Sept. 15 - Doctors Tasha and Ronald Williams, Neuro-psychologists, (no relation) will be sharing insights and expertise on Alzheimer's disease and how it relates to Dementia and Parkinson's disease.
Oct. 20 - Dr. Nancy Jackson, Prof. of Music therapy, IPFW, will be sharing the results of her research with the philharmonic that was conducted last winter, and updating us on a new study being conducted.
Nov. 17 - Dr. Lynn Stafford, podiatrist, will be discussing how podiatry issues (feet, posture, balance, etc.) affect Parkinson's patients.
Dec. - NO MEETING. Celebrate the Christmas season with family and friends.
Jan. 19 - Caring and Sharing Concurrent Sessions.
Feb. 16 - Amy Stir, OT and Driver Rehabilitation Specialist with the Fort Wayne Rehabilitation Hospital will present the program "The Older Driver", and will show us ways to determine when and if it’s time to relinquish our driving privileges.
August Meeting
Special thanks to Dr. Natalie Eddy, DNP, NP, for coming all the way from Valparaiso to share with us her expertise and “passion” about osteoporosis. We gleaned several things from her talk.
Our bones are not designed to break. Broken bones happen but it is not natural. It’s osteoporosis that weakens bones increasing the risk of fracture. Osteoporosis is the most underdiagnosed problem today, especially in postmenopausal women over 50. One in five is diagnosed with osteoporosis. It is the most common type.
Everyone has cells that build new bone. Everyone has cells that remove old bone. When the cells removing old bone work faster than those building new bone, osteoporosis ensues. We all saw the cross-section pictures of old (osteoporotic) and new bone structures, a sort of tight small honeycomb effect vs. larger and weaker honeycombs with lots of space inside the honeycombed area.
CAUSES INCLUDE
Being bed ridden for a long period of time
Chronic rheumatoid arthritis
Kidney disease
Eating disorders
Use of steroids for more the 90 days
Vitamin D deficiency
Large consumption of alcohol, tobacco
Family history of osteoporosis
Hormonal treatment of prostate or breast cancer
Low body weight
SYMPTOMS
Back pain or tenderness
Fractures w/little or no trauma
Weight loss
Low back /neck pain from spinal fractures
Stooped posture (kyphosis)
TESTING
DEXA Scan to measure bone density
Spine CT Scan
QCT – Quantitative Computed Tomography
TREATMENT
Meds – Bio-phosphates: Fosamax, Boniva, Actonel
Hormone Replacement Therapy
Parathyroid Hormones
Exercise
o Weight bearing-walk, jog, dance, tennis
o Resistance-machine/free weights
o Stretch Bands
o Balance-Yoga, Tai Chi
o Stationary bike
o Rowing machine
DIET
Lots of calcium- Cheese, Ice Cream, Leafy Greens, Salmon, Tofu, Yogurt, and other calcium rich foods.
Prevent falls by working on balance, core body strength, using correct shoes, and assistive devices when and where necessary.
Make sure you ask your health care provider about osteoporosis. They undervalue the situation, and you must insist on your provider checking. Medicare does pay for a physical and scans, so insist on them.
Be careful, osteoporosis is no laughing matter.
A NOTE FROM DAN SPANGLER
NINDS Stops Coenzyme Q10 Trial Release date 6/10/2011,
Reprinted from National Parkinson Foundation, www.parkinson.org and PARKINSON NEWS, a publication of the Central Ohio Parkinson Society, July 2011
The National Institute for Neurological Disease and Stroke (NINDS) has announced that they have stopped the clinical trial of Coenzyme Q10, referred to as the Q3 study. The study was designed to test whether fairly high doses of Coenzyme Q10 were effective in slowing the progression of Parkinson’s disease, or neuro-protective. The investigators of the trial determined that there was neither a neuro-protective nor a symptomatic benefit of Coenzyme Q10 for people with early Parkinson’s disease. Everyone who participated in this trial has already been alerted and the open and forthright communications to both investigators and patients should serve as a model for future clinical trial communications.
