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Saturday, December 15, 2018

Build your own pill organizer

Written Sheryl Jedlinski




Does your complicated dosing regimen make it difficult for you to take your medication “on time, every time?” Do you inadvertently skip doses on a regular basis, hampering the successful management of the symptoms and side effects of Parkinson’s disease? Is it reasonable for your doctor to expect you to take a total of 20, 30, or 40 pills a day in unique combinations and over multiple dosing periods without so much as a hiccup? It is doable with the support of additional resources, like a good organizational system, advance planning, and someone to help maintain your medicine inventory. The challenge is these are not things you can readily purchase.

A born problem solver, my husband, Tony, took matters into his own hands and designed a pill organizer that may be just what your doctor ordered to improve your on-time performance, and therefore your health and quality of life. (Full directions for replicating his invention can be found at the end of this article) Unlike most of his gadgets, Tony’s pill organizer is “no tech.” It does not plug in, light up, or make noise, and it is so easy to use, it requires little training.

Comprised of a “chain” of plastic pouches that fold into a compact bundle, Tony’s pill organizer fits in almost any size purse. It is flexible enough to hold pills of a wide variety of sizes and shapes and is easily expandable as dosing regimens change. Each pouch is filled with the specific pills required for that dose and labelled with the time it is to be taken.
Tony sorts, counts, fills, and organizes my pills a week at a time, enabling him to:
  • Know when a particular med is running low and order more before we are out.
  • See whether I occasionally miss a dose and suffer any adverse effects.
  • Keep pills clean and dry.
Follow these simple steps to make your own pill organizer:
  1. Buy enough pill pouches (about a nickel each at Walgreen’s) for a week’s worth of meds. My magic number is 56 as I take eight doses a day.
  2. Attach one day’s bags to one another with red plaid Scotch tape across the front and back. Make up and label one strip for each day of the week.
  3. Lay the strips out on a table and remove enough meds from their containers to make seven lines of pills for the first dose. (See photo).
  4. Transfer pills into the first pouch of each strip, counting as you go, and sealing after filling.
  5. Repeat steps 3 – 4 for each of the other medication times.
  6. Store the completed strips in a safe location, ready to grab on your way out the door. Carry each day’s strip wherever you go.
  7. Save the empty strips to re-use to make up another set of organizers. Pouches last six months or so before the re-closable zippers start to fail, and the lettering wears off the bags.
We are not selling anything. Sharing ideas that work for us is our way of giving back and saying thanks to the Parkinson’s community for all it has given us over the years.

https://livingwellwithparkinsonsdisease.com/2018/12/15/build-your-own-pill-organizer/
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Taking a Careful Look at Apathy: It Could Be Motor Hesitation

