Welcome to Our Parkinson's Place

I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's
diseases as well and thought it would be nice to have a place where
updated news is in one place. That is why I began this blog.
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Saturday, November 7, 2015

Parkinsons Side Effects May Vary (Wildly): 6 Of The Strangest Things Prescription Drugs Are Capable Of

Nov. 7, 2015

Most drugs have side effects of some sort, typically minor things like drowsiness or mood swings. But certain medications can also be the culprit of various other strange effects, like odd dreams or hallucinations — or even colored urine.

Of course, severe side effects are quite rare, and happen to only a handful of people. But side effects can be exacerbated if prescription drugs are mixed with other drugs or alcohol, so be sure to read about your medication before taking it. Below are six of some of the strangest side effects prescription drugs are often responsible for.

Vision Problems

Seeing spots or experiencing blind spots, blurred vision, or sensitivity to light can all be caused by different medications — particularly antihistamines, high blood pressure meds, or drugs that treat malaria or tuberculosis. Viagra, which is used for erectile dysfunction, has been investigated by federal health officials after complaints that the medication caused blindness or sudden vision loss when the optic nerve’s blood flow was blocked. Viagra has also been found to occasionally cause blue vision, or difficulties distinguishing between blue and green. Another drug associated with eye problems is Vasotec, which treats high blood pressure and congestive heart failure.

50 Shades Of Urine

If you’ve ever peed blue because of a drug, you’re aware of the strange things our body can produce. Plenty of prescription drugs can make you produce different shades of urine, such as Flagyl and furazolidone, which can make you pee black (perhaps the weirdest urine color of all). Other drugs, like Dyrenium, which is a diuretic that treats fluid retention and high blood pressure, can turn your pee blue; and Elavil, which is an antidepressant but is also used to regulate children who wet their beds, can turn your urine green.
While rainbow-colored urine may seem cool at first, it could be a sign that there’s something wrong with your body, like severe dehydration or internal bleeding. Be sure to ask your doctor if your drug may cause colored urine, or else make sure you’re not dehydrated, have a liver problem, or have internal bleeding. To find more information about the different colors drugs may induce, click here.

Moods Swings, Gambling Addictions, And Compulsive Behavior

One of the strangest things some prescription drugs can do is alter your behavior or impulse control. Mirapex in particular, which treats Parkinson’s disease and Restless Legs Syndrome (RLS), has been linked to “increased sexual urges, unusual urges to gamble, or other intense urges,” according to Mirapex can also cause the patient to fall asleep suddenly, which is pretty weird. Mirapex increases the production of dopamine in the brain, because people with Parkinson’s often have low levels of dopamine. Dopamine aids in regulating the basal ganglia and movement in the body. In the past, patients taking Mirapex have claimed it led them to alcoholism, shopping addictions, and gambling addictions. While seemingly improbable and bizarre, these side effects are real for some and certain patients have won lawsuits against its creators, Pfizer and Boehringer Ingelheim, after claiming that the drug lost them thousands of dollars in gambling.


Aside from psychedelic drugs like LSD or mushrooms, prescription drugs can cause hallucinations, too. In addition to addictive habits, Mirapex has been linked to hallucinations, or seeing images that aren’t really there. Some Parkinson’s patients on Mirapex report seeing strange things like snakes or people hiding in their closets (which frankly sounds terrifying). Lariam, in addition, which is used for malaria, has caused some patients to exhibit severe psychosis and hallucinatory behavior.

Blacking Out

Used to treat insomnia, the hypnotic Ambien will make you relaxed and drowsy with the aim of helping you sleep. But various reports have shown that Ambien can also wreak havoc on your sleep life and behaviors, even causing you to sleep walk.
Ambien was approved by the FDA in 1992 and quickly rose to become one of the top sleep aids, even though its prescribing information warned of sleep walking, sleep eating, “abnormal thinking,” and “strange behavior.” Since then, Ambien has been the cause of many strange occurrences, including Patrick Kennedy’s car accident in 2006, which he claimed to be because of an “Ambien blackout” during which he remembered nothing. “Ambien zombies” became a term to describe people who began sleep eating strange things like cigarettes and eggshells.According to the Ambien medication guide, “After taking AMBIEN, you may get up out of bed while not being fully awake and do an activity that you do not know you are doing. The next morning, you may not remember that you did anything during the night.” Some people have become addicted to the drug, describing its “high” as relaxed and surreal; but they’ve only been left with gaps in their memory and many blackout nights that could have put them or others on the verge of harm.

