New clues revealed to understand brain stimulation

Date:

September 29, 2014

Source:

Beth Israel Deaconess Medical Center

Summary:

Brain networks -- the interconnected pathways that link brain circuits to one another -- can help guide site selection for brain stimulation therapies, a new study suggests. Over the past several decades, brain stimulation has become an increasingly important treatment option for a number of psychiatric and neurological conditions.

Over the past several decades, brain stimulation has become an increasingly important treatment option for a number of psychiatric and neurological conditions.

Divided into two broad approaches, invasive and noninvasive, brain stimulation works by targeting specific sites to adjust brain activity. The most widely known invasive technique, deep brain stimulation (DBS), requires brain surgery to insert an electrode and is approved by the U.S. Food and Drug Administration (FDA) for the treatment of Parkinson’s disease and essential tremor. Noninvasive techniques, including transcranial magnetic stimulation (TMS), can be administered from outside the head and are currently approved for the treatment of depression. Brain stimulation can result in dramatic benefit to patients with these disorders, motivating researchers to test whether it can also help patients with other diseases.

But, in many cases, the ideal sites to administer stimulation have remained ambiguous. Exactly where in the brain is the best spot to stimulate to treat a given patient or a given disease?

Now a new study in the Proceedings of the National Academy of Sciences (PNAS) helps answer this question. Led by investigators at Beth Israel Deaconess Medical Center (BIDMC), the findings suggest that brain networks – the interconnected pathways that link brain circuits to one another-- can help guide site selection for brain stimulation therapies.

“Although different types of brain stimulation are currently applied in different locations, we found that the targets used to treat the same disease are nodes in the same connected brain network,” says first author Michael D. Fox, MD, PhD, an investigator in the Berenson-Allen Center for Noninvasive Brain Stimulation and in the Parkinson’s Disease and Movement Disorders Center at BIDMC.

“This may have implications for how we administer brain stimulation to treat disease. If you want to treat Parkinson’s disease or tremor with brain stimulation, you can insert an electrode deep in the brain and get a great effect. However, getting this same benefit with noninvasive stimulation is difficult, as you can’t directly stimulate the same site deep in the brain from outside the head,” explains Fox, an Assistant Professor of Neurology at Harvard Medical School (HMS). “But, by looking at the brain’s own network connectivity, we can identify sites on the surface of the brain that connect with this deep site, and stimulate those sites noninvasively.”

Brain networks consist of interconnected pathways linking brain circuits or loops, similar to a college campus in which paved sidewalks connect a wide variety of buildings.

In this paper, Fox led a team that first conducted a large-scale literature search to identify all neurological and psychiatric diseases where improvement had been seen with both invasive and noninvasive brain stimulation. Their analysis revealed 14 conditions: addiction, Alzheimer’s disease, anorexia, depression, dystonia, epilepsy, essential tremor, gait dysfunction, Huntington’s disease, minimally conscious state, obsessive compulsive disorder, pain, Parkinson disease and Tourette syndrome. They next listed the stimulation sites, either deep in the brain or on the surface of the brain, thought to be effective for the treatment of each of the 14 diseases.

“We wanted to test the hypothesis that these various stimulation sites are actually different spots within the same brain network,” explains Fox. “To examine the connectivity from any one site to other brain regions, we used a data base of functional MRI images and a technique that enables you to see correlations in spontaneous brain activity.” From these correlations, the investigators were able to create a map of connections from deep brain stimulation sites to the surface of the brain. When they compared this map to sites on the brain surface that work for noninvasive brain stimulation, the two matched.

“These results suggest that brain networks might be used to help us better understand why brain stimulation works and to improve therapy by identifying the best place to stimulate the brain for each individual patient and given disease,” says senior author Alvaro Pascual-Leone, MD, PhD, the Director of the Berenson-Allen Center for Noninvasive Brain Stimulation at BIDMC and Professor of Neurology at HMS. “This study illustrates the potential of gaining fundamental insights into brain function while helping patients with debilitating diseases, and provides us with a powerful way of selecting targets based on their connectivity to other regions that can be widely applied to help guide brain stimulation therapy across multiple neurological and psychiatric disorders.”

“As we’re trying different types of brain stimulation for different diseases, the question comes up, ‘How does one relate to the other?’” notes Fox. “In other words, can we use the success in one to help design a trial or inform how we apply a new type of brain stimulation? Our new findings suggest that resting-state functional connectivity may be useful for translating therapy between treatment modalities, optimizing treatment and identifying new stimulation targets.”

end text

Story Source:

The above story is based on materials provided by Beth Israel Deaconess Medical Center. Note: Materials may be edited for content and length.

end story_source

Journal Reference:

M. D. Fox, R. L. Buckner, H. Liu, M. M. Chakravarty, A. M. Lozano, A. Pascual-Leone. Resting-state networks link invasive and noninvasive brain stimulation across diverse psychiatric and neurological diseases. Proceedings of the National Academy of Sciences, 2014; DOI: 10.1073/pnas.1405003111

end journal_references

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Beth Israel Deaconess Medical Center. "New clues revealed to understand brain stimulation." ScienceDaily. ScienceDaily, 29 September 2014. <www.sciencedaily.com/releases/2014/09/140929153935.htm>.

