Hopkins Medical Institutions

Parkinson’s is defined by a gradual loss of nerve cells of neurons that produce a chemical called dopamine. Dopamine is essential for normal function of muscles and other body organs.

Researchers have learned that changes in a gene known as DJ-1 also leads to an accelerated loss of dopaminergic neurons and results in the onset of Parkinson’s symptoms at a young age.

Although people naturally lose dopamine-producing neurons as part of the aging process, Parkinson’s patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person.

The ability to modify the activity of DJ-1 could change the progress of the disease, said Dr. Nirit Lev, a researcher at Tel Aviv University. Working in collaboration with Profs. Dani Offen and Eldad Melamed, she has now developed a peptide which mimics DJ-1′s normal function, thereby protecting dopamine-producing neurons.

Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson’s patient or aging normally, Lev said.

The peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.

The new peptide is structured from DJ-1 and has been shown to stop neurodegeneration, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain.

Lev said that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.

In the study, researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle.

“We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain,” said Lev.

In preclinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson’s disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement.

Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.

Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this one does not. Additionally, it provides a safe treatment option because peptides are organic to the body itself.

Lev believes the peptide could fill a gap in the treatment of Parkinson’s disease. “Current treatments are lacking because they can only address symptoms — there is nothing that can change or halt the disease,” she said. “Until now, we have lacked tools for neuroprotection.”

Source: American Friends of Tel Aviv University

Researchers found the latest generation of antidepressant medications can ease depression in Parkinson’s patients without worsening other symptoms of the disease.

“Depression is the number-one factor negatively affecting the quality of life for people with Parkinson’s disease,” said Irene Hegeman Richard, M.D., who led the study.

“It causes a great deal of suffering among patients. The great news here is that it’s treatable. And when the depression is treated adequately, many of the other symptoms become much more manageable for patients.”

The findings are good news for patients with Parkinson’s disease, as about half of Parkinson’s patients also struggle with depression.

“It’s very important to note that these patients are not depressed simply because they are dealing with a chronic neurological condition,” said Richard. “Rather, the depression is caused by the underlying disease process, which also causes problems with movement and balance.”

Older tricyclic depression medications reduced depression but had significant side effects. This discovery caused physician to be cautious in the use of the newer class of antidepressant called selective serotonin reuptake inhibitors (SSRIs).

That led physicians to try newer medications in Parkinson’s patients. However, some smaller studies with these medications had mixed results, leaving some physicians to question whether these drugs were actually of any benefit. In addition, there was some concern that they might worsen patient’s motor symptoms.

The new study sought to review the issue in detail. With funding from the National Institute of Neurological Disorders and Stroke, Richard launched the Study of Antidepressants in Parkinson’s Disease or SAD-PD.

The effort included 115 people with Parkinson’s disease at 20 sites in the United States, Canada, and Puerto Rico. All the participants had Parkinson’s disease and met the criteria for depression.

About one-third of the participants received paroxetine (brand name Paxil), a selective serotonin reuptake inhibitors (SSRIs); one-third received venlafaxine extended release (brand name Effexor), a serotonin and norepinephrine reuptake inhibitor (SNRI); and one-third received a placebo.

On average, the people receiving paroxetine had a 59 percent improvement and those receiving venlafaxine had a 52 percent improvement in their scores, according to the Hamilton Rating Scale for Depression.

People who received the placebo had a 32 percent improvement. Three other depression rating scales showed similar results. The drugs were generally well tolerated and did not lead to any worsening in motor functioning.

The findings culminate a decade-long research effort by Richard. Today, people are becoming more knowledgeable that depression is oftentimes part of the disease, said Richard, who has witnessed striking improvement in many patients after effective treatment.

“After treatment for depression, patients and their families often see a dramatic difference in how they’re feeling, within a few weeks or months. They have more interest in things. They have more energy; they’re sleeping better. And oftentimes there is a great sense of relief, and a huge burden has been lifted,” said Richard.

She added that sometimes it can be difficult to spot depression in patients, because some symptoms overlap with other symptoms of Parkinson’s. For instance, Parkinson’s patients will be less animated, their voice will be less expressive, and many will have sleep difficulties — but they may not be depressed. Therefore, careful diagnosis is crucial.

