Researchers have shown that people with Parkinson’s disease performed markedly better on a test of working memory after a night’s sleep, and sleep disorders can interfere with that benefit.

While the classic symptoms of Parkinson’s disease include tremors and slow movements, Parkinson’s can also affect someone’s memory, including “working memory.”

Working memory is defined as the ability to temporarily store and manipulate information, rather than simply repeat it. The use of working memory is important in planning, problem solving and independent living.

The findings underline the importance of addressing sleep disorders in the care of patients with Parkinson’s, and indicate that working memory capacity in patients with Parkinson’s potentially can be improved with training. The results also have implications for the biology of sleep and memory.

“It was known already that sleep is beneficial for memory, but here, we’ve been able to analyze what aspects of sleep are required for the improvements in working memory performance,” said postdoctoral fellow Michael Scullin, who is the first author of the paper.

The performance boost from sleep was linked with the amount of slow wave sleep, or the deepest stage of sleep. Several research groups have reported that slow wave sleep is important for synaptic plasticity, the ability of brain cells to reorganize and make new connections.

Sleep apnea, the disruption of sleep caused by obstruction of the airway, interfered with sleep’s effects on memory. Study participants who showed signs of sleep apnea, if it was severe enough to lower their blood oxygen levels for more than five minutes, did not see a working memory test boost.

54 study participants had Parkinson’s disease, and 10 had dementia with Lewy bodies: a more advanced condition, where patients may have hallucinations or fluctuating cognition as well as motor symptoms. Those who had dementia with Lewy bodies saw no working memory boost from the night’s rest. As expected, their baseline level of performance was lower than the Parkinson’s group.

Participants with Parkinson’s who were taking dopamine-enhancing medications saw their performance on the digit span test jump up between the fourth and fifth test. On average, they could remember one more number backwards. The ability to repeat numbers backward improved, even though the ability to repeat numbers forward did not.

Patients needed to be taking dopamine-enhancing medications to see the most performance benefit from sleep. Patients not taking dopamine medications, even though they had generally had Parkinson’s for less time, did not experience as much of a performance benefit. This may reflect a role for dopamine, an important neurotransmitter, in memory.

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Public release date: 23-Aug-2012 [ | E-mail | Share ]

Contact: Lisa Merkl lkmerkl@uh.edu 713-743-8192 University of Houston

HOUSTON, Aug. 23, 2012 Scientists at the University of Houston (UH) have discovered what may possibly be a key ingredient in the fight against Parkinson’s disease.

Affecting more than 500,000 people in the U.S., Parkinson’s disease is a degenerative disorder of the central nervous system marked by a loss of certain nerve cells in the brain, causing a lack of dopamine. These dopamine-producing neurons are in a section of the midbrain that regulates body control and movement. In a study recently published in the Proceedings of the National Academy of Sciences (PNAS), researchers from the UH Center for Nuclear Receptors and Cell Signaling (CNRCS) demonstrated that the nuclear receptor liver X receptor beta (LXRbeta) may play a role in the prevention and treatment of this progressive neurodegenerative disease.

“LXRbeta performs an important function in the development of the central nervous system, and our work indicates that the presence of LXRbeta promotes the survival of dopaminergic neurons, which are the main source of dopamine in the central nervous system,” said CNRCS director and professor Jan-ke Gustafsson, whose lab discovered LXRbeta in 1995. “The receptor continues to show promise as a potential therapeutic target for this disease, as well as other neurological disorders.”

To better understand the relationship between LXRbeta and Parkinson’s disease, the team worked with a potent neurotoxin, called MPTP, a contaminant found in street drugs that caused Parkinson’s in people who consumed these drugs. In lab settings, MPTP is used in murine models to simulate the disease and to study its pathology and possible treatments.

The researchers found that the absence of LXRbeta increased the harmful effects of MPTP on dopamine-producing neurons. Additionally, they found that using a drug that activates LXRbeta receptors prevented the destructive effects of MPTP and, therefore, may offer protection against the neurodegeneration of the midbrain.

“LXRbeta is not expressed in the dopamine-producing neurons, but instead in the microglia surrounding the neurons,” Gustafsson said. “Microglia are the police of the brain, keeping things in order. In Parkinson’s disease the microglia are overactive and begin to destroy the healthy neurons in the neighborhood of those neurons damaged by MPTP. LXRbeta calms down the microglia and prevents collateral damage. Thus, we have discovered a novel therapeutic target for treatment of Parkinson’s disease.”