We know that this outcome is disappointing to those who devoted time and energy to participate in this trial as well as people with Parkinson’s and their families who are seeking new therapies. Coenzyme Q10 is available in an over-the-counter supplement and has been shown to support mitochondria function (energy production) in cells. Clinical trials have also shown some benefit in other conditions. It is a safe and well-tolerated, but expensive over-the-counter, especially in the large doses studied in the Q3 trial. Yet despite the result, the Q3 trial will yield important information-even this negative finding helps scientists to close in on several possible mechanisms and to focus on more promising drugs and studies.
At present, there remain several promising new therapeutic approaches that seek to better target symptoms and potentially slow the disease in clinical and pre-clinical development pipeline. These include gene therapy, advances in DBS, and infusion technology, drugs that target better control of motor symptoms, dyskinesia’s and cognitive symptoms, as well as novel pathways to slow the disease, and we remain hopeful that new treatments may be on the horizon.
Anyone with questions about the trial can contact the National Parkinson Foundation’s toll-free Helpline at 1-800-4PD-INFO (2800-473-4636) for more information. .
TIPS TO MAKE YOUR LIFE BETTER By Ed Gatke
CAREGIVER’S CORNER By Ed Gatke
WHAT: AARP 55 Alive Defensive Driving Class
WHEN: 10:00 am - 3:00 pm, Wednesday, October 12, 2011
WHERE: Community Center 233 W. Main St . Ft. Wayne
A One day driving course for seasoned drivers.
This is an "open" course so you do not need to be over 55 years of age to register.
Lunch break with your own sack lunch or at nearby fast food restaurants.
FEE: $14.00 or $12.00 for AARP members with AARP ID card. Make checks payable to AARP.
Registration deadline is October 5, 2011. Call the community Center 260-427-6460 to register or for more information.
____________________________________________________________________________________________
PAACI (Parkinson's Awareness Association of Central Indiana)is conducting their annual Symposium on Saturday, September 10, 2011.
Doors open at noon. The program starts at 1:00 pm. The symposium will be held at the Indy West Conference Center, 402 N. High School Road, Indianapolis, IN 46214. Cost is $15 per person. Families that pay their PAACI dues pay only $10 per ticket for up to four people.
Questions? Contact Sheri at 317-255-1993 or sheripaaci@yahoo.com. Keynote speaker will be Dr. Lawrence Elmer for the University of Toledo who will be speaking on "PD updates: The Revolution Continues". Also, Stephanie Combs from the University of Indianapolis will be discussing "Boxing vs. traditional Exercise". Both will be followed by an exercise break, snack and a question and answer session. There will also be local Parkinson's Support and Exercise Groups represented. There will be works from local PD artists and PAACI merchandise available for purchase. If you would be interested is showing your artistry, please call or email Sheri (317-255-1993 or sheripaaci@yahoo .com to reserve space.
Parkinson's Disease taken from Discovery's Edge Mayo Clinic's Online Research Magazine
@ www.discoverysedge.mayo.edu
Summary
"It's a devastating disorder that affects a million Americans, and millions around the world. It is associated with shortened life, a lot of misery and a seven-fold increased risk of nursing home placement. It is a bad disease."
D.M. Maraganore, M.D.
Due in large part to significant private and government funding, Parkinson's research has advanced to the point that halting progression, restoring function, and even preventing Parkinson's are now considered realistic goals.
Demetrius (Jim) M. Maraganore, M.D.
Parkinson's is about communication. It is very complex, but in a way, it is also that simple. In an area of the brain called the substantia nigra, a specialized set of neurons sends signals in the form of a neurotransmitter called dopamine. The signals travel to the striatum via long fibers called axons. The activity of this pathway controls normal movements of the body.