The study is published online in Neurology.

Source: University of Rochester Medical Center

Elderly man taking meds photo by shutterstock.

“Our research shows that curcumin can rescue proteins from aggregation, the first steps of many debilitating diseases,” said Dr. Lisa Lapidus, MSU associate professor of physics and astronomy. “More specifically, curcumin binds strongly to alpha-synuclein and prevents aggregation at body temperatures.”

Proteins are chains of amino acids that are responsible for doing most of the work in cells. Although scientists understand their structure, it is still unclear how they are built—a process known as folding. Through the use of lasers, Lapidus’ team studied the folding process by correlating the speed at which the protein would fold with its tendency to clump or bind with other proteins.

When curcumin binds to the protein alpha-synuclein, it not only stops clumping, but it also boosts the protein’s folding or reconfiguration rate. As the protein folds at a faster pace, it moves out of the dangerously slow speed zone which would cause it to clump with other proteins.

Doctors won’t be prescribing curcumin pills any time soon, though, Lapidus said.

“Curcumin’s usefulness as an actual drug may be pretty limited since it doesn’t go into the brain easily where this misfolding is taking place,” she said. “But this kind of study showcases the technique of measuring reconfiguration and opens the door for developing drug treatments.”

The study, led by Basir Ahmad, an MSU postdoctoral researcher, is published in the Journal of Biological Chemistry.

Source:  Michigan State University

Mayo Clinic researchers discovered the risk of developing mild cognitive impairment or Parkinson’s disease comes within four years of diagnosis of the sleep disorder.

The muscle relaxation that occurs during REM sleep leaves a person in a state of paralysis; in contrast, people with rapid eye movement sleep behavior disorder (RBD) appear to act out their dreams when they are in REM sleep.

Investigators were able to diagnose RBD by using the Mayo Sleep Questionnaire among people who were otherwise neurologically normal.

Investigators found that approximately 34 percent of people diagnosed with probable RBD developed mild cognitive impairment or Parkinson’s disease within four years of entering the study, a rate 2.2 times greater than those with normal rapid eye movement sleep.

“Understanding that certain patients are at greater risk for mild cognitive impairment or Parkinson’s disease will allow for early intervention, which is vital in the case of such disorders that destroy brain cells. Although we are still searching for effective treatments, our best chance of success is to identify and treat these disorders early, before cell death,” said co-author Brad Boeve, M.D., a Mayo Clinic neurologist.

Previous studies have shown that an estimated 45 percent of people who suffer from rapid eye movement sleep behavior disorder will develop a neurodegenerative syndrome such as mild cognitive impairment or Parkinson’s disease within five years of diagnosis.

“This study is the first to quantify the risk associated with probable RBD in average people, not clinical patients, and it shows that we can predict the onset of some neurodegenerative disorders simply by asking a few critical questions,” said lead author Brendon P. Boot, M.D., a behavioral neurologist. 

• MCI is an intermediate stage between the expected cognitive decline of normal aging and the more pronounced decline of dementia. It involves problems with memory, language, thinking and judgment that are greater than typical age-related changes.
• An estimated 500,000 Americans suffer from Parkinson’s disease, which is characterized by tremor or shakiness, stiffness of the limbs and trunk, slowness of movement, and impaired balance and coordination.

The study is published in the journal Annals of Neurology.

Source: Mayo Clinic

Treatment advances are being tested in patients or are scheduled to begin clinical trials soon.

The long-standing theory regarding glaucoma was that vision damage was caused by unusually high pressure inside the eye, known as intraocular pressure (IOP). Therefore, lowering IOP was the focus of surgical techniques and medications; developing tests and instruments to measure and track IOP was vital to that effort.

Although measuring a patient’s IOP is still a key part of glaucoma treatment, it is no longer the only method an ophthalmologist uses to diagnose glaucoma. Even when surgery or medication successfully lowers IOP, some glaucoma patients continue to lose vision.

Also, some patients find it difficult to use eye drop medications as prescribed by their physicians. These problems encouraged researchers to look beyond IOP as a cause of glaucoma and focus of treatment.

