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.
I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please No advertisers, and No Information about Herbal treatments. Please no advertisements.
This is a free site for all.
Thank you.

Saturday, August 6, 2016

Is Parkinson Disease on the Rise?

Aug. 6, 2016

As the US population continues to age, the number of people living with Parkinson disease (PD) continues to grow and is expected to double between 2010 and 2040. Alarming findings recently published by Rodolfo Savica and colleagues indicate that this growth could be underestimated.

The study, published online in JAMA Neurology last month, revealed a significant increase in the incidence of PD and parkinsonism over 30 years, a trend largely driven by men 70 years of age and older. “These trends may be associated with the dramatic changes in smoking behavior that took place in the second half of the 20th century or with other lifestyle or environmental changes,” the authors speculated.
The authors identified cases of parkinsonism diagnosed in Olmsted County, Minnesota, between 1976 and 2005. In all identified cases, diagnosis was validated through the review of the full medical records by a movement disorder specialist, which strengthens the findings and constitutes an important advantage of this study over most comparable studies.
Of 906 patients with parkinsonism included in the analysis, roughly half (n = 464) had PD. Over the 30-year study period, the incidence rates increased significantly in all men. Men with PD were at a higher relative risk (relative risk [RR], 1.24 per decade; 95% confidence interval [CI], 1.08-1.43) than those with parkinsonism (RR, 1.17 per decade; 95% CI, 1.03-1.33). This increase was attributed to men 70 and older: in this cohort, the incidence rates were increased for both PD (RR, 1.35 per decade; 95% CI, 1.10-1.65) and parkinsonism (RR, 1.24 per decade; 95% CI, 1.07-1.44). In contrast, the incidence rates did not increase in men younger than 70 or in women of all ages.
These findings lend additional support to the protective effect of smoking in PD. In the past several decades, the prevalence of smoking declined substantially for men. For women, the prevalence of smoking has never been as high and hence declined less. This may explain the lack of noticeable increase in PD incidence rate in women. Of other environmental and lifestyle factors that changed dramatically during the past several decades, pesticide use, coffee consumption, and head trauma may be implicated as well.
In addition to secular trends, trends by birth cohort have also been analyzed. The incidence rates were the highest in men born between 1915 and 1924. The risk was also increased, albeit not significantly, in women in this birth cohort. The prenatal and early-life environmental factors that affected this cohort, eg, exposure to influenza virus, could have increased the incidence rate in this cohort.
Possible pitfalls of the study include changes in diagnostic criteria, coding practices, and authorization to use individual medical records in research. In addition, the small size of the study population prohibited the analysis of the trends in less common subtypes of parkinsonism, such as multiple system atrophy.
Despite the limitations, the study’s great methodological precision and unique advantages of the studied population lend additional validity to the findings. The results of this study contrast with previously published data, which show either no change or decrease in the incidence rate of PD. If confirmed, the present findings will have major public health implications. 