When neurons in the substantia nigra degenerate, the resulting loss of dopamine causes the nerve cells of the striatum to fire excessively. This makes it impossible for people to control their movements, leading to the familiar and most obvious symptoms of Parkinson's. Visible symptoms are important here because diagnosis still depends on clinical observation. There are no blood or lab tests that can confirm Parkinson's disease.
Many Parkinson's patients eventually lose 80 percent or more of their dopamine-producing cells. While the cause of this neuronal death remains uncertain, researchers have identified several cellular characteristics that are common in this disease and which appear to play a role in the neurons' degeneration. Chief among these is the presence of Lewy bodies in neurons of the substantia nigra, the brainstem, and other parts of the brain. Lewy bodies are dense clumps of proteins.
Another cellular characteristic of Parkinson's is the presence of Lewy neurites — nerve fibers swollen with proteins. The one critical to our story is called alpha-synuclein. It may interfere with transmission of nerve signals or other important neuronal functions.
On the Edge of One Treatment
Mayo Research: A Triple Threat to Disease
Mayo Clinic conducts complementary research in Parkinson's disease across its three locations – Arizona, Florida and Minnesota. The combination of their respective strengths allows Mayo researchers to observe patients and define the biochemical basis of risk factors, create experimental models in the laboratory, develop therapies and then come back to the patient with a treatment – a very unique collaboration. Researchers in Jacksonville, Florida conduct basic neuroscience research in Parkinson's, while Mayo Clinic in Arizona is a leader in clinical trials for the disease. Discovery's Edge will feature more ongoing Parkinson's investigations by Mayo researchers in future issues.
In 1997, researchers at the National Institutes of Health uncovered the role of alpha-synuclein. Mayo Clinic researchers solidified this evidence. They studied an 80-year span of an Iowa family, discovering that Parkinson's in that family was caused by inheriting three copies of the alpha-synuclein gene from their affective parent. That meant that family members with Parkinson's had four copies of the gene instead of two and were making twice as much of this protein. The protein doesn't have to be abnormally formed or abnormally functioning to cause the disease; there just has to be too much of it. So, why not develop treatments to reduce alpha-synuclein? Such a treatment has been conceived at Mayo Clinic. A patent has been filed. The goal is to reduce the expression of this protein in patients with Parkinson's. The gene can be turned off without affecting normal health. Reducing the protein could halt progression.
Unfortunately, this is probably not the sole cause of Parkinson's. The mutation discovered is a rare cause, but every patient with Parkinson's disease has abnormal accumulations of this protein in Lewy bodies.
A Genomic Map in One Year
In 2004, NIH and The Michael J. Fox Foundation provided approximately $2.8 million in funding to create the first whole genome study, or genetic map, of Parkinson's disease - to be accomplished within one year. Mayo Clinic was chosen from 60 initial applications to be funded. This is a remarkable award of $2.8 million dollars for just one year. The award brought together Mayo Clinic's patient database and Perlegen Sciences, a company that created a high-density array genotyping technology.
"This represents one of the first large-scale whole genome association studies of any disease," said the study's first author, Mayo Clinic neurologist Demetrius Maraganore, M.D. of the Parkinson's Disease Lab, "It is something we've wanted to do for years, and now we finally had the technology and funding to make it happen."
Parkinson's and Alzheimers: More alike than not?
There are many, many different clues supporting a strong relationship between Parkinson's disease and Alzheimer's disease. Two Mayo scientists, Len Kerland and Don Mulder conducted a study in Guam in the 1950's on an epidemic of nerve degeneration on the Island, where there was an abnormal prevalence of ALS, Parkinson's disease and Alzheimer's disease, a strong indication that these disorders may share common underlying mechanisms. Of the 30,000 genes in a human, they only make so many proteins. Further, the Lewy body characteristic in Parkinson's disease is not entirely specific to Parkinson's. There are other Lewy body disorders. Much of the proteins that contribute to Parkinson's disease also contribute to Alzheimer's disease and vice versa. For example, alpha-synuclein was initially discovered as playing a role in modifying amyloidal protein, which is at the very heart of Alzheimer's disease (see DE article).
