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Michael J. Fox Foundation grant to Dr. Samuel Young will provide Parkinson's drug development tools

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Public release date: 3-May-2012 [ | E-mail | Share ]

Contact: Dennis Tartaglia dtartaglia@tartagliacommunications.com 732-545-1848 Tartaglia Communications

Samuel M. Young, Jr., PhD, research group leader at the new Max Planck Florida Institute (MPFI), has received his first grant from The Michael J. Fox Foundation for Parkinson's Research (MJFF). The grant will enable Dr. Young and colleagues to develop a technology that will help scientists working in drug development to research potential treatments that target LRRK2, a Parkinson's-related gene. Globally, five million people have Parkinson's disease.

"We are excited about receiving The Michael J. Fox Foundation grant, as these grants are competitive and MJFF is the world's largest private funder of Parkinson's research," said Dr. Young, who directs MPFI's Molecular Mechanisms of Synaptic Function research group. "We believe that the tools we develop will prove important in advancing Parkinson's research."

Translational researchers working in Parkinson's disease have been hindered in studying the function of the LRRK2 gene in pre-clinical models of Parkinson's. This has been due to difficulty in expressing this gene with commonly used neuroscience research tools known as recombinant viral vectors. Dr. Young will develop tools that will allow researchers to get around this problem.

Mutations in the gene for leucine-rich repeat kinase 2 (LRRK2) are among the most common genetic links to Parkinson's disease yet discovered. LRRK2 has garnered much excitement among drug makers due to its reported protein kinase activity, which appears to be enhanced by Parkinson's disease-causing mutations.

"We are delighted that The Michael J. Fox Foundation has awarded Dr. Young with a grant to lead this critical project," said David Fitzpatrick, PhD, CEO and Scientific Director of MPFI. "This grant recognizes Dr. Young's specialized expertise, as well as our Institute's leadership role in neural circuit research."

Recombinant viral vectors are used by scientists to deliver genetic material into cells. Viruses have evolved specialized molecular mechanisms to efficiently transport their genomes inside the cells they infect. To create the vector, viruses are bioengineered to strip their viral genome or most of their viral genome, which renders them harmless. This enables them to carry transgene expression cassettes to express a gene of interest. The transgene expression cassette is a fragment of DNA that carries the regulatory elements necessary for cells to express specific genes within a cell or organism.

As the principal investigator of the project, Dr. Young will work with collaborators at other institutions to generate the optimal expression cassette to express LRRK2.

Dr. Young has specialized training that makes him the ideal investigator for this project. After training in virology and in recombinant viral vectors during his doctoral studies, Dr. Young switched fields and became a post-doctoral neuroscience researcher, learning electrophysiology techniques. He carried out a second post-doctoral position, gaining further experience with advanced electrophysiological techniques as well as calcium imaging. Using this unique training, which combines techniques in molecular, electrophysiological and biophysical methods, Dr. Young and his group at MPFI study the molecular mechanisms regulating synaptic function. Understanding these mechanisms is critical because the major causes of brain diseases are due to synaptic dysfunction.

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Michael J. Fox Foundation grant to Dr. Samuel Young will provide Parkinson's drug development tools

Michael J. Fox Foundation grant to Dr. Samuel Young will provide Parkinson’s drug development tools

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Public release date: 3-May-2012 [ | E-mail | Share ]

Contact: Dennis Tartaglia dtartaglia@tartagliacommunications.com 732-545-1848 Tartaglia Communications

Samuel M. Young, Jr., PhD, research group leader at the new Max Planck Florida Institute (MPFI), has received his first grant from The Michael J. Fox Foundation for Parkinson's Research (MJFF). The grant will enable Dr. Young and colleagues to develop a technology that will help scientists working in drug development to research potential treatments that target LRRK2, a Parkinson's-related gene. Globally, five million people have Parkinson's disease.

"We are excited about receiving The Michael J. Fox Foundation grant, as these grants are competitive and MJFF is the world's largest private funder of Parkinson's research," said Dr. Young, who directs MPFI's Molecular Mechanisms of Synaptic Function research group. "We believe that the tools we develop will prove important in advancing Parkinson's research."

Translational researchers working in Parkinson's disease have been hindered in studying the function of the LRRK2 gene in pre-clinical models of Parkinson's. This has been due to difficulty in expressing this gene with commonly used neuroscience research tools known as recombinant viral vectors. Dr. Young will develop tools that will allow researchers to get around this problem.

Mutations in the gene for leucine-rich repeat kinase 2 (LRRK2) are among the most common genetic links to Parkinson's disease yet discovered. LRRK2 has garnered much excitement among drug makers due to its reported protein kinase activity, which appears to be enhanced by Parkinson's disease-causing mutations.