2. Savica R, et al. Time trends in the incidence of Parkinson disease. JAMA Neurol. 2016 June 20.

Why we need laughter


We've all felt it before; the wholehearted laughter that seems to come from somewhere deep in our soul. It's contagious and heartfelt, silly and liberating. Laughing is one of the best things we can do each day, yet many of us don't seem to get enough of it.
It's hard to dispute that laughter can increase your overall sense of wellbeing, but did you know that laughter might have other benefits as well? Studies have shown that laughter can help relieve pain, bring greater happiness, and even increase immunity. It increases our overall sense of wellbeing and it feels great.
And let's be honest, it is also an amazing abdominal workout. Try falling into a fit of laughter for 10 or 15 minutes and then notice how tight your ab muscles are!
But probably one of the most significant impacts that laughter has on our lives is stress reduction. Everyone experiences stress in their daily lives, and for years psychologists have recommended laughter as a way to help reduce daily stressors.
According to Dr Lee Berk, an associate professor at Loma Linda University in California, "Laughter appears to cause all the reciprocal, or opposite, effects of stress…it shuts down the release of stress hormones such as cortisol.
"Laughter also triggers the production of feel-good neurochemicals like dopamine, which have all kinds of calming, anti-anxiety benefits. Think of laughter as the yin to stress's yang."
Thanks largely to these stress-quashing powers, laughter has been linked to health benefits ranging from lower levels of inflammation to improved blood flow, Berk says, adding that: "Many of these same things also happen when you sleep right, eat right, and exercise." Because of these effects, he regards laughter as another healthy lifestyle, along with more "traditional" lifestyle activities.
Laughter comes naturally for some people; they are able to find humour in almost every situation. For the rest of us though, we may find it a little more difficult to shrug off the stress in favour of the giggles. If you tend to be a person who is more prone to stress and anxiety, fitting laughter into your day is a great way to start making this mind- and body-boosting activity a part of your life.
Here are 7 ways to get you giggling more!
1. Watch a funny movie or sitcom.
2. Read. Remember the comics section of newspapers that many people used to devour. Rediscover the benefits of the humour of comics and funny books.
3. Surround yourself with people who are positive and humorous. Try to find at least one person you can have contact with daily who makes you laugh.
4. Subscribe to podcasts, YouTube videos, and websites that send out daily bites of humour. Sometimes all we need is a quick break from the daily grind to get a good belly laugh.
5. Slow down. You can't find the humour in things if you are moving too fast. Do something outrageous that you can only accomplish with laughter.
6. Find a kid to hang out with. Kids are often the best source of laughter for us as they are uninhibited and free from the strains of life. Listen to a conversation between a couple of six-year-olds and you will be picking yourself up off the ground.
7. Start a joke jar. Gather your favourite jokes and place them in a jar. Use it at home or at work and ask people to pick and share one joke a day.
So what are you waiting for? Let loose with a belly laugh right now and see how it makes you feel.

Friday, August 5, 2016

Doctor claims Greene Parkinson's patient helped by stem cell treatment

Aug. 5, 2016

MASON CITY — In the three years since Shirley Smith received her Parkinson's disease diagnosis, she has gradually given up painting and traveling.
The progression of her symptoms has been heartbreaking for the once-active Greene woman as she has been losing her ability to walk.
Earlier this year, she decided to take a gamble by trying stem cell therapy at Regenerative Cell Institute in Mason City.
Smith had tremors, an unstable balance and was heavily dependent on a wheelchair, and Dr. Crispino Santos, who runs the practice, was initially skeptical he could offer any effective treatment.
Since 2014, Santos has offered treatments in Mason City for patients who have chronic neck, back, spinal or joint paint, as well as those with arthritis or sports- or work-related injuries.
Santos said Smith is the first patient he has attempted to treat with Parkinson's.
After her first stem cell treatment at his office Jan. 29, where stem cells were taken from her abdomen via liposuction and injected into her spine, Smith appeared to show little improvement, Santos said.
Following a second treatment using umbilical cord stem cells last month, she began to show some improvement, walking a little more independently.
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"After being incapacitated for so long, she didn't have the self-confidence that the rest of us have naturally," said her partner, Eddie Hesalroad.
Santos' stem cell treatments typically cost between $4,000 to $7,000, he said. Patients pay out-of-pocket because the procedures are not typically covered by insurance.
That money came from her retirement fund, Smith said. She estimates she can afford one more treatment, which will be scheduled for next month.
Santos has said he believes his stem cell treatments are responsible for her apparent improvement, because she is not undergoing other treatments. He cautioned he hopes for gradual improvements.
"The reality is we really don't know the improvement (to expect)," he said.
Santos is board-certified in anesthesiology and pain medicine. He previously practiced for nearly a decade in Mason City, where he started the cardiac anesthesia program and pain management center at then-St. Joseph Mercy Hospital.
He currently practices pain management, stem cell therapy, regenerative medicine, aesthetics and platelet-rich plasma therapy in Las Vegas through the Regenerative Cell Institute and Interventional Pain Medicine.