The new research model focuses on the damage that occurs in a type of nerve cell called retinal ganglion cells (RGCs), which connect the eye to the brain through the optic nerve and are vital to vision.

RGC-targeted glaucoma treatments now in clinical trials include: medications injected into the eye that deliver survival and growth factors to RGCs; medications known to be useful for stroke and Alzheimer’s, such as cytidine-5-diphosphocholine; and electrical stimulation of RGCs, delivered through tiny electrodes implanted in contact lenses or other external devices. Human trials of stem cell therapies are in the planning stages.

“As researchers turn their attention to the mechanisms that cause retinal ganglion cells to degenerate and die, they are discovering ways to protect, enhance and even regenerate these vital cells,” said Jeffrey L Goldberg, M.D., Ph.D., assistant professor of ophthalmology at the Bascom Palmer Eye Institute and Interdisciplinary Stem Cell Institute.

“Understanding how to prevent damage and improve healthy function in these neurons may ultimately lead to sight-saving treatments for glaucoma and other degenerative eye diseases.”

Based on these findings, future glaucoma treatments may not only prevent blindness, but may actually restore vision. It may also help scientists determine which factors—such as genetics—make some people more susceptible to glaucoma.

The review is published in Ophthalmology.

Source:  American Academy of Ophthalmology

European scientists discovered Parkinson’s disease patients can suddenly become creative when they take dopamine therapy, producing pictures, sculptures, novels and poetry. However, the extreme focus on the new interests may limit performance of normal daily tasks and social activities.

In the study, Italian researchers studied 36 patients with Parkinson’s disease — 18 with increased artistic production and 18 without — and compared them with 36 healthy controls without Parkinson’s. None of the patients had engaged in artistic hobbies before they took dopamine.

“Patients were included in the artistic group if they started working on creative projects for two or more hours a day after starting taking dopamine” explains lead author Dr Margherita Canesi.

“Our findings suggest that the patients’ newly acquired artistic skills were probably there all along, but did not start to emerge until they took the dopamine therapy.

“They did not appear to be connected with abnormal repetitive behaviors, such as impulse control disorders or punding – stereotyped behavior characterized by an intense fascination with a complex, excessive, non-goal oriented, repetitive activity.

“Other researchers have noted that altered creative drive has been observed in patients who have neurodegenerative diseases or have had a stroke. However the anatomical and physiological understanding of creativity is difficult to establish and quantify.”

Dopamine is a neurotransmitter that helps control the brain’s reward and pleasure centers. It helps to regulate movement and emotional responses and enables people to see rewards and work towards them.
A deficiency in dopamine is the critical factor influencing Parkinson’s disease. Physicians often prescribe dopamine therapy to increase dopamine levels in the brain.

Key findings of the study included:

• The artwork presented by the patients was mainly drawings/paintings (83%), poetry/novels (50%) and sculpture (28%). In 78% of cases, the patients showed more than one skill, normally writing plus painting or drawing.
• Some of the patients produced art that was sold and books that were published, but, at the other end of the scale, some of the creative work was of a very poor quality.
• By using the Torrence Test of Creative Thinking to compare the three groups, the researchers showed that the artistic Parkinson’s Disease patients had similar overall and individual scores to the healthy controls. However the non-artistic patients had significantly lower overall scores than the healthy controls and significantly lower scores than the artistic patients when it came to the elaboration sub-score.
• There was no correlation between the Torrence Test of Creative Thinking scores and the scores obtained using the Barratt Impulsivity Scale, one of the oldest and most widely used measures of impulsive personality traits.
• The researchers also used the Minnesota Impulsive Disorders Interview. This showed that one creative patient was positive for compulsive sexual behaviour, one creative patient for compulsive buying and two creative and three non-creative patients for pathological gambling. However, there was little difference in the Torrence scores for patients who tested positive or negative on the Minnesota scale.
• None of the patients or healthy controls displayed the stereotyped behaviour measured by the Punding Rating Scale.