Vanishing Fingerprints

Though rare, it is a slight possibility that fingerprints might vanish through the use of the cancer drug capecitabine, which is also known as Xeloda. This was first discovered when a Singapore man was detained when entering the U.S. because of his lack of fingerprints — all because he was using the drug. Several other cancer patients had reported the loss of fingerprints individually, according to Dr. Eng-Huat Tan, a senior consultant in medical oncology at the National Cancer Centre in Singapore, who studied the drug’s effects. Capecitabine can cause a side effect known as hand-foot syndrome, which involves chronic inflammation of palms or soles, leading to the peeling of skin off these surfaces, and ultimately develop ulcers or blister — and lose fingerprints.

Lewy body dementia often mistaken for Parkinson's, say local doctors.

NOVEMBER 7, 2015  

Robin Williams with wife Susan, who this week revealed the actor was suffering from Lewy body dementia.

Signs of Lewy body dementia:
* Visual hallucinations
* Rigid muscles
* Sleep difficulties
* Depression
* Cognitive problems
Source: Mayo Clinic
It is the second most common form of dementia after Alzheimer's, say local neurologists – and perhaps the least known.
That is, until this week, when the widow of actor Robin Williams revealed the late star was suffering from Lewy body dementia, in which the onset of hallucinations is swift and the nightmarish spiral to certain death is even swifter.
The mental gymnastics Williams' mind exercised in creating characters both on stage and screen probably couldn't hold a candle to the cruel tricks Lewy would play on him in the end, judging by the way North Jersey neurologists describe the disease, which sounds like a sped-up version of Alzheimer's.
"It is very debilitating, very misunderstood, and very misdiagnosed," says Dr. Monica Chavez, attending physician of internal and geriatric medicine at Holy Name Medical Center in Teaneck.
In Lewy body dementia, protein deposits called Lewy bodies develop in nerve cells in regions of your brain involved in thinking, memory and movement (motor control). "The patients have similar symptoms to that of Parkinson's disease, in the very beginning – tremors, falls, stiffness in the body. Then come early onset hallucinations – very fearful hallucinations. The person gets paranoid. Depressed," Chavez says.
One of the biggest problems is that Lewy body dementia will often be misdiagnosed as Parkinson's at first, according to Chavez. Medications used to treat Parkinson's, however, actually inflame the symptoms of Lewy body dementia. So if you are misdiagnosed and treated for Parkinson's, it can make things much worse.
"Parkinson's medications are absolutely deleterious for this type of dementia. So it is very important to get a proper diagnosis early. A bad diagnosis can be even more stressful for the patient and the caregiver … Unfortunately, there is no one definitive test. The only one is at autopsy, when they can find an abnormal protein in the brain."
It was only at autopsy that Williams – who had been diagnosed with Parkinson's months before his death — was confirmed to have had Lewy body.
His wife, Susan Williams, went public with the diagnosis this week, saying that it wasn't depression that drove him to suicide as many thought, but Lewy body. She said both she and Williams were painfully aware he was suffering from something more than just Parkinson's, based on his increasing mental anguish and rapid loss of certain motor skills. Doctors just couldn't quite put their finger on it, she said, noting she forgave the comedian for killing himself, given what the disease was doing to him.
"It's not easily diagnosed. But we are getting better at ordering newer imaging studies, and identifying certain clinical features in real life. We're learning more about it over time," says Dr. Gary Alweiss, director of neurology at Englewood Hospital and Medical Center. "The diagnosis is frequently made while the patient is still alive but not upon the first few visits. It has to play itself out."
Ultimately, those with Lewy body die the way people with Alzheimer's do – either because of being unable to swallow, or from urinary tract infections, pneumonia or other such complications caused by sheer immobility, according to Alweiss. The only difference is that while Alzheimer's is a gradual decline, Lewy body is much faster, often killing in a matter of just a few years, according to experts.
About 1.4 million people in the United States are believed to have the disease, according to the non-profit Lewy Body Dementia Association of Lilburn, Ga. Though much rarer than Alzheimer's, Alweiss says: "I would encourage anyone who thinks they have dementia to see a neurologist. There are some dementias that are reversible. And if they aren't, we have medications that can at least treat your depression, we can medicate your anxiety, and there is help we can give to the caregivers," he says.
"Though the ultimate prognosis for someone with Lewy body is dismal, we can make the person a lot more comfortable and functional while they are dealing with the disease."