A New Approach to Parkinson’s Disease: How Robotics Can Help

Aug. 5, 2016

Audio Player
There are many insidious diseases that debilitate people, but one of the worst is Parkinson’s. Its level of importance has been highlighted by celebrities including Michael J. Fox and Mohammed Ali, who recently died from complications from the disease. About 60,000 people a year are afflicted with Parkinson’s, and an estimated 7 million to 10 million people around the globe are living with it. Alfredo Muniz and Sade Oba are seniors at the University of Pennsylvania who hope their research in robotics will help improve the quality of life for those living with the disease. They are looking at the effectiveness of using motion sensors to gather data and have founded a company called Xeed. They recently spoke with the Knowledge@Wharton Show on Sirius XM channel 111 about their work and how it can be applied.
An edited transcript of the conversation follows. 
Knowledge@Wharton: Where did the idea come from to gather data on Parkinson’s disease?
Alfredo Muniz: It actually came from a robot. We’re both also roboticists master’s students here at Penn, and it actually started from a robot that could do anything. As amazing as that sounds, no one wanted to buy it. You could think of it as a mobile Amazon Echo. After a good half a year or so of trying to commercialize it, we realized that it wasn’t going to happen. No one wanted this amazing robot because the Amazon Echo was already out.
So we took some sensors in the robot and used them for a different purpose. After talking to a couple of people, we realized that [the sensors] could really track fine motor movement very well. After just a very quick conversation with a physical therapist, we focused in on movement disorders and then focused in even more on Parkinson’s disease. This community is really, really hungry for a new way of tracking the disease, and that’s where we hope that our company comes into play.
Knowledge@Wharton: You had this idea of using a trackable, wearing device. What’s the next step in the process?
Muniz: During our studies with robotics, we realized that if you have a robotic arm, you can make it do anything. The idea is nothing new. People have tried to make human robotic arms. We’re just using the same principles, but without the hardware. So this is actually the tracking part. Now we have prototypes, so we have an order coming in from China that’s about 100 different sensors and we’re going to beta test them with our communities here in Philadelphia.
“This community is really, really hungry for a new way of tracking the disease, and that’s where we hope that our company comes into play.”

Knowledge@Wharton: How quick of a process has this been?
Sade Oba: It was fairly quick. We’ve been working on this for a little over a year, but the transition from a robot to an actual wearable was about a two-month process. It was a realization of, “OK, we need to use only a few sensors, we need to make a wearable, let’s go.” Fortunately, we had had enough experience in our past internships doing product design or bio-wearables to be able to come up with a really quick prototype and iteration to start presenting to people.
Knowledge@Wharton: You mentioned talking with a physical therapist. I’m guessing that you’re getting more interest these days from the medical community?
Oba: Yes. We formed a new partnership with Dr. Alice Chen-Plotkin, assistant professor of neurology at the Perelman School of Medicine at UPenn, who has a small group of 250 Parkinson’s patients who will be able to test our devices, which is great. We’ll get a lot of good feedback.
Knowledge@Wharton: What is it that doctors hope they will be able to gather from tracking all that motion?
Muniz: She’s really interested in the effectiveness of medication and the kind of treatments that she has. She has space at the Penn Tower, and she wants us to participate in this kind of trial where she’ll bring in different patients and have them wear the device. These rooms are videotaped. The patients will be there for a couple hours each day, and we’ll basically monitor them. The doctor will say, “Is the drug working? Are you dyskinetic? Is the drug off? Do you need to take medication now?” We’ll be tracking that with the data from the wearables. With that and a little bit of machine learning, we’ll be able to hopefully map that to even more people.
Knowledge@Wharton: The hope is the doctors will be able to understand the effectiveness of the medication and whether some patients don’t require the medication as much as others, correct?
Oba: Yes. For the patients themselves, many have the question of, “OK, am I meeting tomorrow at 2 p.m. with the other board members of my company? Am I going to be showing signs of having Parkinson’s? How do I prevent that from happening? When do I need to take my medication to prevent that from happening?” You would think that it’s exactly two hours beforehand, for example. But that’s not the case for each and every person. Our company aims to have a personalized care for those with Parkinson’s disease.
Muniz: We’re currently in the manufacturing stage — not mass manufacturing, but just small prototypes. We made our first prototype over a year ago, and it was this really gigantic white box. Basically, a bunch of off-the-shelf components. Then we made it smaller with a batch of 15 of those. We discovered some problems with it. Now, we’re on a third version that we are calling “mark three” that we want to give to patients and have them try out.
Knowledge@Wharton: When people think about a wearable device, they think of a Fitbit or something along that line. Is the ultimate goal to pare the size down to something that is similar to that?
Oba: It actually is quite a few millimeters smaller than a Fitbit right now — that’s where our mark two is at. The one that we’re currently designing is going to be even thinner. We don’t have to worry about it being bulky. You’re not going to attract attention. Ultimately, what our patients want is to be able to track their disease without other people tracking them.
Knowledge@Wharton: Do either of you have a family member who was afflicted by Parkinson’s?
Oba: No, we don’t have a personal family member, but we did have a mentor through our years in college, who would like to remain anonymous, who does have Parkinson’s. It was after working with this individual for years that we realized that [sufferers of this disease could use] some extra assistance from a wearable device such as ours.
Muniz: Even though we have all this technology, there’s still a lot that we don’t know about Parkinson’s, and it’s because they don’t have the tools necessary to objectively quantify what’s going on.
Knowledge@Wharton: Sade, you mentioned a CEO who may be battling Parkinson’s and doesn’t want to show outwardly. We’re talking about a disease that has a stigma attached to it.
Oba:  Yes. One of the focus points of our company is, “How do we provide this service that gives our patients so much information, but doesn’t leak information to other people?” … We’re trying to find a way to give our patients a lot of information on how they can improve their everyday lives without necessarily broadcasting to the world that they have Parkinson’s disease. And that comes with a very small wearable and a phone application that they can use to track their information, and then they can choose who they want to share it with, whether it be their physical therapist or their physician or a family member or a caretaker