 DECEMBER 14, 2018 Dr. C


Depression is often associated with Parkinson’s disease (PD), as is apathy. But there may be a subtle difference between the two. At the risk of oversimplifying, let’s define depression as a state of sadness and loss of interest, and apathy as an apparent lack of motivation. Put sadness and low motivation together and the result looks like someone who has stopped enjoying life. But linking the two together may be a mistake when PD is involved because what looks like a lack of motivation may be the result of motor hesitation and difficulty with set shifting (changing from one motor activity to another). I have seen this motor hesitation in my own life. I feel stuck; not because of a lack of desire but rather an inability to move. It requires a careful examination to recognize the difference.
In a previous column, I talked about scenario looping breakdowns in connection to freezing — a common PD motor symptom. Apathy with PD folks may be linked more to scenario looping breakdowns than to a mood disorder. With PD it speaks to the “unwillingness” to act. But with a breakdown in scenario looping, it may appear as the unwillingness to act when it is actually a form of freezing due to an organic neurological condition. Combine this with the “flat affect face” or facial masking that can come with PD and it can appear to the observer as apathy. A careful look may reveal that often it is not. It is a manifestation of scenario looping breakdowns.
Scenario looping is the brain’s ability to loop through scenarios, exchanging possible actions or responses, until the best course has been determined. This happens with use of language and with motor actions. In every case, the scenario has a starting point. If there is no external cue from the environment to get started, we call that spontaneous initiation; an example is engaging in speech with your partner. You wouldn’t always want to wait until your partner speaks first or provides an external cue. In a normal relationship, each person will often initiate speech spontaneously without external cueing. Patients who have damage to areas of the brain responsible for scenario looping will frequently have problems with spontaneous speech. Does this mean that they are apathetic?
Spontaneously starting a new motor sequence may be difficult for some PD patients. Another example: My partner wants me to put up a new curtain rod. This involves a series of motor tasks: getting the tools and step stool, removing the old curtain rod, and using small screws. These actions involve the use of fine motor skills which are always difficult for those with PD. The curtain rod has been leaning against the wall for a week. Is it apathy that prevents me from engaging in the task? Is it fear? It doesn’t feel that way. It feels like a physical resistance to move my body in the direction of that given sequence of motor actions. PD patients often have motor action hesitancy, and this may be misinterpreted as apathy. In a chapter of “Parkinson’s Disease: Diagnosis and Clinical Management,” Lisa M. Shulman and Mackenzie Carpenter say that great care needs to be taken when ascribing the symptom of apathy to a PD patient, and that more research is necessary.
I need to be taking that careful look, to be clear in my mind that this is motor hesitancy. Doing so will ensure that scenario looping breakdown does not become apathy in my mind, or in the minds of those who care for me. There is a risk of mentally interpreting the motor resistance as “he doesn’t care.” The distinction is very important, and I spend time in mental contemplation making the distinction clear. Muscle hesitancy and difficulty with initiating motor sequences is not apathy. Understanding the difference between apathy and scenario looping breakdown is an opportunity to reframe and enlighten. Taking the time to contemplate on the difference is time well spent.
Write a comment and tell me if you see a difference between apathy and muscle initiation in your own life. Do you have suggestions on how to use this distinction to improve your quality of life? 
***
Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.
To write a comment, please go to:
https://parkinsonsnewstoday.com/2018/12/14/parkinsons-disease-apathy-motor-hesitation-scenario-looping-breakdown-facial-masking/
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Merger of New Mexico Parkinson’s Coalition, PMDAlliance Expected to Improve Patient Services

DECEMBER 14, 2018 BY MARY CHAPMAN 
The recent merger of the New Mexico Parkinson’s Coalition (NMPC) and national nonprofit Parkinson & Movement Disorder Alliance (PMDAlliance) is expected to significantly boost support services for Parkinson’s patients in the New Mexico area, according to the organizations.
“I’m a firm believer in mergers when the organizations share similar missions and are compatible in their purpose and goals,” Sarah Jones, CEO of PMDAlliance, said in a press release. “Bringing everything under one virtual roof creates exponential benefit. It saves money and allows us to serve more people in need.”
As a result, the organizations expect a fourfold increase in the programs offered to patients with Parkinson’s and other movement disorders in New Mexico.
The coalition website states that “the tough decision was made knowing that there would be new, innovative programs and support brought to New Mexico as well as funds to hire a community engagement manager,” adding that more patients will have access to education, exercise programs, and events.
These improvements in services will be expanded to include smaller areas in the state rather than being limited to larger cities such as Albuquerque, Santa Fe, and Las Cruces.
“Working collaboratively, we can expand our reach in New Mexico, including extending services to our Native American neighbors and rural communities,” said Karen St. Clair, a former coalition board member. “PMDAlliance is passionate about services, just as the coalition is. By merging we can allocate more resources to service delivery instead of administration.”
Next year, the PMDAlliance will bring to the state educational events such as a support group for leadership training, a retreat for caregivers and their partners, and a program that focuses on new medical treatments.
The NMPC will be folded into the PMDAlliance umbrella, although it will continue to co-brand — using both organizations’ logos — until the transition is complete in about eight months, St. Clair said in a phone interview with Parkinson’s News Today. After that, its website will discontinue. The coalition was formed the year after the American Parkinson’s Disease Association’s decision in 2013 to leave New Mexico.
Operating nationwide but with no brick-and-mortar base, PMDAlliance provides educational workshops for organization leaders and those affected by movement disorders. Its overall mission is to improve patients’ lives.
According to the Parkinson’s Foundation, about 60,000 U.S. residents are diagnosed with Parkinson’s annually.
https://parkinsonsnewstoday.com/2018/12/14/new-mexico-parkinsons-coalition-pmdalliance-announce-merger/
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Friday, December 14, 2018