“In conclusion, we found that newly acquired creative drive in patients with Parkinson’s Disease, after the introduction of dopaminergic therapy, is not related to impulsivity or impulse control disorders as measured by the Barratt Impulsivity Scale or the Minnesota Impulsive Disorders Interview” says Dr Canesi.

“We believe that their desire to be creative could represent emerging innate skills, possibly linked to repetitive and reward-seeking behaviours. Further studies are needed to support our preliminary observations.”

Source: Wiley-Blackwell

Elderly man holding paint brushes photo by shutterstock.

“While we have known that many different types of exercise can benefit Parkinson’s patients over short time periods, we did not know whether exercise improves the motor symptoms of Parkinson’s over the long term,” said study author Daniel Corcos, Ph.D., with the University of Illinois at Chicago.

For the study, 48 people with Parkinson’s disease were put in one of two groups. The first was assigned to progressive resistance exercise, known as weight training. The other was assigned to the exercise known as fitness counts, which includes flexibility, balance and strengthening exercises.

The groups exercised for one hour, twice a week, for two years.

The severity of symptoms, including tremors, was measured using the Unified Parkinson’s Disease Rating Scale (UPDRS) after six, 12, 18 and 24 months of exercise, Corcos said. Scores were taken when the participants were not taking their medication.

While both forms of exercise reduced symptoms at six months, participants who did weight training saw a 7.3 point improvement in their UPRDS score after two years while the fitness counts group returned to the same scores they had at the start of the study.

“Our results suggest that long-term weight training could be considered by patients and doctors as an important component in managing Parkinson’s disease,” said Corcos.

The study was supported by a grant from the National Institutes of Health.

Source: The American Academy of Neurology

In an exercise study conducted by researchers at the Oregon Research Institute, tai chi training resulted in improved postural stability and walking ability, as well as reduced falls in the participants.

“These results are clinically significant because they suggest that Tai Chi, a low-to-moderate impact exercise, may be used as an add-on to current physical therapies, to address some of the key clinical problems in Parkinson’s disease, such as postural and gait instability,” said Fuzhong Li, Ph.D.

“Since many training features in the program are functionally oriented, the improvements in the balance and gait measures that we demonstrated highlight the potential of tai chi-based movements in rehabilitating patients with these types of problems and, consequently, easing cardinal symptoms of Parkinson’s disease and improving mobility, flexibility, balance, and range of motion.”

In the four-year project funded by the National Institute of Neurological Disorders and Stroke, researchers randomly assigned 195 patients to one of three exercise groups: tai chi, resistance training, or stretching. The patients participated in 60-minute exercise sessions twice a week for 24 weeks.

The results of the study showed that the tai chi group performed consistently better than the stretching group in how far they could lean in any direction without losing balance, as well as demonstrating better levels of directional control of the body and walking ability, such as longer stride length. tai chi participants also outperformed those in the resistance training group on the balance and stride length measures.

Finally, tai chi training was shown to significantly lower the incidence of falls compared to stretching, and was as equally effective as resistance training in reducing falls.

As Parkinson’s disease progresses, patients lose stability and have trouble walking, difficulty managing activities required of daily living, and experience frequent falls. Exercise is an important part of the management of Parkinson’s disease because physical activity has been shown to retard the deterioration of motor function and to prolong functional independence. However, research on alternative forms of exercise, such as tai chi, that could improve balance, gait, and function in patients with Parkinson’s disease is scarce, the researcher notes.

The program developed by Li consisted of six tai chi movements integrated into a routine that focused on weight-shifting, controlled-displacement of the center of gravity over the base of support, ankle sway, and front-to-back and sideways stepping. Natural breathing was integrated into the training routine.

“There are a number of practical advantages to using tai chi to improve motor dysfunction of Parkinson’s disease,” he said. “It is a low-cost activity that does not require equipment, it can be done anywhere, at any time, and the movements can be easily learned. It can also be incorporated into a rehabilitation setting as part of existing treatment. Similarly, because of its simplicity, certain aspects of this tai chi program can also be prescribed to patients as a self-care/home activity.”

Source: Oregon Research Institute

Elderly man performing tai chi photo by shutterstock.

The research on brain activity during competitive social interactions is described in a paper in the Proceedings of the National Academy of Sciences.