Knowledge@Wharton: I guess the way to try and build this out is to have it connect to your smartphone or tablet or laptop so that you have that information available to pass onto a physical therapist, a doctor or a caretaker?
Oba: Correct. One of the interesting challenges is exactly how much information to share. Some people want every single data point. They want to know exactly how their arm was moving. Some people just want to know when they’re leaning on the table for too long, because that’s one of the symptoms. You don’t really realize it until you’re hunched over. Some people want simple information like that. “Oh, can you buzz me when I’m doing that? That’s all I really want to know.” How do we personalize the information on the app such as that? What other bits of information do patients want to know? How do we overlap that with what therapists want and what physicians want? That’s one of the things that we’re currently doing as far as our software development is concerned — how to have a unified, easy-to-use interface that caters to each and every person.
Knowledge@Wharton: How much of a learning experience has this been for you?
Muniz: Even though Sade’s a mechanical engineer and I’m an electrical engineer, during our time at Penn, we had so many resources that we just basically went crazy with learning a bunch of different things and taking advantage of the other students who can help us, and the professors. It’s all new things, but I think we’re kind of used to always learning new things and always pushing ourselves and just really discovering.
Oba: This is the most focused we’ve ever been. We have done a wide variety of projects together the past couple of years. We just never thought we’d come back to a medical device. We have known each other for about nine years now. We went to a high school for health professionals and vowed after spending four years shadowing doctors that we would never do anything in the medical field ever again. Lo and behold, we graduate college and the first thing we do is start a medical device company. It’s been interesting to come full circle and be this focused on one specific thing.
Knowledge@Wharton: Do you already have other areas that you would like to focus on in terms of the potential for this device?
Oba: Yes. At our prime, we hope to move forward and expand to other movement disorders –multiple sclerosis or even the rehabilitation of stroke patients — to really hit on all those people who need to track exactly how they’re moving on a daily basis, who may not actually have a cure in the moment and just need to know, “How can I be better at this exact time tomorrow?”
Knowledge@Wharton: What’s it been like having this company and seeing it develop in the short time that you’ve had it?
Muniz: It’s been really crazy. We have had to make tradeoffs. You can’t be a super human and do everything perfectly all the time. Obviously, our grades suffered a little bit, but we graduated and we got this prize. It was definitely worth it…. People have been contacting us left and right. Every time there’s a news article, there’s always a new partner that wants to try out our devices in their clinic. There are always new patients that just want to beta test. There are also people who are owners of manufacturing companies that [tell us], “I have Parkinson’s. Maybe I can help you.”
Oba: The network is expanding. We’ve been contacted by a lot of people. We’re trying to reel all that in and make sure that we are able to not necessarily cater to each person, but manage it in a way that fits within the timeline of growth within our company. That’s one of the fun things on the entrepreneurship side: How can we make sure all these people fit into our timeline? Is it possible?
Knowledge@Wharton: Is the third version that you’re working on now going to be the one that has the opportunity to be in the market? Or are there still pieces that you’re tinkering with and trying to make better?