###

Gustafsson, professor Margaret Warner, research assistant professor Xin-Jie Tan, and postdoctoral fellows Wanfu Wu and Yubing Dai authored the PNAS study, which is available at http://www.pnas.org/content/early/2012/07/18/1210833109.abstract.

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ScienceDaily (Aug. 23, 2012) Scientists at the University of Houston (UH) have discovered what may possibly be a key ingredient in the fight against Parkinson’s disease.

Affecting more than 500,000 people in the U.S., Parkinson’s disease is a degenerative disorder of the central nervous system marked by a loss of certain nerve cells in the brain, causing a lack of dopamine. These dopamine-producing neurons are in a section of the midbrain that regulates body control and movement. In a study recently published in the Proceedings of the National Academy of Sciences (PNAS), researchers from the UH Center for Nuclear Receptors and Cell Signaling (CNRCS) demonstrated that the nuclear receptor liver X receptor beta (LXRbeta) may play a role in the prevention and treatment of this progressive neurodegenerative disease.

“LXRbeta performs an important function in the development of the central nervous system, and our work indicates that the presence of LXRbeta promotes the survival of dopaminergic neurons, which are the main source of dopamine in the central nervous system,” said CNRCS director and professor Jan-ke Gustafsson, whose lab discovered LXRbeta in 1995. “The receptor continues to show promise as a potential therapeutic target for this disease, as well as other neurological disorders.”

To better understand the relationship between LXRbeta and Parkinson’s disease, the team worked with a potent neurotoxin, called MPTP, a contaminant found in street drugs that caused Parkinson’s in people who consumed these drugs. In lab settings, MPTP is used in murine models to simulate the disease and to study its pathology and possible treatments.

The researchers found that the absence of LXRbeta increased the harmful effects of MPTP on dopamine-producing neurons. Additionally, they found that using a drug that activates LXRbeta receptors prevented the destructive effects of MPTP and, therefore, may offer protection against the neurodegeneration of the midbrain.

“LXRbeta is not expressed in the dopamine-producing neurons, but instead in the microglia surrounding the neurons,” Gustafsson said. “Microglia are the police of the brain, keeping things in order. In Parkinson’s disease the microglia are overactive and begin to destroy the healthy neurons in the neighborhood of those neurons damaged by MPTP. LXRbeta calms down the microglia and prevents collateral damage. Thus, we have discovered a novel therapeutic target for treatment of Parkinson’s disease.”

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Ed McCaskey has lived with Parkinsons disease for six years, and now hes trying to help others like him mitigate some of their symptoms through exercise.

McCaskey, 59, was diagnosed with Parkinsons in 2006. He lives in Roscoe, Ill., and he joined the Stateline Family YMCA Roscoe Branch the same year, and he typically works out five days a week.

Exercise has been found to help reduce some of the symptoms like shaking and tremors associated with Parkinsons. That is why the YMCA of Greater Cleveland in Ohio developed a program called Pedaling for Parkinsons with the help of Cleveland Clinic physician Dr. Jay L. Alberts, a staff member with the Biomedical Engineering Center for Neurological Restoration.

The program in which participants exercise on indoor spin/cycling bikes and tandem bikes launched earlier this year, and McCaskey read about it in a Parkinsons newsletter and pitched it to his local YMCA. Research by Cleveland Clinic showed a 35 percent reduction in symptoms with the act of pedaling a bicycle at a rapid pace optimally 80 to 90 revolutions per minute.

The YMCA staff in Roscoe, Ill., agreed, and the one-hour class will meet three days a week starting Sept. 24 through Nov. 16. Its free to YMCA members and nonmembers alike.

Some class participants may need a relative or friend to drive them to the class, and McCaskey said YMCA officials will let those people use the Y facilities free of charge while they wait during the class.

More than 1 million people nationally are living with Parkinsons disease, and nearly 60,000 new cases are diagnosed each year, according to the National Parkinson Foundation. Parkinsons is a chronic degenerative disease that occurs when nerve cells in parts of the brain stem die or degenerate.

McCaskey recently traveled to Washington state and tried the Pedaling for Parkinsons class there. It was pretty easy for the marathon runner and regular spin-class participant, but he said its a great opportunity for Parkinsons patients to get moving and realize the benefits of exercise.