Experts say this is the first investigation to use a computational approach to analyze differing patterns of brain activity during these interactions.

“When players compete against each other in a game, they try to make a mental model of the other person’s intentions, what they’re going to do and how they’re going to play, so they can play strategically against them,” said University of Illinois postdoctoral researcher Kyle Mathewson, Ph.D. “We were interested in how this process happens in the brain.”

Previous studies have tended to consider only how one learns from the consequences of one’s own actions, called reinforcement learning, Mathewson said.

These studies have found heightened activity in the basal ganglia, a set of brain structures known to be involved in the control of muscle movements, goals and learning. Many of these structures signal via the neurotransmitter dopamine.

“That’s been pretty well studied and it’s been figured out that dopamine seems to carry the signal for learning about the outcome of our own actions,” Mathewson said.

“But how we learn from the actions of other people wasn’t very well characterized.”

Researchers call this type of learning “belief learning.”

Investigators used functional magnetic resonance imaging (fMRI) to track activity in the brains of participants while they played a competitive game, called a Patent Race, against other players.

The goal of the game was to invest more than one’s opponent in each round to win a prize (a patent worth considerably more than the amount wagered), while minimizing one’s own losses (the amount wagered in each trial was lost). The fMRI tracked activity at the moment the player learned the outcome of the trial and how much his or her opponent had wagered.

A computational model evaluated the players’ strategies and the outcomes of the trials to map the brain regions involved in each type of learning.

“Both types of learning were tracked by activity in the ventral striatum, which is part of the basal ganglia,” Mathewson said. “That’s traditionally known to be involved in reinforcement learning, so we were a little bit surprised to see that belief learning also was represented in that area.”

Belief learning also spurred activity in the rostral anterior cingulate, a structure deep in the front of the brain. This region is known to be involved in error processing, regret and “learning with a more social and emotional flavor,” Mathewson said.

The findings offer new insight into the workings of the brain as it is engaged in strategic thinking, says co-author Ming Hsu. This in turn may aid the understanding of neuropsychiatric illnesses that undermine those processes.

“There are a number of mental disorders that affect the brain circuits implicated in our study,” Hsu said.

“These include schizophrenia, depression and Parkinson’s disease. They all affect these dopaminergic regions in the frontal and striatal brain areas. So to the degree that we can better understand these ubiquitous social functions in strategic settings, it may help us understand how to characterize and, eventually, treat the social deficits that are symptoms of these diseases.”

Source: University of Illinois

Woman playing cards photo by shutterstock.

The finding, reported in the online version of The Lancet Neurology journal is published by researchers at the University of Florida and 14 additional medical centers.

In the study, sponsored by a manufacturer of DBS devices, researchers found a constant current device helped to manage the symptoms of Parkinson’s.

Investigators say the device is designed to reduce tremors, improve the slowness of movement, decrease the motor disability of the disease and reduce involuntary movements that often are a side-effect of Parkinson medications.

After treatment, researchers analyzed 136 patient diaries and discovered longer periods of effective symptom control — known as “on time” — without involuntary movements.

“On time” for patients who received stimulation increased by an average of 4.27 hours compared with an increase of 1.77 hours in the group without stimulation.

Patients also noted overall improvements in the quality of their daily activities, mobility, emotional state, social support and physical comfort.

“I think it is safe to say since dopamine treatment emerged in the 1960s, DBS has been the single biggest symptomatic breakthrough for Parkinson patients who have experienced the fluctuations associated with levodopa therapy,” said Michael S. Okun, M.D., first author of the study, and the National Medical Director for the National Parkinson Foundation.

“This study validates the use of mild electrical currents delivered to specific brain structures in order to improve Parkinson’s disease in select patients with advanced symptoms, and additionally, it explored a new stimulation paradigm. Future improvements in devices and the delivery systems for DBS will hopefully provide exciting new opportunities for Parkinson’s sufferers.”

Researchers studied the effects of DBS on patients who have had Parkinson’s disease for five years or more. They were randomly assigned to a control group that delayed the onset of stimulation for three months, or a group whose stimulation began shortly after surgery.