OUT-THINKING PARKINSON'S

December 14, 2018

Quality of Life Improvement for People Affected by Parkinson's Disease


DANCE THERAPY FOR PARKINSON'S DISEASE

INTRODUCTION

Of all the therapies and modalities we’ve discussed here, I believe the most beneficial overall for progressive symptom reduction and movement recovery are Dance based. Here we define Dance Therapy broadly and simply as “moving to music or a beat”. The importance of Dance for symptom reduction was confirmed to me by an article on the BBC show “How to Stay Young”. According to one of the presenters, Angela Rippon,
“All the experts we met confirmed that holding back neurodegeneration is possible as long as you keep making brain cells and enabling neural connections. So this means trying new things, and setting challenges“.
“When I visited a group in Germany to assess the relative merits of gym work versus dancing, I was delighted (and as a lifelong dancer, not at all surprised) to see that doing the twist was far more beneficial overall than merely lifting weights. Again, the real difference seemed to be the added value of the endorphin boost dancing invoked, plus the novelty of learning new routines, and what you could call the ‘sociability quotient’.”
Indeed, Dance Therapy incorporates a number of other beneficial therapies which we’ve previously explored, including:

MUSIC-AS-MEDICINE FOR PARKINSON'S DISEASE;

SOCIAL ENGAGEMENT AND PARKINSON'S DISEASE;

MIRRORING AND REHEARSAL THERAPIES FOR PARKINSON'S DISEASE;

BUILDING ALIVENESS WITH PARKINSON'S DISEASE.

Here, we’ll demonstrate the benefits of Dance Therapy for people with Parkinson’s Disease, mainly through video examples, starting with my own experience, and then considering other real world examples where Dance has clearly improved quality of life for people with Parkinson’s.

MY JOURNEY THROUGH DANCE

Here is a very early entry from my diary, back in Aprill 2016, when I first discovered Dance and its benefits. Interestingly, in this one I discuss and demonstrate how Dance Therapy is not just important for helping us to move physically again, but also to move our emotions through our system. This is critical too, as people with Parkinson’s Disease are just as emotionally frozen as they as physically, see:

MENTAL HEALTH AND PARKINSON'S DISEASE.




I soon discovered the importance of “Mirror Dancing”: passively watching a music video over and over, and then actively trying to copy the dance moves of people in them. This brings into play the firing of my Mirror Neurons to enhance access to and relearning movement (see the article on Mirroring and Rehearsal Therapies linked to in the Introduction for more about this). Here is a diary entry from July 2016, below which I have also included the music video that I am mirroring, so the reader can match up my moves to those seen in the original.

https://youtu.be/0eNHm_iTz4c


Another example of Mirror Dancing is below, again together with the video that I’m attempting to copy. It is important to note in all my diary entries that I am in a “off” state, which means the previous dose of my PD medication has worn off, and I have lost free access to movement. Thus, crucially, it is the sound and the visual cues provided by the music video which is allowing me to move as seen.



Indeed, after practicing Mirror Dancing daily for a while, I soon found that I could dance more freely by myself without the need for the visual cues. At times, the joy of being able to access free movement again could temporarily unlock me completely from the stiffness, rigidity, pain and freeze of my PD, via a positive feedback loop, as this entry from November 2016 demonstrates.


This second example, from January 2017, shows the results of an experiment where I was trialling combining wearable light therapy glasses with Dance.


Continuing practice daily, when my symptoms and energy would allow, by the time of this next diary entry, from October 2017, my balance, fluidity of movement, range of motion and confidence have clearly markedly improved. I also found that expressiveness of the hands was a vital ingredient to the success of Dance Therapy, and that tactile feedback could enhance this. Thus in this entry, you will see me wearing a pair of work gloves.


I have also found that dancing outside can boost the feel-good factor, as shown in this more recent update from July 2018.


MORE EXAMPLES OF DANCE THERAPY FOR PARKINSON’S DISEASE

First up is the TEDx talk by Federico Bitti, a fellow traveller who also kept a video diary of his journey through Dance. Here, Federico demonstrates how Dance Therapy allowed him to escape from severe Dystonia (abnormal muscle rigidity and pain) - Dystonias are strongly related to Parkinson’s Disease, and most people with PD will suffer from some form of this.


Next is another TEDx talk, by Rafi Eldor, who found that he could maintain his health and access to movement through ballroom dancing.


Indeed, Tango dancing is being found to be particularly beneficial for people with PD as a therapy.


Here is another form of Dance which is showing significant benefit to the real lives of people with PD, namely “Body Popping”.