Im still pretty lucky because my symptoms are minimal, McCaskey said. After a good workout, a lot of those symptoms dissipate for a good part of the day. The exercise recommendation came from my doctor, but following up on it really reinforces what he says. Im experiencing the positive benefits.

Melissa Westphal: 815-987-1341; at mwestpha@rrstar.com

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By Jason Napodano, CFA

Parkinson’s Disease

Parkinsons disease (PD) is a neurodegenerative brain disorder that results from the death of dopamine-generating cells in the substantia nigra region of the midbrain. PD is also characterized by the accumulation of a protein called alpha-synuclein into inclusions called Lewy bodies in neurons. The cause of PD is generally idiopathic, although some atypical cases have a genetic origin. The disease is named after the English doctor James Parkinson, who published the first detailed description in An Essay on the Shaking Palsy in 1817.

PD patients often exhibit marked reduction in motor control and an increase in parkinsonism (tremors, hypokinesia, rigidity, bradykinesia, and postural instability). However, as the disease progresses, patients often exhibit non-motor symptoms that include autonomic dysfunction, neuropsychiatric problems (mood, cognition, behavior or thought alterations, psychosis), and sensory and sleep difficulties. Parkinsons disease psychosis (PDP) is common in nearly 50% of PD patients a decade after initial diagnosis. Anxiety and depression are common co-morbidities. Initial signs of PD include shaking, loss of smell, difficulty writing, trouble sleeping, constipation, and poor posture. Diagnosis of a typical case is mainly based on symptoms, with tests such as neuroimaging used for confirmation.

There is no cure for PD. Instead, physicians attempt to manage the symptoms of the disease through a multidisciplinary approach that may include pharmacological, social, and surgical options. The most common pharmaceutical treatment options are those which look to increase the level of dopamine in the brain. These include dopamine replacement therapies (DRT) combined with dopa decarboxylase inhibitors, dopamine agonists, and MAO-B inhibitors. The treatment option is often tailored specifically for the patient based on the stage and severity of the disease and the balance between good symptom control and side-effects resulting from enhancement of dopaminergic function.

Despite these co-formulations, Levodopa carries significant risk of side-effects, including dyskinesia. As a result, despite its effectiveness in reducing motor symptoms associated with Parkinsons disease, physicians often attempt to delay Levodopa therapy until the disease progresses to a more moderate-to-severe stage. Most early-stage PD patients start out on MAO-B inhibitors and / or dopamine agonists, or low-dose Levodopa. However, PD is a progressive and degenerative disease, and patients typically progress to the point where starting Levodopa or increasing the Levodopa dose is necessary in five years after initial diagnosis. After a decade on therapy, almost all PD patients require high doses of Levodopa, as well as surgical options including deep brain stimulation (DBS). As the dose and use of Levodopa increases, the incidence of dyskinesia also increases.

Levodopa also has a relatively short half-life, requiring dosing averaging three to four times a day. Peak plasma concentrations of Levodopa occur 60 to 90 minutes after dosing. Unfortunately, this is also when peak side effects such as dyskinesia occur. The hefty dosing requirement of Levodopa creates compliance issues, especially at night when patients may sleep through their dose schedule dosing every six hours. The peaks and troughs associated with Levodopa create significant on and off treatment times for PD patients.

Levodopa-Induced Dyskinesia

Levodopa-Induced Dyskinesia (LID) is a major side-effect of Levodopa use. LID is characterized by hyperkinetic movements, including chorea (abnormal involuntary movement), dystonia (sustained muscle contraction, abnormal posture), and athetosis (involuntary convoluted movements). It is most common at times of peak L-DOPA plasma concentrations (peak-dose dyskinesia), although it may also occur when plasma concentrations of L-DOPA rise and fall (diphasic dyskinesia) or during off-time (off-period dystonia).

In the U.S., there are an estimated 500,000 to 1 million patients suffering from Parkinsons disease. There are no approved treatment options for PD-LID. Approximately 50% of PD patients will experience LID after 4 to 6 years on L-DOPA therapy. The number rises to 90% after 10 to 15 years on L-DOPA therapy.

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Multiple sclerosis is a prevalent disease that affects about 250,000 to 350,000 Americans, according to the National Institute of Health. This disease afflicts the brain and spinal cord, which make up the central nervous system, and causes the inflammation of the meninges, a lining of cells that cover the surface of the brain.