All patients were followed for 12 months.

The deep brain stimulation procedure involves surgeons implanting small electrodes into an area of the patient’s brain that controls movement. The electrodes are connected to a device precisely programmed to use mild electrical current to modulate problematic brain signals that result in movement problems.

Technological advances over the past decade have greatly improved the ability to deliver and control DBS.

In the current study, voltage-controlled DBS devices delivered pulses of current that varied slightly with surrounding tissue changes.

Researchers believe the current system enables patients to have better motor control and an improvement in their quality of life when compared to the control group. The U.S. Food and Drug Administration approved the use of DBS for Parkinson’s disease in 2002.

At least 500,000 people in the United States suffer from Parkinson’s with about 50,000 new cases reported annually, according to the National Institute of Neurological Disorders and Stroke. These numbers are expected to increase as the average age of the population rises.

“The study answered some very important questions concerning cognition and mood with lead implantation (alone) versus implantation with stimulation. It also refutes the hypothesis that DBS increases depressive symptoms,” said Gordon H. Baltuch, M.D., Ph.D.

“The group’s results also showed a decrease in the infection rate to 4 percent from previously published 10 percent. It shows that American neurosurgeons and neurologists with their industry partners are improving the safety of this procedure and working in a collaborative fashion.”

Comparable with other large DBS studies, the most common serious adverse event revealed was infection, which occurred in five patients. Likewise, some participants also reported an increase in the occurrence of slurred speech, known as dysarthria.

“Technology is on the move, and we expect to see continued improvements to DBS approaches, equipment and materials,” said Okun. “DBS has set the bar high for the development of new therapies for advanced Parkinson’s disease patients.”

Source: University of Florida

PET technology is an advanced radiological method that provides functional images of biological processes. In the analysis, researchers discovered a molecular imaging technique that combines PET with an injected biomarker called 18F-FDG helps to pinpoint key areas of metabolic decline in the brain indicating dementia.

Researchers believe use of PET will provide clinicians with physiological evidence of neurodegenerative disease. This knowledge will expedite and improve the accuracy of physician diagnosis.

“The new data support the role of 18F-FDG PET as an effective addition to other diagnostic methods used to assess patients with symptoms of dementia,” said Nicolaas Bohnen, M.D., Ph.D., lead author of the study.

“The review also identified new literature showing the benefit of this imaging technique for not only helping to diagnose dementia but also for improving physician confidence when diagnosing a patient with dementia. This process can be difficult for physicians, especially when evaluating younger patients or those who have subtle signs of disease.”

Dementia is a challenging diagnosis because it is not a specific illness but a pattern of symptoms characterized by a loss of cognitive ability. Cognitive decline may be caused by injury or progressive disease affecting areas of the brain that control attention, memory, language and mobility.

Alzheimer’s is most commonly associated with progressive memory impairment, although dementia with Lewy bodies can be associated with symptoms of Parkinson’s and prominent hallucinations. Another disorder, called frontotemporal dementia, is found in patients showing uncharacteristic personality changes and difficulties in relating and communicating.

Researchers believe expanded use of FDG-PET will help physicians diagnose dementia and help differentiate between disorders.

Already, the diagnosis of dementia includes a criteriion that physicians use evidence from molecular imaging studies.

“For the first time, imaging biomarkers of Alzheimer’s disease are included in the newly revised clinical diagnostic criteria for the disease,” said Bohnen.

“This is a major shift in disease definition, as previously an Alzheimer’s diagnosis was based mainly on a process of evaluating patients to exclude possible trauma, hemorrhage, tumor or metabolic disorder. Now it is becoming a process of inclusion based on biomarker evidence from molecular imaging.”

“The earlier we make a diagnosis, the more we can alleviate uncertainty and suffering for patients and their families.”

The biomarker 18F-FDG is among a variety of imaging agents being investigated for its efficacy in Alzheimer’s imaging.

As treatments for dementia become available for clinical use, PET will no doubt play an important role in not only the diagnosis of these diseases, but also the assessment and monitoring of future therapies.

According to the World Health Organization, an estimated 18 million people worldwide are currently living with Alzheimer’s disease. That number is projected to almost double by 2025.