Friday, November 6, 2015

Parkinsons disease patients showed improved reward learning from placebo effect researchers say

A placebo used in a study about Parkinson’s disease treatment stimulated learning-related brain activity just as well as the actual Parkinson’s medication, according to researchers from Columbia University and the University of Colorado at Boulder. The details of the new Parkinson’s disease research have been published in the journal Nature Neuroscience. The study’s findings hold up results from previous studies that found that patients with Parkinson’s disease who have positive expectations of their treatment demonstrate greater improvement in their brains.
Medical News Today calls the findings of the Parkinson’s disease study, “a clear example of how psychology and medicine interact” that demonstrates “the powerful effect of expectation on the brain.”
Known as “the placebo effect,” people can sometimes respond to treatment that includes no medication if the patient believes they are taking medication. Tor Wager, an associate professor of psychology and neuroscience, and co-author of the study, believes that the new Parkinson’s research, which was funded by the Michael J. Fox Foundation for Parkinson’s Research,”highlights important links between psychology and medicine.”
Parkinson’s disease is a motor disorder. It is believed to occur when a person’s brain loses dopamine-producing cells. Dopamine is a naturally occurring brain chemical that controls reward and pleasure and regulates emotional responses, as well as bodily movements. Because of the loss of dopamine-producing cells, Parkinson’s disease sufferers have difficulties with “reward learning,” according to the study’s authors, since this form of learning requires a dopamine release in response to positive rewards offered after particular actions.
One of the ways physicians treat patients with Parkinson’s disease is to give them dopamine-boosting medication, according to the authors. For the study, Wager and his team compared using this medication against using a placebo. Parkinson’s disease patients were tasked with playing a computer game that centered around reward learning. While playing the game, the participants had functional magnetic resonance imaging (fMRI) scans taken of their brains.
The participants in the Parkinson’s placebo-based study had their learning measured as they discovered, by trial and error, which of two symbols would lead to a reward. The rewards that were offered were receiving money and “avoiding the loss of money,” according to Medical News Today. The patients with Parkinson’s disease played the computer game three different times. One time, orange juice was given and acted as a placebo. Another time, orange juice with medication was given. The participants with Parkinson’s disease did not know which was which. On another try, they were given neither a placebo, nor medications.
The researchers compared the results of the game to the fMRI results. They found that the dopamine-rich areas of the participants’ brain were just as active when they took the placebo as when they took the medication. Some holistic practitioners are questioning whether or not the researchers took into account any effect the nutrients in the orange juice itself might have had on the positive results recorded from the placebo part of the study.
The researchers found the results of their placebo-based study significant and full of potential.
“Recognizing that expectation and positive emotions matter has the potential to improve the quality of life for Parkinson’s patients, and may also offer clues to how placebos may be effective in treating other types of diseases,” Wager said.

By:Dawn Papple

Simple Things To Do At Home To Reduce Parkinson’s Symptoms

Parkinson’s symptoms can be difficult. Each new day brings on something new, from stiffness, to weakness, and eventually to tremors. When it becomes more difficult to perform even the most mundane tasks – buttoning a shirt, for instance – it can become frustrating.