"We are delighted that The Michael J. Fox Foundation has awarded Dr. Young with a grant to lead this critical project," said David Fitzpatrick, PhD, CEO and Scientific Director of MPFI. "This grant recognizes Dr. Young's specialized expertise, as well as our Institute's leadership role in neural circuit research."

Recombinant viral vectors are used by scientists to deliver genetic material into cells. Viruses have evolved specialized molecular mechanisms to efficiently transport their genomes inside the cells they infect. To create the vector, viruses are bioengineered to strip their viral genome or most of their viral genome, which renders them harmless. This enables them to carry transgene expression cassettes to express a gene of interest. The transgene expression cassette is a fragment of DNA that carries the regulatory elements necessary for cells to express specific genes within a cell or organism.

As the principal investigator of the project, Dr. Young will work with collaborators at other institutions to generate the optimal expression cassette to express LRRK2.

Dr. Young has specialized training that makes him the ideal investigator for this project. After training in virology and in recombinant viral vectors during his doctoral studies, Dr. Young switched fields and became a post-doctoral neuroscience researcher, learning electrophysiology techniques. He carried out a second post-doctoral position, gaining further experience with advanced electrophysiological techniques as well as calcium imaging. Using this unique training, which combines techniques in molecular, electrophysiological and biophysical methods, Dr. Young and his group at MPFI study the molecular mechanisms regulating synaptic function. Understanding these mechanisms is critical because the major causes of brain diseases are due to synaptic dysfunction.

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Michael J. Fox Foundation grant to Dr. Samuel Young will provide Parkinson's drug development tools

Freezing Parkinson's in its tracks: Researcher developing therapy to halt symptoms in Parkinson's patients

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ScienceDaily (May 2, 2012) Parkinson's disease, a disorder which affects movement and cognition, affects over a million Americans, including actor Michael J. Fox, who first brought it to the attention of many TV-watching Americans. It's characterized by a gradual loss of neurons that produce dopamine. Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson's symptoms at a young age.

The ability to modify the activity of DJ-1 could change the progress of the disease, says Dr. Nirit Lev, a researcher at Tel Aviv University's Sackler Faculty of Medicine and a movement disorders specialist at Rabin Medical Center. Working in collaboration with Profs. Dani Offen and Eldad Melamed, Dr. Lev has now developed a peptide which mimics DJ-1's normal function, thereby protecting dopamine-producing neurons. What's more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.

Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. Dr. Lev says that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.

Guarding dopamine levels

As we age, we naturally lose dopamine-producing neurons. Parkinson's patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson's patient or aging normally, says Dr. Lev.

The researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle. "We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain," explains Dr. Lev.

In pre-clinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson's disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.

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

Filling an urgent need

According to Dr. Lev, this peptide could fill a gap in the treatment of Parkinson's disease. "Current treatments are lacking because they can only address symptoms -- there is nothing that can change or halt the disease," she says. "Until now, we have lacked tools for neuroprotection."

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Freezing Parkinson's in its tracks: Researcher developing therapy to halt symptoms in Parkinson's patients

Freezing Parkinson’s in its tracks: Researcher developing therapy to halt symptoms in Parkinson’s patients

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ScienceDaily (May 2, 2012) Parkinson's disease, a disorder which affects movement and cognition, affects over a million Americans, including actor Michael J. Fox, who first brought it to the attention of many TV-watching Americans. It's characterized by a gradual loss of neurons that produce dopamine. Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson's symptoms at a young age.

The ability to modify the activity of DJ-1 could change the progress of the disease, says Dr. Nirit Lev, a researcher at Tel Aviv University's Sackler Faculty of Medicine and a movement disorders specialist at Rabin Medical Center. Working in collaboration with Profs. Dani Offen and Eldad Melamed, Dr. Lev has now developed a peptide which mimics DJ-1's normal function, thereby protecting dopamine-producing neurons. What's more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.

Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. Dr. Lev says that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.

Guarding dopamine levels

As we age, we naturally lose dopamine-producing neurons. Parkinson's patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson's patient or aging normally, says Dr. Lev.

The researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle. "We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain," explains Dr. Lev.

In pre-clinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson's disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.

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

Filling an urgent need

According to Dr. Lev, this peptide could fill a gap in the treatment of Parkinson's disease. "Current treatments are lacking because they can only address symptoms -- there is nothing that can change or halt the disease," she says. "Until now, we have lacked tools for neuroprotection."

See the article here:
Freezing Parkinson's in its tracks: Researcher developing therapy to halt symptoms in Parkinson's patients

Concerns as nurse leaves

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By Andrew Clarke

Published at 11:11, Thursday, 03 May 2012

HEALTH chiefs have moved to reassure people living with Parkinsons disease that they will not suffer a loss of service in the Copeland area.