The research is found in the current issue of The Journal of Nuclear Medicine.

Source: Society of Nuclear Medicine

Low levels of vitamin D already are associated with a range of health condition including osteoporosis, cardiovascular diseases, neurological ailments and many other disorders. However, experts do not agree on the ideal level of the vitamin and even if supplements can improve health.

In the new study — published in Mayo Clinic Proceedings – researchers believe they have confirmed that an inverse relationship does exist between vitamin D and depression. The issue turned muddy after smaller studies produced conflicting results about the relationship between vitamin D and depression.

Major depressive disorders affect nearly one in 10 adults in the U.S.

“Our findings suggest that screening for vitamin D levels in depressed patients – and perhaps screening for depression in people with low vitamin D levels – might be useful,” said Dr. E. Sherwood Brown, professor of psychiatry at UT Southwestern and senior author of the study. “But we don’t have enough information yet to recommend going out and taking supplements.”

Researchers examined the results of almost 12,600 participants from late 2006 to late 2010. Brown and colleagues found that higher vitamin D levels were associated with a significantly decreased risk of current depression, particularly among people with a prior history of depression.

This could reflect the fact that vitamin D levels are influenced by getting ultraviolet-light exposure, often by exercising in the outdoors — a behavior that reduces depression. Further, high Vitamin D levels could occur because a person has a strong self-worth and follows a healthy diet.

Among the study participants, researchers discovered low vitamin D levels were associated with depressive symptoms, particularly those with a history of depression. Because of this, investigators believe assessing Vitamin D levels among primary care patients with a history of depression may be an effective screen for potential relapse.

The study did not address whether increasing vitamin D levels reduced depressive symptoms. And, experts have not determined the exact relationship — whether low vitamin D contributes to symptoms of depression, whether depression itself contributes to lower vitamin D levels, or chemically how that happens.

However, vitamin D may affect neurotransmitters, inflammatory markers and other factors, which could help explain the relationship with depression, said Brown.

Vitamin D levels are now commonly tested during routine physical exams, and they already are accepted as risk factors for a number of other medical problems: autoimmune diseases; heart and vascular disease; infectious diseases; osteoporosis; obesity; diabetes; certain cancers; and neurological disorders such as Alzheimer’s and Parkinson’s diseases, multiple sclerosis, and general cognitive decline.

Source: UT Southwestern Medical Center

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Researchers say the evidence suggest that young women who display signs of either depression or binge eating should be screened for both disorders.

“Binge-eating prevention initiatives should consider the role of depressive symptoms and incorporate suggestions for dealing with negative emotions,” say the authors.

This study could provide important new opportunities to address the nation’s obesity epidemic, according to senior author Alison Field, Sc.D., an epidemiologist at Harvard Medical School and the Harvard School of Public Health.

Researchers say the new investigation is the largest to look at the relationship between binge eating and depression during adolescence, when most eating disorders develop.

The study authors defined binge eating as eating a large amount of food in a short amount of time and feeling a lack of control over eating during the episode. Researchers labeled girls who ate large amounts of food but did not feel out of control “overeaters.”

The findings rely on surveys conducted as part of the nationwide Growing Up Today Study.

The authors focused on girls because eating disorders and depression are more common in females than in males. Investigators analyzed data from nearly 5,000 girls aged 12 to 18 who answered questions in 1999, with follow-up surveys in 2001 and 2003.

Teens and young women who reported in the first survey that they always or usually felt “down in the dumps” or “depressed” were about twice as likely as others were to start overeating or binge eating during the following two years.

“The most common approach to obesity has been to focus on eating better and exercising more, but many pathways can lead to being overweight,” said Marian Tanofsky-Kraff, Ph.D., who studies eating disorders, told the Health Behavior News Service. 

“There is a group of people where it may be more psychologically driven. Targeting some of these psychological factors might help prevent obesity.”

“Binge eaters or overeaters can be very secretive, so parents may be unaware that there’s a problem. That’s a really important message for clinicians,” added Field. “If they have patients who are depressed, they need to ask about disordered eating patterns and vice versa.”

Source: Health Behavior News Service

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