As the medical world begins understanding more about the disease, certain things have become apparent in the overall treatment. At the top of the list is exercise. Exercise increases your flexibility and can help relieve many of the symptoms common to everyday life. Just a few stretching and flexibility exercises can help relieve stiffness and soreness, and allow you to do many of the things that were once just a part of your normal routine.
You can work with a personal trainer or fitness instructor that understands mobility issues. He or she can add common, everyday movements into a routine to help maintain your flexibility. It doesn’t have to involve weights or complex machines. Sometimes simple things can do just as much good.
Like standing next to a wall for support, and gradually stretching your arms upwards towards the ceiling. Hold that for a number of seconds. Release your arms and put your hands on the wall. Stretch out your back and your arms.
You can also sit on a chair as you lift your arms towards the ceiling, then release them down and back, stretching out your shoulders. Do only what feels comfortable and what doesn’t put your balance in jeopardy.
Tremors are a fact with Parkinson’s. To control them as much as possible, stick to a rigorous schedule when taking medicines. They are designed to help control the tremors between intakes. If you begin noticing tremors in between your dosage, talk with your doctor. It may be something as simple as upping the dosage of your medicines.
Diet also comes into play. Diets heavy in protein, for instance, can limit your body’s absorption of levodopa, which is a common medication used in the treatment of Parkinson’s. As a result, many doctors ask patients to limit their protein intake to around 12 percent of their daily calories. Many also recommend increasing the amount of fruits and vegetables, which may help protect nerve function and decrease the symptoms of the disease.
If balance and walking is at issue, certain things can quickly be improved around the home. You can work with an occupational therapist, who will help with room placement and creating a user friendly environment. Also focus in on creating a highly moveable space. Place furniture with enough space to move around easily. Install handrails in the bathrooms. Choose floor coverings wisely to avoid tripping hazards. Whenever you notice a problem, quickly find a solution to make it more livable space.
And finally, focus in on making the best of every day. When walking becomes a challenge, find ways to improve the situation. Rubber soles can easily stick to the floors as a person shuffles; choose soles that make the process easier. Practice walking in a safe place, and put more focus on your everyday movements. Each day is a new process in your journey, the safer you can make it, the more enjoyable it will be.

How Parkinson Disease Affects Emotions Of A Person


When you or a family member is diagnosed with Parkinson’s, you will experience a range of emotions and go through several stages of adjustment to the disease. As Parkinson’s progresses, bringing new challenges, you will go through many of the emotions and stages of adjustment again and again. Each person will experience the stages in their own order and at their own pace.
Remember, everything you are feeling is normal.

Denial, Disbelief, Shock

This response may be prolonged if symptoms are mild 
  • or the correct diagnosis is not made early in the course of the disease.
  • Ironically, denial can be a useful coping mechanism if it allows you to largely ignore symptoms and go on with life as usual.
  • However, if a person refuses to take medication, or goes to extremes seeking second opinions, it may indicate denial as an unhealthy response.
What to do
  • Take time to explore your feelings and be honest with yourself and others. Journaling or telling your story may help.
  • Knowledge is power. Learn about Parkinson’s, and focus on abilities rather than inabilities. Remember that each person’s experience of PD is unique.

Discouragement, Searching for an Explanation

In this phase, people look for some direct cause for the health problems they are experiencing.

  • You might become preoccupied with the “why me?” question, while searching for something or somebody to blame for the unwanted circumstances occurring in your life.
What to do
  • Symptoms of depression are common in any stage of PD. In some cases, depression is an early symptom. Don’t be afraid to tell your doctor if you feel depressed.

Shifting Abilities, Role Reversals

People with Parkinson’s often need more time to perform activities because of changes in hand coordination, muscle stiffness or slowness. Conflict may arise as it becomes necessary to reevaluate who is responsible for what tasks in the family and around the home.

  • Changing abilities and assuming new roles can cause frustration and emotional upheaval.
  • Stress makes PD symptoms worse.
What to do
  • Maintain open communication with your loved ones.
  • Prioritize daily tasks. Get outside help as needed for some tasks such as yard work, housecleaning or home maintenance.
  • Regular exercise can help manage stress.
  • Seek help from a counselor to resolve relationship conflicts.

At this point, you realize that PD has had an impact on your life. You are willing to take on the work of achieving your optimal level of independence.

  • You are also willing to seek out others with the same condition for education and encouragement.
What to do
  • Explore new opportunities to find self-fulfillment.


  • You once again feel some control in your life.
What to do
  • Take an active role in your health and care. For example, work with your health care providers to optimize your medications.
  • Communicate openly about your priorities.
  • Set realistic expectations.