The West Cumbria branch of Parkinsons UK has voiced its concerns after Georgie Berry, a nurse specialising in Parkinsons care in the area, left her post for a new role last month.

Members say they have been left in limbo in the light of Ms Berrys departure, and are seeking clarification about the future provision of services.

However, a spokeswoman for the North Cumbria University Hospitals Trust says measures are in place to ensure that patients will continue to receive to same level of care.

John Kane, chairman of the West Cumbria branch of Parkinsons UK, said: There were four Parkinsons nurses in Cumbria, and Georgie covered Copeland and Aller-dale.

Georgie was dedicated in her role and was a lifeline for people with Parkinsons disease. She could alter peoples medication to what best suited their symptoms, which is crucial as there are more than 20 different types of medication to help deal with this awful condition.

We still have a support officer, but he is there to offer practical and emotional support, but is not able to deal with the medical side of things.

Parkinsons is on the increase we have over 300 members in our branch and there is a lot of concern about the gap in services that now exists.

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Concerns as nurse leaves

Once-Marginalized Parkinson's Disease Theory May Be Valid

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Editor's Choice Main Category: Parkinson's Disease Article Date: 02 May 2012 - 11:00 PDT

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Current Article Ratings:

4.5 (2 votes)

By using powerful computer tools and laboratory tests, the scientists managed to obtain a step-by-step explanation of how a "protein-run-amok" aggregates within the membranes of neurons, puncturing them and causing Parkinson's disease symptoms. The process describes how -synuclein (a-syn) can turn against us, especially as we get older. The results of the model demonstrate how -syn monomers penetrate cell membranes and how they become coiled and aggregate within nanoseconds into dangerous ring structures that are harmful for neurons.

Lead researcher Igor Tsigelny, a research scientist at the San Diego Supercomputer Center and Department of Neurosciences at UC San Diego, declared:

Numerous cases of familial Parkinson's disease are caused by a limited number of protein mutations, the most toxic of which is A53T. Tsigelny's team demonstrated that the mutant form of -syn both penetrates neuronal membranes substantially faster compared with a normal -syn, and that the mutant protein also accelerates ring formation.

Tsigelny explained:

The researchers discovered that their modeling results also proved consistent with electron microscopic images of neurons in Parkinson's disease patients that have shown damaged neurons are riddled with ring structures.

The researchers immediately turned to search for drug candidates that can inhibit ring formation in neuron membranes. The highly complex modeling consists of various sophisticated scientific realms, which intersect between chemistry, physics, and statistical probabilities. A wide spectrum of interacting forces within this realm cause circumstances comparable to an earthquake, in which the a-syn proteins bump and tremble, coil and uncoil and join up in pairs or larger groups.

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Once-Marginalized Parkinson's Disease Theory May Be Valid

Once-Marginalized Parkinson’s Disease Theory May Be Valid

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Editor's Choice Main Category: Parkinson's Disease Article Date: 02 May 2012 - 11:00 PDT

email to a friend printer friendly opinions

Current Article Ratings:

4.5 (2 votes)

By using powerful computer tools and laboratory tests, the scientists managed to obtain a step-by-step explanation of how a "protein-run-amok" aggregates within the membranes of neurons, puncturing them and causing Parkinson's disease symptoms. The process describes how -synuclein (a-syn) can turn against us, especially as we get older. The results of the model demonstrate how -syn monomers penetrate cell membranes and how they become coiled and aggregate within nanoseconds into dangerous ring structures that are harmful for neurons.

Lead researcher Igor Tsigelny, a research scientist at the San Diego Supercomputer Center and Department of Neurosciences at UC San Diego, declared:

Numerous cases of familial Parkinson's disease are caused by a limited number of protein mutations, the most toxic of which is A53T. Tsigelny's team demonstrated that the mutant form of -syn both penetrates neuronal membranes substantially faster compared with a normal -syn, and that the mutant protein also accelerates ring formation.

Tsigelny explained:

The researchers discovered that their modeling results also proved consistent with electron microscopic images of neurons in Parkinson's disease patients that have shown damaged neurons are riddled with ring structures.

The researchers immediately turned to search for drug candidates that can inhibit ring formation in neuron membranes. The highly complex modeling consists of various sophisticated scientific realms, which intersect between chemistry, physics, and statistical probabilities. A wide spectrum of interacting forces within this realm cause circumstances comparable to an earthquake, in which the a-syn proteins bump and tremble, coil and uncoil and join up in pairs or larger groups.

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Once-Marginalized Parkinson's Disease Theory May Be Valid

18th Annual Parkinson's Unity Walk Raises More Than $1.5 Million in Support of Parkinson's Research

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KINGSTON, N.J., May 2, 2012 /PRNewswire/ --The 18th Annual Parkinson's Unity Walk (PUW), held on Saturday, April 28, 2012 in New York City's Central Park, raised more than $1.5 million thus far and united 10,000 walkers, The Parkinson Alliance announced today.