“One of the interesting challenges is exactly how much information to share.”
Muniz: It’s not in the market for sale yet because of government regulations — the Federal Communications Commission and also, potentially, the FDA. Those are certifications that we must have before we’re able to sell the physical device. However, the service can be sold. But at this point, we’re not interested in making money yet; we’re just interested in refining the device. There are still one or two more iterations before we can actually go into mass manufacturing and legally sell the device.
Knowledge@Wharton: Why do you need FCC approval?
Oba: Because of our wireless communication. If you wirelessly communicate in a device that you’re making, then you need to have this certification. It’s kind of a gray area when you’re buying someone else’s chip off the market or if you’re designing your own. But currently at our stage, we would need FCC approval to be able to do that.
Knowledge@Wharton: How far away do you think you are from going to the FDA?
Oba: By the end of 2017. We’re not that far away. What helps is to have a physician on hand who has a set of patients that they’re doing studies on, so you’re able to do a trial beta test. Now that we have those individuals and our new devices are being made and the only thing that’s really being tweaked is the software, we’re almost at that point after a few months of testing with these individuals … to be able to approach the FDA and get the process started.
Knowledge@Wharton: Is tackling something like Parkinson’s easier to do these days because of the technology?
Muniz: This technology is not new. There are companies that have these sorts of devices, but the problem is that they’re really expensive. A hospital will only have one or two of these because they can’t afford to give one to each patient, let alone have them take it home. What we’re doing here is creating a new price point, bringing that sort of technology to the consumer, to the patients, to everyone that needs it.
Knowledge@Wharton: When you started at Penn a few years ago, this was not the path that you originally thought you were going to go down, correct?
Oba: We both thought that we would end up in product design firms in California with all of our other peers.
Muniz: When you enter engineering, the dream is California. You’re working for Apple or Google. But once you intern there, it’s kind of like, “Oh, that’s it?”
Knowledge@Wharton: It has to feel very good that you have gone down this path and that there is a light at the end of the tunnel.
Oba: This has been the most rewarding thing. I think the light isn’t as bright as we would want because once you start working in the Parkinson’s space, the biggest light, the brightest light, the actual end of the tunnel is a cure. Our company does not provide a cure. We don’t advertise that because it’s not possible on our end. But what we do strive for is to make all the other moments of your life easier for you, more bearable for you, more manageable. So you feel as if you have some of the control back that the disease has taken from you. That’s the best thing that we can provide and what we get the greatest feedback on…. That we’re in this space and that we’re making active change and that we’re moving as quickly as we can — people really, really appreciate that and are getting really excited about it.
Knowledge@Wharton: What is your hope for the company in the next 10 to 15 years?
Oba: In the next 10 to 15 years, I think we definitely want to get acquired because we’d want to be able to expand our outreach to the point where a smaller startup wouldn’t be able to do that. But in the next five years, it’s the whole expanding to other movement disorders, tackling Parkinson’s, having a good network of therapists and physicians in this area to help continue improving therapy regimens or knowing which medications are best for each patient and when they need to be taken. Then, it’s moving onto other conditions that also need the same treatment that the Parkinson’s community is now getting from Xeed.


Microscopic collisions help proteins stay healthy

Aug. 5, 2016

This is a model of the structure of clathrin, a protein that researchers at The University of Texas Health Science Center at San Antonio used to study how a heat shock protein disassembles protein complexes. Drs. Eileen Lafer and Rui Sousa/UT Health Science Center at San Antonio