    1. Many people in the Pacific island of Guam have developed Parkinson’s Disease, due to feasting on flying foxes, a species of bat that can be as big as six feet across. This is because the bats eat cycad seeds which contain a potent neurotoxin.

    2. For reasons unknown, Bulgarian Gypsies appear to be almost immune to developing Parkinson’s Disease. All other Bulgarians are ten times more likely to get Parkinson’s Disease.
    3. In 1875, Henri Huchard had a patient that had all of the symptoms of Parkinson’s Disease who was only three years old.
    4. The Parsi, a Zorastrian community in Bombay, India have almost the world’s highest prevalence of Parkinson’s Disease due to the poisonng effects of a ritual in which they burn Aspand seeds in order to rid their children of the Evil Eye – a sickness transmitted by someone who is envious, jealous, or covetous.
    5. Although L-dopa is widely used to raise L-dopa levels, no other common substance reduces L-dopa formation more than L-dopa itself.

    6. Anti-cholinergics, used to treat Parkinson’s Disease, are found in nature as Deadly Nightshade, a plant that is so poisonous that just one leaf could kill an adult.
    7. Although it is claimed that Parkinson’s Disease becomes more likely with age, amongst the very oldest of people, those between 110 and 120 years old, Parkinson’s Disease is virtually unknown.
    8. L-dopa, in seed form, was being used in India to treat the symptoms of Parkinson’s Disease over 6000 years ago.
    9. James Parkinson, who Parkinson’s Disease was named after, never knew that Parkinson’s Disease was called Parkinson’s Disease.
    10. There are two films of Adolf Hitler’s last public appearance, one that was shown in which he displayed no symptoms of Parkinson’s Disease, and another that was not shown in which he was displaying the symptoms of Parkinson’s Disease.