The event, kicked-off by Michael J. Fox, drew a record number of 527 registered teams participating in the PUW's 18 year history to help raise funds for Parkinson's disease (PD) research. The funds raised are distributed evenly among the nation's seven leading Parkinson's foundations, and the PUW will continue to accept contributions for the 2012 event through May 28, 2012.

A number of leading advocates and representatives from the Parkinson's community spoke at the PUW, including Congresswoman Carolyn Maloney, 14th CD; Michael Jones, Divisional VP & General Manager, Abbott; May May Ali, Writer and Comedian; and Martin Tuchman, Chairman of the Parkinson's Unity Walk.

"Collaboration and sharing two words that are extremely important to the success of this community," said Carol Walton, Chief Executive Officer of The Parkinson Alliance. "People living with Parkinson's, researchers, healthcare professionals, volunteers and foundations all working together to assure that one day a year, the most comprehensive day of community and education takes place for people with Parkinson's and their families."

The PUW is the largest awareness and fundraising event for PD research in the United States.

"The Parkinson's Unity Walk is important, not only for members of the Parkinson's community but also for the field of Parkinson's disease research," said Todd Sherer, Chief Executive Officer of the Michael J. Fox Foundation for Parkinson's Research. "It brings together so many of us who are deeply invested in finding a cure, and the funds raised help speed progress for patients today. The Michael J. Fox Foundation is grateful to be a part of this inspiring event."

For Walk participants, the PUW represented much more than a one-day event. It was an opportunity for patients, caregivers and organizations to all come together in support of the community.

"Year after year, I'm humbled by the consistent support from my friends, family and colleagues," said Jim McNasby, Team Captain of top fundraising team, Team McMoss, and PUW Board Member. "Their generosity is both extraordinary and impactful because all of the donations go directly to research. And when I hear about the research especially some of the genetic research supported by the Walk it gives me hope for the future. Hope keeps me going."

In addition to individual and team fundraising efforts, Abbott, a leading global health care company and premier sponsor of the PUW, helped raise an additional $30,000, which will be donated directly to the PUW in support of research.

Additional sponsors included Boehringer Ingelheim, Teva CNS, Chelsea Therapeutics, LSVT Global, Medtronic, Novartis, and UCB.

Continued here:
18th Annual Parkinson's Unity Walk Raises More Than $1.5 Million in Support of Parkinson's Research

18th Annual Parkinson’s Unity Walk Raises More Than $1.5 Million in Support of Parkinson’s Research

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KINGSTON, N.J., May 2, 2012 /PRNewswire/ --The 18th Annual Parkinson's Unity Walk (PUW), held on Saturday, April 28, 2012 in New York City's Central Park, raised more than $1.5 million thus far and united 10,000 walkers, The Parkinson Alliance announced today.

The event, kicked-off by Michael J. Fox, drew a record number of 527 registered teams participating in the PUW's 18 year history to help raise funds for Parkinson's disease (PD) research. The funds raised are distributed evenly among the nation's seven leading Parkinson's foundations, and the PUW will continue to accept contributions for the 2012 event through May 28, 2012.

A number of leading advocates and representatives from the Parkinson's community spoke at the PUW, including Congresswoman Carolyn Maloney, 14th CD; Michael Jones, Divisional VP & General Manager, Abbott; May May Ali, Writer and Comedian; and Martin Tuchman, Chairman of the Parkinson's Unity Walk.

"Collaboration and sharing two words that are extremely important to the success of this community," said Carol Walton, Chief Executive Officer of The Parkinson Alliance. "People living with Parkinson's, researchers, healthcare professionals, volunteers and foundations all working together to assure that one day a year, the most comprehensive day of community and education takes place for people with Parkinson's and their families."

The PUW is the largest awareness and fundraising event for PD research in the United States.

"The Parkinson's Unity Walk is important, not only for members of the Parkinson's community but also for the field of Parkinson's disease research," said Todd Sherer, Chief Executive Officer of the Michael J. Fox Foundation for Parkinson's Research. "It brings together so many of us who are deeply invested in finding a cure, and the funds raised help speed progress for patients today. The Michael J. Fox Foundation is grateful to be a part of this inspiring event."

For Walk participants, the PUW represented much more than a one-day event. It was an opportunity for patients, caregivers and organizations to all come together in support of the community.

"Year after year, I'm humbled by the consistent support from my friends, family and colleagues," said Jim McNasby, Team Captain of top fundraising team, Team McMoss, and PUW Board Member. "Their generosity is both extraordinary and impactful because all of the donations go directly to research. And when I hear about the research especially some of the genetic research supported by the Walk it gives me hope for the future. Hope keeps me going."