Hopeful New Drug Therapy Being Developed at University of Alabama

Alpha-synuclein is one of the most prevalent proteins found in human brains.  It is also the one that when it fails to conform to its normal configuration, or mis-folds, contributes to the neurodegeneration seen in PARKINSON’S DISEASE.  Researchers at the University of Alabama led by Andrew West, Ph.D. think they may have found a key to prevent alpha-synuclein from misfolding and aggregating.

The gene LRRK2 has been linked to PARKINSON’S DISEASE and West’s lab demonstrated that the known mutations of this gene all increase its activity.  Other studies have shown that it is related to alpha-synuclein in several ways.  This study has shown that blocking the expression of LRRK2 in mouse models that are genetically very similar to human models, blocked the over-expression of alpha-synuclein.  Blocking alpha-synuclein may prevent the death of dopamine producing cells in the substantia nigra, thus offering a potential treatment to prevent or slow the progress of PARKINSON’S DISEASE.  The search for a drug to inhibit the expression of LRRK2 is now underway.

LRRK2 is known to be significantly involved in the genetic forms of PARKINSONS, in populations of Ashkenazy Jews from Eastern Europe and from Mediterranean ethnic populations such as the Berbers of North Africa, but is not as highly involved in non inherited forms of the disease.   Still, West’s team thinks LRRK2 has more than one method of action as seen in the genetic forms.  It may interact with alpha-synuclein in other ways.

He asks, “What would happen if you simply remove all LRRK2 activity?  Modern approaches allow us to approximate what a perfect drug would do in rats and mice.  We think LRRK2 is plugging into PARKINSON’S DISEASE in more than one way.  It is making the disease more likely to happen and making it progress faster when it does happen.  So we think knocking out LRRK2 will do the opposite–slow the disease or make it much less likely to develop.”

Simply slowing the progress of the disease would be a major break through.  It could extend the length of time that levodopa effectively alleviates the symptoms and could even reduce or eliminate some of the side effects that can sometimes be worse than the disease.

Southern Research Institute is pharmaceutical research company partnering with Dr. West’s lab to develop a drug to inhibit LRRK2.  They hope to be able to test it in humans early next year.

J. P. L. Daher, L. A. Volpicelli-Daley, J. P. Blackburn, M. S. Moehle, A. B. West.Abrogation of  -synuclein-mediated dopaminergic neurodegeneration in LRRK2-deficient rats. Proceedings of the National Academy of Sciences, 2014; DOI: 10.1073/pnas.1403215111

Review by Marcia McCall

Picture Credit

http://cssb2.biology.gatech.edu/kinomelhm/kinases/LRRK2_Hsap.html

http://www.scidacreview.org/0704/html/parkinsons.html

http://www.walker-facts.com/Case-Studies-Parkinson-Disease.asp

New PARKINSON’S Gene Discovery Could Lead to New Treatment

The new molecular sciences continue to delve deeper into the mysteries of the cellular actions and interactions to unlock the keys to PARKINSON’S DISEASE.  A team of genetic researchers at the University of California at Los Angeles headed by Dr. Ming Guo has found one more clue, a gene that mediates the interactions of two mutated genes and helps cells maintain their health to prevent neurodegeneration.

The genes PINK1and Parkin play important roles in protecting the energy producing mitochondria of cells.  When these genes are mutated, they do not operate correctly and allow for accumulations of unhealthy cells with damaged mitochondria that leads to the early on-set of PARKINSON’S DISEASE.  Working in fruit flies and mouse models of disease, Guo and her team found that a gene called MUL-1 mediated the interaction of PINK-1 and Parkin and contributed to the health of the mitochondria. When MUL-1 was removed from the interaction with PINK-1 and Parkin in the neurons in the mouse model, they found it caused deterioration of the mitochondria, but when an extra amount of MUL-1 was added, the mitochondrial damage was repaired.

The discovery of this new genetic interaction is exciting, showing a new mechanism for improving the function of mitochondria and maintaining the health of the cell, but also because it may lead to the development of a drug that could enhance its presence and prevent neurodegeneration.  Such a new drug would be of immense benefit to people with PARKINSON’S DISEASE.

Further studies will test these findings in more complex biological organisms and will help to find more cellular interactions related to MUL-1.  Testing for drugs that will enhance MUL-1  and become a basis for treatment is another a priority.  The team will also be looking for mutations of the MUL-1 gene and to understand its heritability to see if it exists in all PARKINSON’S patients or if it is found only in the inherited forms of PARKINSON’S.