    Levodopa Add-On Disappoints in Late-Stage Parkinson's


    Investigators blame poor trial design and execution
    The adenosine 2A (A2A) receptor antagonist preladenant didn't reduce "off" time in Parkinson's in two trials, but that may have been due to poor trial design and management at individual sites, researchers reported.In one of the trials, the active control rasagiline also failed, Robert Hauser, MD, of the University of South Florida in Tampa, and colleagues reported online in JAMA Neurology.
    "Because the active control (rasagiline) also failed to demonstrate a significant reduction in off time, it is not possible to determine from these results whether they represent a finding of inefficacy for preladenant, or are related to issues of study design or conduct," the researchers wrote.
    Three adenosine 2A receptor antagonists -- istradefylline, preladenant, and tozadenant -- are in development for Parkinson's disease, and this is the second phase III trial with disappointing results with this class of agents.
    All three drugs yielded positive results in phase II trials, but istradefylline had mixed results in phase III, preladenant just failed its two phase III trials, and tozadenant is still in phase III development.
    The drugs provide a nondopaminergic target for Parkinson's and are thought to work by reducing overactivity of striatopallidial output neurons. They're intended to be an add-on to levodopa in Parkinson's patients who have motor fluctuations.
    Hauser and colleagues conducted the two 12-week randomized controlled trials in several international centers, with moderate-to-severe Parkinson's patients who were already taking levodopa.
    The first trial enrolled 778 patients who were randomized to an add-on of placebo, rasagiline, or one of three doses of preladenant twice daily: 2 mg, 5 mg, or 10 mg.
    In the second trial, 476 patients were randomized to placebo or to one of two twice-daily doses of preladenant: 2 mg or 5 mg.
    The primary outcome in both studies was the change in "off" time from baseline to week 12.
    In the first trial, they found that neither preladenant nor rasagiline was superior to placebo in reducing "off" time during that time period. Here are the reductions in "off" time compared with placebo; none of which amount to a significant difference:
    • 2 mg: -0.10 hour (95% CI −0.69 to 0.46 hour)
    • 5 mg: -0.20 hour (95% CI −0.75 to 0.41 hour)
    • 10 mg: -0.00 hour (95% CI −0.62 to 0.53 hour)
    • Rasagiline mesylate 1 mg/d: -0.30 hour (95% CI −0.90 to 0.26 hour)
    The percentage of responders with at least a 30% decrease in "off" time at week 12 was similar among all three groups, ranging from 31% to 36%, the researchers reported.
    Similarly, in the second trial, preladenant wasn't superior to placebo in reducing "off" time, with no significant differences compared with placebo:
    • 2 mg: -0.20 hour (95% CI −0.72 to 0.35 hour)
    • 5 mg: -0.30 hour (95% CI −0.86 to 0.21 hour)
    The mean increases in "on" time without dyskinesia at week 12 were similar across groups, the researchers added.
    They noted, however, that preladenant was well tolerated, with the most common adverse event being constipation, occurring in 6% to 8% of those in the drug groups compared with 1% to 3% for those on placebo.
    They also noted that there was one suicide in the second trial -- a self-inflicted gunshot wound to the chest -- which was considered possibly related to the study drug by the investigator.
    Hauser and colleagues said the studies offer several lessons for trial design in further development of these drugs, which they highlight in a boxed section of the article.
    A post-hoc analysis of the first trial revealed a large placebo effect at sites in Turkey, India, and Latin America, prompting a need for careful choice of sites and regions, as well as specialized training to mitigate placebo response, they wrote.A second lesson is that more patients are not always better, they said. In both trials, enrollment sped up significantly as the trial went on, which "could potentially have degraded the quality of patients that sites were enrolling," they wrote.
    "We hypothesize that sites enroll their most ideal patients first and then may 'scrape the bottom of the barrel' to find additional patients to enroll," they wrote.
    Having ideal patients is important, they said, because the studies rely on patient diaries. Patients have to be taught to recognize motor states and complete their diary in a timely and acute manner.
    "It seems likely that these requirements would be easiest to accomplish at a small number of expert sites with a successful clinical trial track record and a large population of well-known patients from which to draw, which appears to be the case for phase II trials but becomes more difficult in phase III trials, when more sites and more participants are required," they wrote.
    Their solution to this challenge: avoid having to enroll more patients than necessary.
    The studies were funded by Merck. Some study authors are employees of Merck.
    Hauser disclosed relevant relationships with Merck, Pfizer, UCB Biosciences, Teva, Chelsea, Impax, Lundbeck, AstraZeneca, AbbVie, Avadia, Biotie, and the National Parkinson Foundation.
    Co-authors disclosed relevant relationships with Merck, Lundbeck, UCB Biosciences, Britannia, Teva, BIAL, Agence Nationale de la Recherche, Centre Hospitalier Universitaire Toulouse, FranceParkinson, Institut National de la Santé et de la Récherche Médicale-Direction de l'Hospitalisation et de l'Organisation des Soins, Recherche Clinique Translationelle, Michael J. Fox Foundation, Programme Hospitalier de Recherche Clinique, Boehringer Ingleheim, AbbVie, Ono, Mundipharma, Sanofi, Servier, Xenoport, Zambon, Neuroderm, Novartis, and Eli Lilly.
    Associate Clinical Professor ofMedicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

    Exploring current state of knowledge about mild cognitive impairment in Parkinson’s disease


    The current issue of Neurodegenerative Disease Management explores evolving viewpoints on the role of mild cognitive impairment in Parkinson’s Disease (PD-MCI), a medical issue which currently lacks consensus.
    Neurodegenerative Disease Management is published by Future Science Group. The article is also available free of charge to members of Neurology Central, FSG’s online community for the international neurology community.The article explores the growing acknowledgement of mild cognitive impairment as both a construct of and a risk factor for dementia in patients with Parkinson’s disease. The authors review lessons learned from Alzheimer’s disease research that has already explored disease precursors and biomarkers, disease trajectory and clinical trial considerations.“Recent research on mild cognitive impairment in Parkinson’s disease (PD-MCI), has sought to define its characteristics and risk factors as well as possible precursors of Parkinson’s dementia,” said Jennifer Goldman, MD, MS, who co-authored the article with Neelum T. Aggarwal, MD, and Cynthia D. Schroeder, MHS colleagues from Rush University Medical Center Department of Neurological Sciences.
    “Precursors under investigation include serum, cerebrospinal fluid, and neuroimaging biomarkers, some of which may be similar in concept or in scientific findings to those found in Alzheimer’s disease,” said Goldman. “Lessons learned from the Alzheimer’s disease field may help Parkinson’s disease clinicians and researchers further the development of good screening and accurate diagnostic algorithms, which may predict future cognitive decline, and ultimately assist in making treatment decisions.”
    The article explores MCI-AD research, including the evolution of MCI definitions over the years, clinical trials that now incorporate biomarkers and genetics in the study design, and emerging therapeutic strategies targeting specific biological mechanisms, novel compounds and delivery systems, and earlier stages of cognitive impairment with potential disease-modifying or prevention trials.
    “The authors elegantly synthesize advances and challenges in PD-MCI, a complex field which currently lacks consensus, and make comparisons with the more advanced field of AD-MCI,” said Daphne Boulicault, Commissioning Editor. “We are pleased to offer this thoughtful review in both our MEDLINE-indexed journal, and free of charge on our industry portal, Neurology Central.”