In addition to individual and team fundraising efforts, Abbott, a leading global health care company and premier sponsor of the PUW, helped raise an additional $30,000, which will be donated directly to the PUW in support of research.

Additional sponsors included Boehringer Ingelheim, Teva CNS, Chelsea Therapeutics, LSVT Global, Medtronic, Novartis, and UCB.

Continued here:
18th Annual Parkinson's Unity Walk Raises More Than $1.5 Million in Support of Parkinson's Research

Tennis: Court is in Session on Multiple Sclerosis

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I have been told by several people that there is no way that I can continue to play the sports I love, because of my multiple sclerosis. These people consist of family, friends, and some people that I have hardly ever met before. I love to play sports, and have even been encouraged to keep as much of a normal life as possible by my doctors.

This is the reason that I try to take as many vacations as I can, and try to get involved in some sort of sport or physical activity while I'm away. I have been playing tennis for the last three years now, and have taken a few vacations to get away, and play a game or two of tennis.

This is why I proudly bring to you my list of the best five tennis courts I have played on. Some of these have been on vacations with my husband, and some here in my own home state of Colorado.

Tennis court number one

The Broadmoor Hotel right here is Colorado Springs, Colo., is our first stop on this tour. The reason I like playing at the Broadmoor Hotel on occasion, is that the Broadmoor Hotel has inside courts that you can play on. This makes it easier for me to enjoy a game of tennis with my multiple sclerosis. I do not have to contend with the heat while playing on the indoor courts here, which is what makes it easier to deal with my multiple sclerosis.

Tennis court number two

The Walt Disney World Dolphin Resort in Orlando, Fla., is our second stop on this tour. Yes, most people come to Disney World for the rides, and other attractions, but when you have had enough fun for a day on the rides, and want to enjoy the hotel this is a great escape from the crowds. These courts are lighted which means that you can enjoy them even in the evening time when the temperature has gone down a little bit. This is the reason that I enjoy these tennis courts.

Tennis court number three

The Sailport Waterfront Suites Hotel in Tampa, Fla., is our third stop on this tour. This hotel has its own fishing dock, which allows for me to unwind after a good game of tennis. I do not usually fish from the dock, but I do like to go down there to unwind. This is the reason that this hotel has been a favorite of mine for awhile now to stay at when I go on a tennis trip to Florida.

Tennis court number four

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Tennis: Court is in Session on Multiple Sclerosis

Mayo Clinic: Dementia Risk Reduced by Exercise and Computers

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Exercise and computer use can help stave off dementia, according to research (Reuters)

Combining exercise and computer use could help to reduce the risks of dementia, a study claims.

Researchers in Minnesota found an association between engaging in moderate exercise and mentally stimulating activities in reducing the risks of dementia, according to a study published in Mayo Clinic Proceedings.

The study had more than 920 people between the ages of 70 and 93 in Olmsted County, Minnesota, complete questionnaires detailing the amount of time they exercise and spend on computers over the previous year.

Of those who both exercised and used a computer, 18.3 percent showed signs of mild cognitive impairment (dementia), compared to 37.6 percent who did neither. Of those who did both, 36 percent were declared cognitively normal, while 20.1 percent were normal in the group that did neither.

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Experts warn that the world's ageing population will lead to major increases in the number of people who sufferer from dementia and other degenerative mental conditions, such as Alzheimer's.

A spokesman for the Alzheimer's Society said: "There is already considerable evidence to show that donning the walking shoes, or hitting the tennis courts can have real benefits for your head as well as your heart.

"Although we need to know more before we can say for sure whether using computers has real additional benefits and why this could be, we would encourage any older people who enjoy using them to keep it up.

"The best way to reduce your risk of dementia is to exercise regularly, eat a healthy diet, don't smoke and get your blood pressure and cholesterol checked by your GP."

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Mayo Clinic: Dementia Risk Reduced by Exercise and Computers

Missing Woman with Dementia in Chicago

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Chicago - A woman with dementia has been missing since last week from her Calumet City home is believed to be traveling on CTA buses in the South and West sides of Chicago.

An adult daughter was caring for Earcell Hines, 71, of the 1600 block of Downs Drive in Calumet City, when she left her home April 24 by possibly receiving a ride to Chicago, according to a release from Calumet City police. There is no indication of foul play.

She suffers from early onset dementia, the release said.

Hines is using her CTA pass to travel throughout the South and West sides of Chicago on buses, possibly visiting numerous churches, as she is deeply religious, the release said.

She contacted a relative Friday, April 27 in the 1700 block of North Parkside saying she was on her way over, but never arrived, the release said. Hines made the phone call from a McDonalds restaurant at Kedzie Avenue and Roosevelt Road.