Studies at The University of Texas Health Science Center at San Antonio are providing basic new understanding about "heat shock proteins," also called "chaperone proteins." These proteins, first identified in cells subjected to heat, are very important under many stressful and non-stressful metabolic conditions. They maintain proper protein function and, importantly, prevent the inappropriate accumulation of damaged proteins. For example, accumulation of damaged proteins such as beta amyloid, tau and synuclein are thought to be very important in the development of diseases of the brain such as Alzheimer's disease and Parkinson's disease.
Aug. 1 in the journal Nature Structural & Molecular Biology, a Health Science Center research team led by Rui Sousa, Ph.D., and Eileen M. Lafer, Ph.D., both professors of biochemistry in the School of Medicine, presented data that show how heat shock proteins break apart protein complexes. They found that when heat shock proteins with molecular weight 70 (Hsp70s) are recruited to protein complexes, rather than simply binding to these complexes, the Hsp70s collide with them and generate a force that dissolves the complexes.
"No one knew how the heat shock proteins pull apart bad protein complexes," Dr. Sousa said. "At the molecular level, everything is moving, colliding and bumping, and smashing into other components of the cells. We found that the system moves Hsp70s to where they are needed. Once this occurs, collision pressures pull things apart."
Model system
Previous attempts to glean this information failed because the proteins studied were too heterogeneous--of too many different sizes, shapes and actions--to isolate the Hsp70 behavior.
The UT Health Science Center team studied clathrin, a protein that is uniform in size and shape and is important in making intracellular cages that transport other proteins. Previously clathrin was only available from animal specimens, making it very difficult to manipulate experimentally. Dr. Lafer made a technical breakthrough when she was able to grow clathrin in bacteria for the first time using recombinant DNA technology. The clathrin could then be genetically engineered for mechanistic studies.
Dr. Lafer grew clathrin "cages"--shaped like microscopic soccer balls--that provided the biological raw material for Dr. Sousa and the team to study the force that occurs with Hsp70 collisions. The clathrin model system could be manipulated to yield precise results.
A wrecking machine
Dr. Sousa gave this analogy of the study: The heat shock protein is like a worker with an ax who, when moved to a wood pile, begins swinging. The wood pile represents a protein complex. The scientists give the worker both thick trees and thin trees to swing at, and spindly wood and hard wood. They change the angle of the wood pile, and every other variable, to learn how this affects the chopping.
By making variants of clathrin with recombinant DNA technology, team members were able to manipulate this biological material in ways that allowed them to determine the mechanism by which it is taken apart by Hsp70.
"This work was a tour de force, requiring the convergence of exceptional biochemical and molecular genetic skills with a deep understanding of the principles of physical chemistry," said Bruce Nicholson, Ph.D., chair of the Department of Biochemistry at the Health Science Center. "Such insights into the most basic aspects of protein chemistry and cell biology are often, as in this case, driven by a curiosity to find out how the molecular machines that drive our bodies work. But from these basic pursuits of scientific curiosity will often stem great benefits to human health."
Hsp70 in disease
Understanding Hsp70 behavior may have relevance to human disease. By increasing Hsp70 function, scientists cured Huntington's, a neurodegenerative disease, in a fly model. Cancer is another interesting focus. Tumors rely on Hsp70s to survive, so lowering Hsp70 function is a topic in cancer research.
"This is an impressive study that not only improves our understanding of cellular biology, but could lead to therapeutic discoveries for neurodegenerative diseases," said Francisco González-Scarano, M.D., dean of the School of Medicine and executive vice president for medical affairs of the Health Science Center. "It is a tribute to scientists who ask hard questions and develop tools to answer them. My congratulations to the team."
"We attacked this problem because it was a really important question in cellular biology," Dr. Lafer said. "We didn't do it because we wanted to cure neurodegenerative disease or cancer. We know, however, that when we attack really important questions in science and biology, it ultimately leads to translational applications down the line."
"Sometimes as a scientist you just increase understanding of the way the world works," Dr. Sousa said. "This is something scientists have wanted to know."
News online
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About the UT Health Science Center at San Antonio
The University of Texas Health Science Center at San Antonio, with missions of teaching, research and healing, is one of the country's leading health sciences universities. Its schools of medicine, nursing, dentistry, health professions and graduate biomedical sciences have produced 33,000 alumni who are advancing their fields throughout the world. With six campuses in San Antonio and Laredo, the university has a FY 16 revenue operating budget of $801.8 million and is the primary driver of its community's $30.6 billion biomedical and health care industry. For more information on the many ways "We make lives better®," visit

Therapeutic strategies targeting Alzheimer's disease-related molecules

Aug. 5, 2016

Therapeutic strategies targeting Alzheimer's disease (AD)-related molecule β-amyloid (Aβ), Tau protein and BACE enzyme have been recently explored. However, the therapeutic efficacy for a single target is not ideal. The clinical trials that clean Aβ from the brain in AD patients were largely unsuccessful. It is well known that the inflammatory response is one component of AD pathogenesis, leading to a series of irreversible pathological events. Epidemiological evidences show that long-term use of non-steroidal anti-inflammatory drugs has a sparing role in AD, but it failed to prevent the progression of symptoms in AD patients in randomized clinical trials. Possible reasons for the failure of anti-inflammatory drugs may be associated with: 1) the advanced state of disease or the dosing regimens of drugs; 2) most of the available anti-inflammatory drugs are not really "anti-inflammatory"; 3) these "anti-inflammatory" drugs only prevent the pro-inflammatory responses, but do not trigger the anti-inflammatory responses.