    Thursday, November 5, 2015

    Alzheimer's may be a collection of diseases that should be treated separately

    Nov. 5, 2015

    'It is essential to carefully characterize and classify the mechanisms that underlie Alzheimer's disease, in order to allow for the development of novel therapies that can be prescribed according to the patient's relevant disease sub-type.'

    Deciphering the mechanism that underlies the development of Alzheimer's disease in certain families but not in others, researchers at the Hebrew University of Jerusalem's Faculty of Medicine have proposed that the malady is actually a collection of diseases that probably should be treated with a variety of different approaches.
    Neurodegenerative diseases are incurable and debilitating conditions that result in degeneration or death of cells in the nervous system. Conditions such as prion disorders (the most famous of which is "Mad Cow Disease"), Alzheimer's Disease and Parkinson's Disease share two key features: they emerge as a result of aberrant protein folding and aggregation, and their onset is late in life. These maladies emerge either sporadically or as familial, mutation-linked illnesses (certain prion disease can be also infectious).
    Most sporadic cases are diagnosed during the patient's seventh decade of life or later, while familial cases typically manifest during the fifth or sixth decade. Despite their relative rareness, mutation-linked cases are very important, as they provide hints that can help decipher the mechanisms that underlie the development of the disease.
    The late onset feature typical to distinct neurodegenerative diseases, and the common temporal emergence patterns of these maladies, raise key questions: first, why do individuals who carry disease-linked mutation show no clinical signs until their fifth or sixth decade of life? In addition, why do apparently distinct disorders share a common temporal emergence pattern?
    One possible explanation is that as people age, the efficiency of the mechanisms that protect younger people from the toxic aggregation of proteins declines, thus exposing them to disease. Indeed, previous studies clearly indicate that the aging process plays key roles in enabling neurodegenerative disorders to onset late in life.
    These finding raised the question of what mechanisms are negatively regulated by aging, allowing the emergence of neurodegeneration in the elderly.
    Since neurodegenerative disorders stem from aberrant protein folding, an international research team, led by Prof. Ehud Cohen and Dr. Tziona Ben-Gedalya at The Institute for Medical Research Israel - Canada (IMRIC) in the Hebrew University's Faculty of Medicine, postulated that an aging-associated decline in the activity of proteins that assist other proteins to fold properly, may be one mechanism that exposes the elderly to neurodegeneration.
    To identify such mechanisms, they searched for similar mutational patterns in different proteins that are linked to the development of distinct neurodegenerative disorders. Their research showed that the development of Alzheimer's disease in certain families, and of a familial prion disorder in other families, originate from very similar mutational patterns.
    Based on this discovery, they identified that the malfunction of the protein "cyclophilin B," which helps nascent proteins to attain their proper spatial structures, is responsible for the manifestation of both maladies. They also comprehensively characterized the mechanism that underlies the development of Alzheimer's disease in individuals who carry these mutations, and found that it has no relevance to the emergence of the disease in patients who carry other Alzheimer's-linked mutations.
    According to Prof. Ehud Cohen: "This study provides important new insights: first, it shows that the development of distinct neurodegenerative disorders stems from a similar mechanism. More importantly, it indicates that Alzheimer's disease can emanate from more than one mechanism, suggesting that it is actually a collection of diseases that should be classified."
    The new insights derived from this study may reinforce the efforts to develop novel therapies to the different subtypes of Alzheimer's disease, providing new hope to those who suffer from this incurable disorder and to their families.
    Prof. Ehud Cohen added: "Our study proposes that the failure to develop efficient Alzheimer's therapy emanates from the pooling, in clinical experiments, of patients who suffer from distinct disorders that eventually lead to Alzheimer's symptoms. Therefore it is essential to carefully characterize and classify the mechanisms that underlie Alzheimer's disease, in order to allow for the development of novel therapies that can be prescribed to the individual patient according to their relevant disease subtype."