"What we learn from curing Parkinson's disease will allow us to cure Alzheimer's disease or multiple sclerosis or other brain disorders much earlier because it will set the stage for how to successfully discover the causes of the disease and how to successfully cure it," says Dr. Maraganore.
The combination of Mayo's extensive patient experience, Perlegen's state-of-the-art genotyping technology and significant funding, accelerated Parkinson's research by quickly providing a comprehensive source of information to scientists everywhere. These genomic findings also have high potential for translation: identifying new targets for drug therapies, or a biomarker, or diagnostic test.
The team met the aggressive timeframe, and in September 2005, published the first large-scale whole genome map of genetic variability associated with Parkinson's disease. Their results highlight changes in 12 genes that may increase the risk for Parkinson's in some people.
Significance and Key Findings
Nearly 200 million gentic tests (genotypes) were completed. The team looked at the DNA from 1,000 individuals: 500 sibling pairs—one of whom has Parkinson's disease and one of whom does not, by studying more than 200,000 single nucleotide polymorphisms (SNPs -- pronounced "snips"), unique genetic markers that are spread evenly across the human genome. The purpose was to determine those that vary most between the Parkinson's and non-Parkinson's samples. After identifying these markers, they were furthered analyzed in an additional population consisting of 300 people with Parkinson's and 300 unrelated people as controls.
In the first tier of the whole genome scan, researchers examined DNA from 443 case-sibling pairs; in the second tier, they genotyped 332 case-control pairs. That's a total of 775 pairs or 1,500 individuals total, with the goal of identifying all the major Parkinson's disease susceptibility genes as well as risk factor profiles associated with a high risk for the disease.
"To be most effective, a whole genome association study requires accurate testing of a large number of SNP markers that are distributed across the human genome in a dense and informative pattern. In this respect, our collaborators at Perlegen have set a new standard," said Dr. Maraganore.
The research also confirmed that variation in two previously known regions of the genome, PARK10 and PARK11, are likely associated with Parkinson's disease susceptibility. The study also identified ten additional SNPs that appear to be associated with Parkinson's susceptibility. Some are in or near genes with direct biological relevance to the disease.
Susceptibility genes are genes that may make some persons more or less likely to develop a disease, but do not directly cause the disease. In this study, the size of the effect was small for any single SNP; combinations of gene variants or interactions with environmental factors may be necessary to develop Parkinson's.
If confirmed, the finding of 12 potential susceptibility genes is significant. However, equally significant is that the study found no strong single genetic determinant of Parkinson's disease.
We are now meeting for exercise on
Mondays AND Wednesdays
10:30 a.m. in the usual place.
We hope newcomers will choose the Monday class, as the Wednesday class is running at, or near, capacity of twenty-five participants.
Turnstone
Turnstone has several activities going on throughout the summer and fall:
"
"Harley Motorcycle Raffle Drawing - September 3
"Golf Outing" - September 8 - At Autumn Ridge Country Club.
"Corvette Raffle Drawing" - October 13
Want to volunteer at Turnstone?
Turnstone is a special place, with special people, helping special people. In your own way, if you want to be a part of all of this, visit www.turnstone.org for more details about all we have mentioned. Turnstone helps FWPSG, so get involved in helping Turnstone.
COGNITIVE COMMUNICATION CLASS
There are two sessions per week. ($6.00 for one session or $10 for both) Mondays and Wednesdays from 9:30 to10:15 a.m. at theTurnstone Auditorium, 3320 N Clinton in Ft Wayne.
Peg Maginn, Speech Pathologist, is instructor. (260-483-2100)(260-483-2100, Ex.229) The class addresses speech, voice, swallowing, and cognitive thinking.