SUMMARY

Dance Therapies of many forms have been shown to have potentially massive benefits for people with PD. I hope the examples demonstrated herein will encourage, inspire and motivate people with Parkinson’s, and their partners or caregivers, to start dancing daily.

http://www.outthinkingparkinsons.com/articles/dance?fbclid=IwAR2BqIzkZD2QAC7MDlvnmFL3zn88cv1CCj8YERPh-71PiZ8VeRcveQGxySI#.XBPaqWS_3_I.facebook
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New Neurodegeneration Challenge Network Puts Focus on Causes of Parkinson’s, Other Disorders

DECEMBER 14, 2018 BY MARY CHAPMAN IN NEWS.


A new network launched by Facebook CEO Mark Zuckerberg and his wife, Priscilla Chan, will unite leading investigators from various biomedical fields, as well as biologists and physicians, in gaining insight into why neurodegenerative disorders such as Parkinson’s occur.
The Chan Zuckerberg Initiative’s (CZI) Neurodegeneration Challenge Network will focus on neurodegenerative diseases as a group of disorders that share common features — and possibly future cures.
”Neurodegenerative disorders, including Alzheimer’s, Parkinson’s, Huntington’s disease and ALS, are a class of diseases that affect millions of people worldwide,” CZI science program officer Katharine Brose said in a press release. “Meanwhile, the causes of most degenerative diseases are only partly understood, and there still are no effective therapies to cure, prevent or even treat most of these disorders.”
Research projects were selected in a competitive process. Grantees include 17 early-career investigators and nine collaborative teams. Each team — seven from the U.S, one from Sweden, and one from Belgium — will receive $1.05 million.
The Belgian team, led by Patrik Verstreken, PhD, plans to develop a new chip to study how Parkinson’s works. He will work alongside researchers Wim Vandenberghe, MD, PhD, and Dries Braeken, PhD.
”We will produce human neuronal microcircuits that are relevant to Parkinson’s disease on a multi-electrode array chip,” Braeken said. “This chip will be used to measure electrophysiological changes between neuronal circuits of cells obtained from healthy people and from an extensive collection of Parkinson’s patients.”
The 2D chip is needed to form a 3D human-relevant model for brain function and disorder.
Verstreken said he hopes to “print” small parts of the human brain on a unique chip, allowing scientists access to brain tissue from healthy individuals and patients. He explained that the technology can be used to monitor disease progression and to look for potential solutions.
”While we will develop this chip using tissue from Parkinson’s patients, the same technology can be used to create better models for Huntington’s disease or any other neurodegenerative disease, for that matter,” Vandenberghe said.
Years of research notwithstanding, there remains much about Parkinson’s and related diseases that scientists don’t yet understand.
“By supporting these nine interdisciplinary collaborations and generating shared tools, resources and platforms, we hope to inspire a new approach to tackling neurodegenerative disease — one that leverages the combined power of basic science and technology to accelerate progress toward clinical goals,” Brose said.
Zuckerberg is Facebook’s co-founder and CEO. Chan is a pediatrician and philanthropist. Founded by Zuckerberg and Chan in 2015, the CZI aims to use technology to solve some of the world’s toughest problems. Its focus areas are science, education, justice, and opportunity.
https://parkinsonsnewstoday.com/2018/12/14/focus-parkinsons-other-disorders-new-neurodegeneration-challenge-network/
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Thursday, December 13, 2018

Here’s why laughter is the best medicine—besides actual medicine

John Murphy, MDLinx | December 13, 2018
As the old saying goes, laughter is the best medicine—but for what? Can laughter cure cancer or defeat the common cold? Can laughing fix erectile dysfunction? Hmm, probably not.

Laughter really is good (if not the best) medicine for a range of ailments, from chronic pain to improved cardiovascular function


We know that laughing has the intangible ability to make us feel better—it reduces tension and helps us cope. But laughter has also shown measurable clinical effects in the body: It releases endogenous opioids
and endorphins in the brain, increases the activity of natural killer cells to strengthen the immune system, and lowers cortisol levels in blood circulation for stress reduction. Moreover, laughter is known to increase tolerance to pain and improve vascular function.
All in all, that’s pretty good medicine. Here are a few more examples of how laughter can be effective (if not the best) medicine.