    Gait difficulties in Parkinson's linked to new blood vessels in brain

    Targeting the formation of unwanted blood vessels in the brain could be a way to help Parkinson's disease patients whose balance and walking difficulties persist despite dopamine-restoring medication.

    The researchers found links between cerebrospinal fluid markers of new blood vessel formation in the brain and gait difficulties in patients living with Parkinson's disease.
    This is the potential implication of a study published in the journal Neurology that found biomarkers of blood vessel formation in the brain are increased in patients living with Parkinson's disease, and they are linked to gait difficulties.
    The study confirms similar findings by other researchers who analyzed brain tissue obtained postmortem from Parkinson's patients.
    Study leader Dr. Oskar Hansson, from Lund University in Sweden, says:
    "The strength of our study is the number of participants, and the fact that they are alive. Because many suffer from several parallel diseases at the final stage of their lives, it is difficult to analyze samples from deceased persons."
    Despite adequate medication, many people with Parkinson's disease eventually develop problems with walking and balance. Also, some cannot tolerate full doses of dopamine-restoring medication because of the side effects.
    Parkinson's disease arises from the death of brain cells in a few restricted areas of the brain. The affected brain cells release dopamine, a chemical messenger that is important for the control of movement, emotional responses and other functions.
    As the disease progresses, levels of available dopamine fall, and symptoms like tremors, slowness, impaired balance and stiffness get worse. Normal life erodes - at different rates in different people - as walking, talking and looking after oneself become increasingly difficult.
    There is no cure for Parkinson's disease, and patients must rely mainly on drug-based treatments to control their symptoms. The drugs are designed to increase dopamine in the affected parts of the brain.

    Angiogenesis linked to walking and balance difficulties in Parkinson's

    The formation of new blood vessels, or angiogenesis, in the brain is also a feature of Parkinson's disease and other neurodegenerative disorders. The reason for this is not clear, but one theory is that the death of cells triggers it. Angiogenesis can also be triggered by inflammation and damage to tissue.
    It is possible to assess the extent of angiogenesis in the brain by measuring biomarkers in cerebrospinal fluid.
    In their study, Dr. Hansson and colleagues found clear links between several markers of angiogenesis and walking or balance difficulties in patients with Parkinson's disease.
    Dr. Hansson says they also noted "an increased permeability of the blood-brain barrier, which leads to blood components potentially leaking into the brain and causing damage."
    The team arrived at these results by comparing the cerebrospinal fluid from 100 Parkinson's patients with that of 38 healthy people (the controls). They measured levels of a number of angiogenesis markers and also, from magnetic resonance imaging (MRI) scans, they assessed any damage to brain tissue (for example, white matter lesions and small bleeds). They then confirmed the results in two further patient groups of approximately the same size.
    The results showed that cerebrospinal fluid markers of brain angiogenesis are "upregulated" in Parkinson's disease.
    The authors note that the increased angiogenesis was linked with gait difficulties, blood-brain barrier dysfunction, and signs of damage to brain tissue in the Parkinson's patients but not the controls, and write that "these interactions are specific" for Parkinson's disease.
    Regarding the study's implications, Dr. Hansson notes:
    "Medication for angiogenesis already exists. If we can confirm our results in further studies, these drugs can be tested on Parkinson's patients in the future."
    Before embarking on human trials, the team plans to carry out animal studies first, so as to understand more about the underlying mechanisms, and also to screen for the most appropriate candidate drugs.
    Angiogenesis has also been implicated in other neurodegenerative diseases. For example, in 2011, Medical News Today reported a study where researchers suggest that a profusion of blood vessels may explain how Alzheimer's disease destroys the brain.