Though this is, as yet, an incurable disease, MS has many treatment and therapeutic options for patients. A group of Wayne State researchers, along with colleagues in Canada, have found a possible pathway that leads to disease progression which could lead to new therapies for patients.

WSU School of Medicine neurology associate chair and professor Joyce A. Benjamins, neurology professor Robert P. Lisak, neurology and immunology & microbiology assistant professor Samia Ragheba, neurology research assistants Liljana Nedelkoskaa and Jennifer Barger all contributed to the study.

The main idea behind the study was to see if B cells from patients with MS make substances that could be secreted that could damage CNS cells, Lisak said.

B cells are a type of lymphocytes, or white blood cells, that produce antibodies, which help the body in immune responses. In patients with multiple sclerosis, however, the B cells produce molecules that damage oligodendrocytes, which make myelin, Lisak said.

Myelin is a type of insulation for the axons of the nerve cells, neurons, in the CNS. If these protective coats are damaged and degraded, chemical communication between the brain and the rest of the body will be halted. Therefore, body movements such as walking, talking or bladder and bowel control are greatly hindered.

Benjamins said damage is not only done to the myelin sheath, but also to the neurons in a region of the brain called gray matter due to the dense population of neurons. Areas of gray matter are also called the cerebral cortex, and it is seen that damage in this area occurs early in the progression of the disease. The experiment to investigate B cells was conducted with the help of Canadian counterparts, Lisak said.

Our collaborators in Montreal isolated and cultured B cells from the blood of seven patients with MS and four healthy individuals, Lisak said.

The liquid from the cultures was sent to WSU where it was put in CNS culture. By analyzing the results, researchers found that the liquid from the B cells of MS patients killed oligodendrocytes, but not from the liquid of normal individuals.

This lead to the researchers conclusion that MS patients B cells secrete some sort of molecules or substances that directly attack CNS cells. These results are quite relevant and important for the study of progression. Lisak said these results show a new way through which B cells can damage neurons in MS; this novel pathway can lead the direction of how future therapies and treatment target the disease.

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For each Teen BurgerTM sold in Canada , $1 will be given to the MS Society

MONTREAL , Aug. 20, 2012 /CNW Telbec/ – For a fourth consecutive year, the Multiple Sclerosis Society of Canada invites Quebecers to join the fight against MS as part of its annual fundraising and awareness event, in collaboration with A&W Food Services of Canada Inc. (AW-UN.TO).

How can I contribute?

Exclusively on Thursday, August 23 , for each Teen Burger sold across the country, one dollar will be donated to help fight MS. The A&W Rendez-vous event will also feature several fundraising activities in participating restaurants, including games, raffles, prizes and even personal appearances by the Great Root Bear himself! Well-known personality Patricia Paquin will be at the Plateau-Mont-Royal A&W restaurant, located at 4501 St-Denis Street, between 11:30 a.m. and 1 p.m.

Furthermore, until August 23:

“The A&W Rendez-vous to end MS campaign greatly contributes to financing ongoing MS cause and treatment research, as well as services offered to Canadians suffering from this illness, which is diagnosed in three Canadians per day, explains Yves Savoie, President and CEO, MS Society of Canada . We are very grateful toward all donors, as well as A&W guests and employees, for the active role they play year after year to ensure that this important fundraising event is a resounding success.”

Canada posts one of the world’s highest multiple sclerosis incidence rates. Indeed, an estimated one out of every two Canadians knows someone suffering from MS, and approximately 50,000 to 75,000 Canadians are currently fighting this disease. Of this figure, nearly 20,000 live in Qubec. While the cause of this often debilitating illness remains unknown, researchers are getting closer to a solution. The MS Society of Canada , the foremost organization in MS research, funds services to those suffering from MS and their families.

“In three years, A&W guests, employees and franchisees have raised over two million dollars to help fight MS, said Paul Hollands , President and CEO, A&W Food Services of Canada Inc. We’re thrilled by this success and invite everyone to help make this incredible feat a reality by participating in the A&W Rendez-vous to end MS on August 23.”

About multiple sclerosis and the MS Society of Canada Multiple sclerosis is a chronic, often disabling disease of the brain and spinal cord. It is the most common neurological disease of young adults in Canada . Most people with MS are diagnosed between the ages of 15 and 40, and the unpredictable effects of MS last for the rest of their lives. The MS Society provides services to people with MS and their families and funds research to find the cause and cure for this disease. Please visit mssociety.ca or call 1800 268-7582 to make a donation or for more information.