Fasudil, a selective Rho kinase (ROCK) inhibitor, may be a more appropriate therapeutic option in the treatment of patients with AD. Our previous studies provided many evidence that Fasudil inhibited the inflammatory response in both experimental autoimmune encephalomyelitis (EAE) and Parkinson's disease (PD) models through converting inflammatory M1 microglia/macrophage to anti-inflammatory M2 cells. The investigations from other groups also demonstrated therapeutic potential in EAE, PD and amyotrophic lateral sclerosis (ALS). It should be noted that the inhibition of inflammatory microglia is essential for the neuroprotective effects of ROK inhibitor on MPTP-induced dopaminergic cell death. Based on these reasons, we designed the study to observe therapeutic potential of Fasudil, and explored possible mechanisms in APP/PS1 transgenic .
Our results show that administration of Fasudil improved learning and memory deficits in APP/PS1 Tg mice. The expression of Aβ1-42 in hippocampus and brain of mice was clearly observed in APP/PS1 Tg mice, while treatment of Fasudil reduced the expression of Aβ1-42 in hippocampus of APP/PS1 mice. Tau protein intracellular neurofibrillary tangles (NFTs) pathology is the major correlation between clinical symptoms and main feature in AD. Tau-induced animal models reproduce neuronal and glial Tau pathology, leading to the progressive cognitive and/or motor impairment and premature death. Our results demonstrated that the treatment of Fasudil decreased the number of p-Tau/Ser396-positive cells and expression of p-Tau/Ser396 protein in brain of APP/PS1 Tg mice. BACE is a β-site APP cleaving enzymes that is a major drug target for AD because of BACE-mediated cleavage of APP and decrease of Aβ. To investigate whether Fasudil intervention influences the levels of BACE, we observed the expression of BACE in the hippocampus and brain. The expression of BACE protein in brain of App/PS1+saline mice was elevated significantly compared with those of wild-type mice and were dramatically downregulated upon treatment with Fasudil for 8 weeks. PSD-95 is a synaptic protein regulating glutamate receptor anchoring, synaptic stability and certain types of memory that is regulated by Aβ. The treatment of Fasudil increased the expression of PSD-95 in App/PS1 mice. Taken together, Fasudil ameliorated learning and memory deficits, accompanied by reduced Aβ deposition, Tau phosphorylation, BACE expression, as well as increased PSD-95 expression in hippocampus.
It has become increasingly apparent that neuroinflammation plays an important role in the pathology of AD. Our results found that the treatment of Fasudil also inhibited TLR-2/4, MyD88, p-NF-κB/p65, IL-1β, IL-6 and TNF-α, and induced IL-10 in App/PS1 mice.
AD is a complex aging-related disease caused by a variety of genetic and environmental factors. Currently therapeutic agents approved by the US Food and Drug Administration (FDA), including donepezil, rivastigmine, galantamine and memantine, are unable to prevent or reverse disease progression and are only modestly efficacious. A series of irreversible pathological events coexist in the pathogenesis of AD, including , toxic to neurons, oxidative stress, activated microglia and loss of Aβ clearance ability. The novel therapeutic strategy should target multiple aspects of AD, e.g., attenuates the Aβ burden and Tau phosphorylation, and/or converts beneficial microglia polarization. Fasudil exhibited a multitarget therapeutic effect in APP/PS1 transgenic mice by the reduction of Aβ deposition and Tau phosphorylation, the decrease of BACE and the increase of PSD-95, as well as inhibition of TLRS-NF-κB-MyD88 inflammatory axis. However, these results still need to be repeated and confirmed before clinical application.