Hines is described as an African American woman, 5-feet-3, 160 pounds, with dark hair, the release said.

She has a bible and wire rimmed prescription glasses, which she would never travel without the release said. She possibly has her state drivers license that has an address in the 8500 block of South Morgan Street in Chicago.

Anyone with any information regarding this case is encouraged to contact Calumet City police at (708) 868-2500.

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Missing Woman with Dementia in Chicago

Woman with dementia missing from Calumet City

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Sun-Times Media Wire May 3, 2012 6:09AM

storyidforme: 29884076 tmspicid: 10828886 fileheaderid: 4958257

Updated: May 3, 2012 6:23AM

A woman with dementia has been missing since last week from her Calumet City home and is believed to be traveling on CTA buses in the South and West sides of Chicago.

An adult daughter was caring for Earcell Hines, 71, of the 1600 block of Downs Drive in Calumet City, when she left her home April 24 by possibly receiving a ride to Chicago, according to a release from Calumet City police.

There is no indication of foul play.

She suffers from early onset dementia, the release said.

Hines is using her CTA pass to travel throughout the South and West sides of Chicago on buses, possibly visiting numerous churches, as she is deeply religious, the release said.

She contacted a relative April 27 in the 1700 block of North Parkside Avenue saying she was on her way over, but never arrived, the release said.

Hines made the phone call from a McDonalds restaurant at Kedzie Avenue and Roosevelt Road.

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Woman with dementia missing from Calumet City

Valley hospice program leader lauded for dementia work

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by Connie Cone Sexton - May. 2, 2012 12:56 PM The Republic | azcentral.com

When Maribeth Gallagher came to work for Hospice of the Valley in 2005, she assisted a team that focused on dementia.

Gallagher, a psychiatric nurse practitioner with a doctorate in nursing practice from Arizona State University, now leads the team as its director. It's an area that has brought her great joy and her experience on the job has given her enough fortitude to weather "days that are really difficult." But Gallagher believes her work is "a calling.

"It just felt right, within me."

On March 29, she was recognized by the London-basedInternational Journal of Palliative Nursing for her leadership providing exceptional end-of-life care for dementia patients. Gallagher flew to London to accept her first-place award in the "non-cancer" category in an awards contest sponsored by the journal.

In other honors, Gallagher will be presented with the Program Manager of the Year award Thursday by the Visiting Nurse Associations of America at its annual meeting in Phoenix.

The not-for-profit Hospice of the Valley cares for 4,000 patients a day in Maricopa and northern Pinal counties. About 12 percent of those patients have a primary diagnosis of dementia; more than half have dementia along with other diseases or conditions.

Gallagher has heard from some people who ask her why she likes focusing on patients with dementia. "They say, 'What can you possibly do for people in last stages of dementia?' "

But she points out that dementia is a disease of verbal language; the patient still has a heart and soul to be nurtured and recognition for who they are.

The HOV dementia team educates agency staff, community health-care providers and the public about non-invasive, non-pharmacological ways to maximize quality of life for dementia patients.

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Valley hospice program leader lauded for dementia work

ViroPharma to Participate in Two May Healthcare Investor Conferences

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EXTON, Pa., May 2, 2012 /PRNewswire/ --ViroPharma Incorporated (VPHM) today announced that Charles Rowland, vice president and chief financial officer of ViroPharma, will present at the Deutsche Bank 37th Annual Healthcare Conference at 2:50 P.M. ET on Monday, May 7, 2012. The conference is being held at the InterContinental Hotel in Boston.

ViroPharma also announced that Vincent Milano, president and chief executive officer will present at the Bank of America/Merrill Lynch 2012 Healthcare Conference at 8:40 A.M. PT (11:40 AM ET) on Wednesday, May 16, 2012. The conference is being held at the Encore at the Wynn Hotel in Las Vegas.

ViroPharma's presentations will be webcast live for investors through http://www.viropharma.com and available for a period of 14 days following the conferences.

About ViroPharma Incorporated

ViroPharma Incorporated is an international biopharmaceutical company committed to developing and commercializing novel solutions for physician specialists to address unmet medical needs of patients living with diseases that have few if any clinical therapeutic options. ViroPharma is developing a portfolio of therapeutics for rare and Orphan diseases including C1 esterase inhibitor deficiency, Friedreich's Ataxia, and adrenal insufficiency; and recurrent C. difficile infection (CDI). Our goal is to provide rewarding careers to employees, to create new standards of care in the way serious diseases are treated, and to build international partnerships with the patients, advocates, and health care professionals we serve. ViroPharma's commercial products address diseases including hereditary angioedema (HAE), seizures and C. difficile-associated diarrhea (CDAD); for full U.S. prescribing information on our products, please download the package inserts at http://www.viropharma.com/Products.aspx; the prescribing information for other countries can be found at http://www.viropharma.com.