A&W Food Service of Canada Inc. is a purely Canadian company and one of the most recognized brands within the Canadian food service industry. A&W is the country’s second largest hamburger restaurant chains, operating 730 locations across Canada . A&W restaurants offer their famous menu, which includes the Burger FamilyTM, Chubby ChickenTM and A&W Root BeerTM. For more information, please visit http://www.aw.ca.

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Health

Posted on 06:40 PM, August 23, 2012

PEOPLE who keep their teeth and gums healthy with regular brushing may have a lower risk of developing dementia later in life, according to a US study.

Researchers at the University of California who followed nearly 5,500 elderly people over an 18-year-period found that those who reported brushing their teeth less than once a day were up to 65% more likely to develop dementia than those who brushed daily.

Not only does the state of your mind predict what kind of oral health habits you practice, it may be that your oral health habits influence whether or not you get dementia, said Annlia Paganini-Hill, who led the study, published in the Journal of the American Geriatrics Society.

Inflammation stoked by gum disease-related bacteria is implicated in a host of conditions including heart disease, stroke and diabetes.

Some studies have also found that people with Alzheimers disease, the most common form of dementia, have more gum disease-related bacteria in their brains than a person without Alzheimers, Paganini-Hill said.

Its thought that gum disease bacteria might get into the brain, causing inflammation and brain damage, she said.

Paganini-Hill and her team followed 5,468 residents of a Californian retirement community from 1992 to 2010. Most people in the study were white, well-educated and relatively affluent. When the study began, participants ranged in age from 52 to 105, with an average age of 81. All were free of dementia at the outset, when they answered questions about their dental health habits, the condition of their teeth and whether they wore dentures.

When the researchers followed up 18 years later, they used interviews, medical records and in some cases death certificates to determine that 1,145 of the original group had been diagnosed with dementia.

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Aug 24 2012

People in Scotland are “in the dark” when it comes to caring for those with dementia, according to a private healthcare firm.

A poll by Ipsos MORI for Bupa Care Homes suggests that 29% of people in Scotland do not know the best way to support someone with dementia and that 31% do not know what to expect as the symptoms get worse.

Around 800,000 people across the UK have dementia and this is expected to rise to at least one million by 2021, according to Bupa.

Family members are usually the first to identify symptoms of the condition and often try to care for their loved ones for as long as possible.

Bupa said many people struggle to find basic information and guidance to help them.

In response, Bupa has launched a series of films offering advice to people who find themselves caring for someone with dementia. Bupa Care Homes, which provides specialist dementia care, has teamed up with choreographer Arlene Phillips to make the films for the company’s Understand Dementia campaign.

Ms Phillips, whose father had dementia, said: “I know from my own experience how frightening it can be when someone you loved lived with dementia. I wanted to make these films to help others.

“Had I known what I do now, my relationship with my father needn’t have been so fraught and difficult.”

Professor Graham Stokes, Bupa Care Homes’s director of dementia care, said: “When families bring a loved one to our care homes, they often tell us how they struggled for many years caring for them, sometimes on their own with little support.

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Singer Amy Grant’s father has been diagnosed with dementia.

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Dr. Burton Grant, 80, began showing signs of a faltering memory in late 2008, and the Grammy winner and her sisters finally forced him to seek help from doctors who determined he was dealing with a loss of overall brain function.

She tells People magazine, “Watching his brilliant mind go away was tough.”

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The news prompted the singer to retire her dad’s medical license and hire around-the-clock caregivers, and the 51-year-old admits the disease has presented a new set of challenges for her family.

Grant says, “He might not know my name, but I sense familiarity. … It’s a new reality. He doesn’t make sense, but it’s the comfort of hearing him talk and talking back to him. I wouldn’t have guessed this is the way my dad’s life played out. But I wouldn’t change it. The unexpected and hard aspects of life draw us together.”

RELATED: Carrie Underwood: ‘Country Music Is for Real People’

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The Irish Times – Thursday, August 23, 2012

BENEDICT CAREY

OLDER MEN are more likely than young men to father a child who develops autism or schizophrenia, because of random mutations that become more numerous with advancing paternal age, scientists reported yesterday, in the first study to quantify the effect as it builds each year. The age of mothers had no bearing on the risk for these disorders, the study found.

Experts said the finding was hardly reason to forgo fatherhood later in life, though it may have some influence on reproductive decisions. The overall risk to a man in his 40s or older is in the range of 2 per cent at most, and there are other contributing biological factors that are unknown.