Statin Use Tied to Reduced Risk of Parkinson’s in Diabetes

Aug. 4, 2016

For patients with diabetes, statin use is associated with reduced incidence of Parkinson's disease, according to a study published online July 29 in the Annals of Neurology.

For patients with diabetes, statin use is associated with reduced incidence of Parkinson's disease (PD), according to a study published online July 29 in the Annals of Neurology.
Kun-Der Lin, M.D., from the Kaohsiung Municipal Ta-Tung Hospital in Taiwan, and colleagues examined the correlation between statin dosage and risk of PD in patients with diabetes. Data were included for 50,432 patients with diabetes, of whom half were statin users.

The researchers found that the incidence of PD was lower in statin users versus non-users, with crude hazard ratios of PD incidence of 0.65 and 0.60 in female and male statin users, respectively, versus non-users. All statins except lovastatin had protective effects on PD incidence, and there was evidence of a significant dose-dependent trend.

"In Taiwanese diabetic patients, the risk of PD is lower in statin users than in non-users of statins. Statin users, except lovastatin users, are dose-dependently associated with a decreased incidence of PD compared with non-users of statins," the authors write. "This finding provides a new indication for statin beyond lipid control and cardiovascular events in diabetic patients."

Large Scale Study Assesses Statin Use and Incidence of Parkinson's Disease

AUG. 5, 2016

Protective effects for all statins, except lovastatin; evidence of dose-dependent trend

HealthDay News — For patients with diabetes, statin use is associated with reduced incidence of Parkinson's disease (PD), according to a study published online July 29 in the Annals of Neurology.

Kun-Der Lin, MD, from the Kaohsiung Municipal Ta-Tung Hospital in Taiwan, and colleagues examined the correlation between statin dosage and risk of PD in patients with diabetes. Data were included for 50,432 patients with diabetes, of whom half were statin users.

The researchers found that the incidence of PD was lower in statin users versus non-users, with crude hazard ratios of PD incidence of 0.65 and 0.60 in female and male statin users, respectively, versus non-users. All statins except lovastatin had protective effects on PD incidence, and there was evidence of a significant dose-dependent trend.

"In Taiwanese diabetic patients, the risk of PD is lower in statin users than in non-users of statins. Statin users, except lovastatin users, are dose-dependently associated with a decreased incidence of PD compared with non-users of statins," the authors write. "This finding provides a new indication for statin beyond lipid control and cardiovascular events in diabetic patients."

Research finds way to measure Parkinson's gene mutation

Aug 2, 2016

A team of scientists, led by Professor Dario Alessi from the University of Dundee, has developed a new way to measure the effect of mutations in LRRK2 – a gene linked to Parkinson's.
The findings, published in the Biochemical Journal, could pave the way to a test for this form of Parkinson's and the ability to develop drugs that target it.

Inherited Parkinson's

A number of genetic changes, or mutations, are known to increase the risk of Parkinson's.
While inheriting one of these genetic changes is rare, accounting for around 5% of Parkinson's, mutations in LRRK2 are one of the most common causes of inherited Parkinson's.
This new discovery could lead us to a new type of treatment that tackles a root cause of Parkinson's rather than mask its symptoms.
Dr Beckie Port, Senior Research Communications Officer
Mutations in the LRRK2 gene often cause the resulting protein to be more active than normal.
And scientists believe that reducing the activity of the LRRK2 protein may help people with this form of inherited Parkinson's.
This new research has identified a simple way to measure the activity of LRRK2 indirectly by looking at one of the proteins that LRRK2 interacts with.
The researchers believe this could be turned into a simple test to find people where overactive LRRK2 plays a role in their Parkinson's.

Identifying different types of Parkinson's

Beckie Port, Senior Research Communications Officer at Parkinson's UK, comments:
"Research is uncovering different types of Parkinson's that may respond to treatments in different ways. Understanding this is essential for developing new and better treatments that can slow or stop the progression of Parkinson's.
"Identifying people with LRRK2-related Parkinson's would allow researchers to test new drugs that target this type of the condition.
"While less than 1% of all people with Parkinson's has changes in the LRRK2 gene, the LRRK2 protein may also play a key role in non-inherited Parkinson's.
"This new discovery could lead us to a new type of treatment that tackles a root cause of Parkinson's rather than mask its symptoms."