ViroPharma routinely posts information, including press releases, which may be important to investors in the investor relations and media sections of our company's web site, http://www.viropharma.com. The company encourages investors to consult these sections for more information on ViroPharma and our business.

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ViroPharma to Participate in Two May Healthcare Investor Conferences

Searching for a cure

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BeeJay Acker-Hitta looked at Kiela, her 10-year-old daughter, uncertain of how to tell her she had Friedreichs ataxia, a disease that would overcome her body and eventually end her life.

Mom, do I have it? Kiela asked.

Yes, you do, answered her mother.

What does that mean? Kiela asked.

Tears streamed down Kielas face as she attempted to understand what the diagnosis meant for her future.

Twelve years later Kiela and Acker-Hitta have participated in countless fundraisers to raise awareness for the deadly disease, which has no treatments or cure. Kiela will be escorted by her uncle to the Ride Ataxia, a cycling fundraiser in Davis on May 5.

Friedreichs ataxia is a life-shortening, degenerative neuro-muscular genetic disorder that affects 1 out of 50,000 people in the United States. Symptoms include loss of coordination, fatigue, vision impairment, curvature of the spine, diabetes and heart conditions.

The mental capabilities of people with FA remain intact, although the progressive loss of coordination and muscle strength leads to motor incapacitation and the full-time use of a wheelchair.

Kiela started showing symptoms at age 6. She had cardiomyopathy, often referred to as heart muscle disease, which usually leads to heart failure. She started using a walker by the fifth grade and was wheelchair bound by middle school. After more than four years of testing at UC San Francisco, Acker-Hitta took her daughter to Shriners Hospitals for Children in Sacramento. After a muscle biopsy, a spinal tap and blood tests, Acker-Hitta received a phone call.

It was the worst day of my life.

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Searching for a cure

Davis bike ride to raise funds for disease

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Hundreds of supporters are set to take part in a nationwide bike ride in Davis Saturday in an effort to raise funds -- and hope -- for a cure to Friedreich's Ataxia.

Friedreich's Ataxia is a debilitating, life-shortening degenerative neuromuscular disease typically affecting children and young adults, according to Megan Brewster of National Strategies Public Relations on behalf of the nonprofit Friedreich's Ataxia Research Alliance.

Ride Ataxia Norcal begins at 7:30 a.m. at the Veterans Memorial Center, 203 East 14th St. in Davis. The ride will offer 15-, 30- and 50-mile flat plus 55 and 68 mile hilly cycling routes on scenic country roads.

UC Davis graduate Kyle Bryant, founder and director of Ride Ataxia, was diagnosed with Friedreich's Ataxia at the age of 17.

He was told his abilities would deteriorate over time, would soon be in a wheelchair, would lose the ability to take care of himself and would likely die a premature death due to heart failure.

"That was a heavy load," said Bryant in a news release. "I was scared for the future."

During his junior year at UCD Bryant met a researcher who was studying the disease.

"It was the first time I was filled with hope," said Bryant.

The 2005 engineering graduate became a full-time employee of Friedreich's Ataxia Research Alliance in 2009.

Ride Ataxia cycling events across the country have raised invaluable awareness for Friedreich's Ataxia and funded more than $1 million in FA research

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Davis bike ride to raise funds for disease

It might not be autism

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With autism constantly in the headlines the Centers for Diseases Control & Prevention estimates that 1 in 88 children has the disorder its crucial to help parents determine if their child should be screened. One of the first indicators of autism is a speech delay. However, that does not automatically mean the child has the disorder. According to the American Speech-Language-Hearing Association (ASHA), more than five million children in the United States have a speech, language and/or hearing disorder and, often, parents are uninformed and unsure about what to do.

May is Better Hearing and Speech Month (BHSM), an ideal opportunity for schools and the community to educate parents about communication disorders so that their childrens ability to socialize, learn and succeed academically is not impaired.

Here are some communication red flags that parents and teachers should be aware of: A child does not follow directions, imitate or respond when name is called; poor eye contact; delayed speech and language development; loss of words the child could previously speak; and problems answering questions or finding objects named.

While some of these might be warning signs for autism, the child may have other developmental delays. If parents notice any of these symptoms, they should speak with the childs pediatrician and request a referral to an ASHA certified speech-language pathologist.

Treatment is crucial because it can improve the quality of life for a child who may have problems speaking, understanding or hearing. If autism is diagnosed, there is hope. While there is no known cure, early intervention (before age 3) can effectively treat speech, language, social and behavioral problems.