Improv improves ADLs in Parkinson’s patients

There’s nothing funny about Parkinson’s disease—but maybe there should be.
After performing in an improv comedy course, people with Parkinson’s disease showed significant improvement in activities of daily living, reported researchers at Northwestern University Feinberg School of Medicine, Chicago, IL, in Parkinsonism & Related Disorders.
For this study, the researchers recruited patients with Parkinson’s disease to participate in a 12-week course operated by The Second City®, an improvisational comedy group known for launching the careers of professional funny people like John Belushi, Bill Murray, Steve Carrell, Tina Fey, and many others. At the end of the course—in which all but one participant attended at least 80% of the once-weekly classes—patients showed significantly improved scores on a ratings scale of activities of daily living (ADLs).
For people with Parkinson’s disease, “as mobility becomes limited, spontaneity of thought and action also becomes impaired,” the researchers wrote. “Because the success of an improv scene requires an element of risk-taking, playfulness, and support, the personal development benefits of practicing may include a greater ability to ‘live in the moment’ and focus.”  

A laugh a day keeps the cardiologist away

Can laughter prevent cardiovascular disease? Researchers in Japan have found that people who said they never or almost never laugh had 1.21 times higher prevalence of heart disease compared with people who reported laughing every day, even after adjustment for confounding risk factors. The prevalence ratio for stroke was even greater: 1.60 times higher among never-laughers compared with daily laughers, the researchers reported in the Journal of Epidemiology.
For this study, the researchers analyzed cross-sectional data of 20,934 men and women aged 65 years or older from the Japan Gerontological Evaluation Study. After adjusting for hyperlipidemia, hypertension, depression, body mass index, and other risk factors, the researchers determined that daily laughter is associated with lower prevalence of cardiovascular diseases.
“Although our study could not clearly show any preventive effect of laughter on cardiovascular diseases due to its cross-sectional nature, the present findings are consistent with such an effect, since those who reported having been diagnosed with stroke or heart disease were found not to laugh as often as those who did not have a history of stroke or heart disease,” the amusing authors hilariously concluded.
They acknowledged that their study did have limitations. For one, they couldn’t rule out “reverse causality”—meaning that people with serious illnesses, such as stroke and heart disease, may have less frequent occasions to feel cheerful. Another limitation: Laughter itself may be a sign of having a physically and/or mentally positive lifestyle.
“People who have a more positive outlook on life may be more motivated to engage in healthy behaviors, such as exercise, healthy diet, and moderation in alcohol consumption,” the authors wrote. “Although we controlled for many of these behaviors, the possibility of residual confounding cannot be ruled out.” 

Laughter lightens chronic pain in seniors

“Humor therapy” is an effective nonpharmacological intervention for chronic pain in nursing home residents, according to researchers in a study published in the Journal of Aging Research.
Because many older people simply accept pain as a part of aging, they don’t seek help until their pain becomes severe and unbearable. To add insult to injury, chronic pain not only impairs functional mobility and increases health-care costs, but also often results in social isolation, loneliness, and depression in older folks, the researchers observed.
To that end, they recruited two groups of similar residents in similar nursing homes to find out if humor therapy could reduce chronic pain and loneliness, and improve happiness. In one nursing home, 36 residents participated in an 8-week humor program, while 34 residents in another nursing home were evaluated but not offered the program. About two-thirds of all residents reported chronic pain.
During the humor program, participants made a “happy” scrapbook, heard and told jokes, had laughing exercises, and participated in other funny activities and games. Researchers found that at the end of the program, participants had significant reductions in pain scores and loneliness measures, as well as significant increases in happiness and life satisfaction scores. Sadly, those in the control group had no such improvements. (But don’t worry—the team visited these folks after the study and provided humor activities for them, too.)
The researchers concluded that humor therapy is an effective—and appealing—intervention for reducing pain and loneliness, and increasing happiness and life satisfaction.
“Nurses and other healthcare professionals can incorporate humor in caring for their patients. Telling a joke and encouraging clients to tell a funny story may have a therapeutic effect,” the authors suggested. “Regardless of their physical condition, patients need to allow themselves to be happy, to let humor play a greater role in their lives, and to enjoy life.”
https://www.mdlinx.com/internal-medicine/article/3190
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Is Alzheimer's Infectious? Intriguing Findings From New Mouse Study


Experiment shows amyloid beta pathology can be transmitted
Human growth hormone samples extracted from cadavers decades ago were able to "seed" amyloid beta pathology in mice, researchers reported.

While these findings do not demonstrate that Alzheimer's disease can be transmitted, they provide experimental evidence for the hypothesis that amyloid beta pathology can be transmitted by iatrogenic means, said John Collinge, MD, of University College London, and colleagues, in Nature.