But the study, published online in the journal Nature, provides support for the argument that the surging rate of autism diagnoses over recent decades is attributable in part to the increasing average age of fathers, which could account for as many as 30 per cent of cases.

The findings also counter the long-standing assumption that the age of the mother is the most important factor in determining the odds of a child having developmental difficulties. The risk of chromosomal abnormalities such as Down syndrome increases for older mothers but when it comes to some complex developmental and psychiatric problems the lions share of the genetic risk originates in the sperm, not the egg, the study found.

Previous studies had strongly suggested as much but the new report quantifies that risk for the first time, calculating how much it accumulates each year.

The research team found the average child born to a 20-year-old father had 25 random mutations that could be traced to paternal genetic material. The number increased steadily by two mutations a year, reaching 65 mutations for offspring of 40-year-old men. The average number of mutations coming from the mothers side was 15, no matter her age, the study found.

This study provides some of the first solid scientific evidence for a true increase in the condition of autism, said Dr Fred Volkmar, director of the Child Study Centre at the Yale School of Medicine, who was not involved in the research. It is extremely well done and the sample meticulously characterised.

The new investigation, led by the Icelandic firm Decode Genetics, analysed genetic material taken from blood samples of 78 parent-child trios, focusing on families in which parents with no signs of a mental disorder gave birth to a child who developed autism or schizophrenia.

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PHILADELPHIA, Aug. 22, 2012 /PRNewswire/ –A federal court in Philadelphia yesterday granted class action status to a lawsuit brought by the parents of an autistic child against CIGNA Corporation and related CIGNA entities for their policy of denying insurance coverage for an autism treatment known as Applied Behavior Analysis (ABA) therapy. In their lawsuit, the plaintiff, Kristopher Churchill and Luis Rolando, allege that the CIGNA companies have a nationwide policy of classifying ABA as experimental, and therefore they do not provide insurance coverage for this therapy. The plaintiffs claim that the classification of ABA as experimental and the denial of insurance coverage for ABA violates federal laws governing insurance plans. The court’s order today means that the case will proceed as a nationwide class action on behalf of all families having children with autism who were denied coverage by CIGNA for ABA therapy.

According to the lawsuit, ABA is a well recognized and scientifically valid form of autism treatment for children. Numerous authorities and organizations have supported using ABA to treat autism. For example, the use of ABA for treating autism has been endorsed by the U.S. Surgeon General and the National Institute of Mental Health. The American Academy of Pediatrics has said that the effectiveness of ABA “has been well documented through 5 decades of research.” Currently, 31 states mandate insurance coverage for ABA-type autism treatments.

In the Court’s Order entered yesterday, Judge Juan R. Sanchez held that the following subclass shall be certified pursuant to FRCP 23(b)(3):

All individuals who, on or after November 24, 2006, (1) were enrolled in a plan administered by a CIGNA Defendant, or insured under health insurance coverage offered by CIGNA Defendant in connection with a plan, and (2) are currently enrolled in a CIGNA-affiliated plan, and (3) who, on or after November 24, 2006, made a claim or make a claim for Applied Behavior Analysis and/or Early Intensive behavioral Treatment for Autism Spectrum Disorder which was denied on the grounds that such treatment is deemed by a CIGNA Defendant to be investigative or experimental.

Churchill and Rolando are represented by Gerard Mantese, Brian Saxe, and John J. Conway of Michigan. Mantese and Conway are counsel in several cases seeking insurance coverage for ABA therapy. In 2010, Mantese and Conway obtained final approval of a class action against Blue Cross Blue Shield of Michigan requiring payment of $1 million in claims for ABA. They are also currently counsel for several military beneficiaries seeking coverage of ABA from the military’s Tricare insurer. On July 26, 2012, a federal court in Washington D.C. granted summary judgment ordering that ABA Therapy be provided to military beneficiaries in that case.

Contact information for Churchill’s attorneys follows:

Gerard Mantese, Esq. Brian Saxe, Esq. Mantese Honigman Rossman and Williamson, P.C. 1361 E. Big Beaver Road Troy, Michigan 48083 248-457-9200 Office 248-515-6419 Cell

John J. Conway, Esq. John J. Conway, P.C. 26622 Woodward Avenue, Suite 225 Royal Oak, MI 48067 313-961-6525 Office 313-574-2148 Cell

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