Millie Martinez Suarez, M.S., founder and director, Speech Pathology Educational Center, Miami

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It might not be autism

Autism, ADHD, and children's learning — insights from Psychological Science

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Public release date: 3-May-2012 [ | E-mail | Share ]

Contact: Anna Mikulak amikulak@psychologicalscience.org 202-293-9300 Association for Psychological Science

Critical issues in learning, ADHD and autism will be explored during the Association for Psychological Science annual convention in Chicago, from May 23 to the 27th. Leaders in the field studying attention deficit hyperactivity disorder, autism spectrum disorders, learning, and childhood development will present the latest in psychological science research that will shed light on treatment options, disorder management, memory and school performance.

There will be two major offerings in ADHD research.

Four experts on ADHD will present current research, and discuss future directions for treating and assessing the disorder. Howard Berenbaum from the University of Illinois at Urbana-Champaign and Arnaud Rey from Aix-Marseille University, France will moderate the session. Friday, May 25, 2012 10:30 AM 11:50 AM Chicago Ballroom X

Children with ADHD typically have great difficulty in both following and creating linear narratives. What does this reveal about the disorder and how can the creation of narratives actually address some of the problems that these children encounter in school? Richard S. Milich from the University of Kentucky has focused on this subject and will discuss the academic difficulties of children with ADHD and how they are connected to the difficulty that they have in creating coherent narratives.

Richard S. Milich, Professor of Psychology, University of Kentucky millich@email.uky.edu

The brain chemistry of children with ADHD will be discussed by Tiago V. Maia from Columbia University. What neurotransmitters are involved in producing the cognitive and behavioral symptoms that characterize this disorder? No one knows for sure, but by using a computer simulation of the role of norepinephrine in attention, these researchers found that low levels of norepinephrine produce many of ADHD's symptoms.

Tiago V. Maia, Assistant Professor of Clinical Neurobiology, Columbia University MaiaT@columbia.edu

The part of our brain that keeps us organized, that helps us prioritize various situations with order and agility is known as executive function. One characteristic of children with ADHD is that the part of their brain responsible for executive functioning is compromised. As a result, when they should react with speed and clarity, they respond slowly and with uncertainty. But executive function is not simply a single process. By isolating response times into different components, Cynthia Huang-Pollock from Pennsylvania State University teases out the connections between poor executive function performance and the response times. This connection can lead to new understanding about ADHD and may lead to new strategies for treating the disorder.

Read the original here:
Autism, ADHD, and children's learning -- insights from Psychological Science

Autism, ADHD, and children’s learning — insights from Psychological Science

Posted on by

Public release date: 3-May-2012 [ | E-mail | Share ]

Contact: Anna Mikulak amikulak@psychologicalscience.org 202-293-9300 Association for Psychological Science

Critical issues in learning, ADHD and autism will be explored during the Association for Psychological Science annual convention in Chicago, from May 23 to the 27th. Leaders in the field studying attention deficit hyperactivity disorder, autism spectrum disorders, learning, and childhood development will present the latest in psychological science research that will shed light on treatment options, disorder management, memory and school performance.

There will be two major offerings in ADHD research.

Four experts on ADHD will present current research, and discuss future directions for treating and assessing the disorder. Howard Berenbaum from the University of Illinois at Urbana-Champaign and Arnaud Rey from Aix-Marseille University, France will moderate the session. Friday, May 25, 2012 10:30 AM 11:50 AM Chicago Ballroom X

Children with ADHD typically have great difficulty in both following and creating linear narratives. What does this reveal about the disorder and how can the creation of narratives actually address some of the problems that these children encounter in school? Richard S. Milich from the University of Kentucky has focused on this subject and will discuss the academic difficulties of children with ADHD and how they are connected to the difficulty that they have in creating coherent narratives.

Richard S. Milich, Professor of Psychology, University of Kentucky millich@email.uky.edu

The brain chemistry of children with ADHD will be discussed by Tiago V. Maia from Columbia University. What neurotransmitters are involved in producing the cognitive and behavioral symptoms that characterize this disorder? No one knows for sure, but by using a computer simulation of the role of norepinephrine in attention, these researchers found that low levels of norepinephrine produce many of ADHD's symptoms.

Tiago V. Maia, Assistant Professor of Clinical Neurobiology, Columbia University MaiaT@columbia.edu

The part of our brain that keeps us organized, that helps us prioritize various situations with order and agility is known as executive function. One characteristic of children with ADHD is that the part of their brain responsible for executive functioning is compromised. As a result, when they should react with speed and clarity, they respond slowly and with uncertainty. But executive function is not simply a single process. By isolating response times into different components, Cynthia Huang-Pollock from Pennsylvania State University teases out the connections between poor executive function performance and the response times. This connection can lead to new understanding about ADHD and may lead to new strategies for treating the disorder.

Read the original here:
Autism, ADHD, and children's learning -- insights from Psychological Science