"This represents a new way of thinking about Alzheimer's disease," Collinge said in a press briefing. "There may be certain circumstances -- hopefully, they're rare medical circumstances -- in which transmission of the pathology can occur."

In 2015, Collinge's group reported evidence of early amyloid beta pathology in the brains of seven people who had died of iatrogenic Creutzfeldt-Jakob disease (CJD). These patients had been treated with human growth hormone from cadaveric pituitary glands, a practice that was stopped in 1985 when some recipients were found to have developed CJD. What was unknown at the time was whether these patients developed amyloid beta pathology from the cadaveric samples or whether the samples contained amyloid beta.

Since then, Collinge and colleagues obtained vials of the growth hormone the patients were exposed to and found a number of them tested positive for both amyloid beta and tau protein. They injected samples into mice models of Alzheimer's disease and found that the animals developed accelerated amyloid deposition in the brain parenchyma and around the cerebral vessel walls over time. These deposits were almost completely absent in control mice, including mice that received synthetic recombinant human growth factor.

"This data indicate that the vials used for human treatment indeed contained amyloid beta material that was competent to seed the accumulation of pathological amyloid," said Claudio Soto, PhD, of the University of Texas McGovern Medical School at Houston, who was not involved with the study. "This study, added to the previous one, strongly suggests that amyloid beta deposition seen in patients was induced in a manner reminiscent to prions."

More than 15 years ago, Soto had developed a hypothesis that beta-amyloid plaques were a disorder of protein folding, analogous to prion pathology, such that one misfolded amyloid protein could catalyze misfolding of others to form toxic aggregates.

The question still remains whether transmission of Alzheimer's pathology is restricted to these rare conditions -- such as the use of human-derived products for treatment -- or can occur under more common medical practices like blood transfusions, Soto told MedPage Today.

Concerns about transfusions have been around for some time, noted Bart De Strooper, MD, PhD, of the University College London in England. "Several studies using mice that were similarly genetically primed to develop Alzheimer's disease-like symptoms have shown that this route of transmission is theoretically possible," he told the U.K. Science Media Centre. 

These findings prompted a large retrospective study in Sweden and Denmark that found no evidence for increased rates of Alzheimer's or Parkinson's disease in patients who received blood from donors who went on to develop those diseases. "Those results provided real-world evidence that any such risk is extremely small," De Strooper said. "Nevertheless, it is worth monitoring these risks."

While Collinge emphasized there is no suggestion Alzheimer's disease is contagious or transmissible by blood, he noted it's important to evaluate the risks of iatrogenic transmission of amyloid beta pathology.

"We have now provided experimental evidence to support our hypothesis that amyloid beta pathology can be transmitted to people from contaminated materials," he said. "It will be important to review risks of transmission of amyloid pathology by other medical procedures still done today, including instruments used in brain surgery, drawing on other research and what we already know about accidental CJD transmission."

Mice in this study received samples injected directly into their brains, while people who received the cadaveric human growth hormone preparations decade ago had injections intravenously or intramuscularly, observed Tien-Phat Huynh, MD-PhD candidate, and David Holtzman, MD, both of Washington University in St. Louis, in an accompanying editorial.

"Future studies in animals should assess whether the route of administration influences the ability of material containing misfolded amyloid beta to cause brain amyloid beta pathology, and should investigate the minimum amount of material that has pathological effects," they wrote.

It's worth noting that the stored vials had been maintained at ambient temperature since the mid-1980s, they added. "Their ability to transmit amyloid beta pathology seen in this study corroborates the idea that amyloid beta seeds are remarkably stable," they noted. "This property of amyloid beta seeds emphasizes the importance of not using biological material prepared from the human central nervous system for injection or transplantation into patients during neurosurgical or medical procedures, unless these materials are adequately screened or there is no other option."

The mice in this study were genetically modified to be prone to amyloid beta pathology, but not tau. The samples of human growth hormone people were exposed to also contained tau, Collinge said, and future studies will assess whether the tau in these vials can seed aggregation in other mice.

This study was funded by the U.K. Medical Research Council, the National Institute of Health Research, University College London, the Leonard Wolfson Experimental Neurology Centre, and the National Institute on Aging.

Collinge is a shareholder and director of D-Gen Limited. No other researchers disclosed competing interests.

https://www.medpagetoday.com/neurology/alzheimersdisease/76895
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