J. Yun, R. Puri, H. Yang, M. A. Lizzio, C. Wu, Z.-H. Sheng, M. Guo. MUL1 acts in parallel to the PINK1/parkin pathway in regulating mitofusin and compensates for loss of PINK1/parkin. eLife, 2014; 3 (0): e01958 DOI:10.7554/eLife.01958

Review by Marcia McCall

Picture Credits

http://cssb2.biology.gatech.edu/kinomelhm/kinases/PINK1_Hsap.html

http://newsavalanche.com/2013/05/10/the-watchdog-protein-research-leads-to-new-therapies-for-parkinsons/

http://www.novusbio.com/MUL1-Antibody-5H62D5_NBP2-31361.html

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IMPROVEMENT SEEN IN FIRST CLINICAL TRIAL OF MAGNETIC STIMULATION FOR PARKINSON’S DISEASE

A double blind, randomized trial tested two targets of magnetic stimulation as well as a sham stimulation on 60 subjects that had moderate PARKINSON’S DISEASE.  They received their usual Parkinson’s medications in addition to the stimulation. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive treatment that researchers hope will augment pharmaceutical treatments for PARKINSON’S DISEASE.  This trial has safety and efficacy as its primary outcome measures as well as improving clinical results when the subjects were off their drugs. While other studies have reported mixed results from transcranial magnetic stimulation, this trial used a larger, unique coil with the ability to generate a larger field of stimulation that penetrated deeper into the brain.

Principal investigator of this trial was Mario FIchera, M.D. from the Institute of Experimental Neurology at the Scientific Institute Hospital San Raffaele in Milan, Italy who presented his findings at the 24th Meeting of the European Neurological Society on June 1, 2014. He stated that compared to the group receiving sham stimulation, both groups that received targeted stimulation improved significantly, with no serious adverse events.  In addition to reported improvements as measured by the Unified Parkinson’s Disease Rating Scale (UPDRS) part III, subjects reported they experienced a better quality of life, but he cautioned that a further trial should be done to “validate the efficacy seen in this trial and to gauge the duration of the effects.”

Transcranial Magnetic Stimulation is a relatively new technique that changes neuronal function by using an electromagnetic field generated by a coil.  Electricity passes in opposite directions through the shape of the coil and where the current crosses it generates an electrical field, whose intensity can be modified by regulating the amount of electrical current.  Pulses can be applied singly or repetitively and at varying intensities.  The strength and frequency of the pulses can determine excitability or inhibition of the target neurons. The coil is placed against the scalp and the magnetic field passes through the skull to change the electrical field of the underlying neurons.  In this study TMS was applied in repetitive pulses, timed milliseconds apart.  TMS treatment is usually done several times a week for several weeks.

In this study, all groups of subjects received treatment three times a week for four weeks. One group received treatment on the motor cortex region, contralateral to their affected side, and also to the prefrontal cortex.  Group two received treatment to the motor cortex region, but sham treatment on the prefrontal cortex.  Group three received sham treatments on both treatment sites. Both groups that received actual treatment showed reductions in the motor symptoms and tremors compared to the sham group.

Dr. Josep Valis-Solis, a neurologist and neurophysiologist at the Hospital Clinic in Barcelona, Spain said “I think that we have to promote a bit this kind of treatment that is noninvasive and nonpharmacological, so some hope that we are escaping from toxicity from drugs.”  It is still early and there needs to be more investigation into the types and differences of effects from different coils.  Cost and availability of the equipment and training and availability of personnel to administer treatment is another issue that needs to be studied together with the rate of retreatment necessary to maintain a positive effect over an as yet unknown, period of time.

Magnetic Stimulation Improves Parkinson’s Symptoms, Medscape Jun 17, 2014

Review by Marcia McCall.

Picture Credits

http://www.magventure.com/en-gb/products/stimulators/magprocompact.aspx

http://phys.org/news171037372.html

http://blogs.scientificamerican.com/guest-blog/2013/02/28/challenges-in-simulating-a-human-

NEW TECHNIQUE FOR DOPAMINE CELL REPLACEMENT IN PARKINSON’S DISEASE

Love those Italians…. they excel in fashion design and make the best designer shoes!  Now they have taken design to the cellular level and are creating designer drugs for designer receptors on those cells.  They call it DREADD (designer receptor exclusively activated by designer drug.  But this is really serious science.

Cell transplantation in PARKINSON’S DISEASE, while in theory, sounds very plausible, in practice has yielded mixed results with the development of serious dyskinesias or even tumors being a major problem. Because it is a particular type of neuronal cell that is affected in PARKINSON’S DISEASE, cell therapy with dopamine producing cells could yield a potential therapeutic treatment.  If dopamine producing cells could be developed, transplanted and become effective and efficient producers of dopamine, the troublesome motor symptoms that plague people with PARKINSON’S could be banished.

Embryonic stem cells or induced pluripotent stem cells have been developed from both mouse and human cells and have been somewhat effective in alleviating motor symptoms when transplanted into animal models of PARKINSON’S DISEASE.  But if the differentiation from stem cell to dopamine producing cell is not well controlled, tumors can develop.  Cells developed from human fibroblasts can be induced to become neurons, but are more difficult to produce, with more opportunity for potential error.  Much stem cell technology exists only in petri dishes, and the degree to which these reprogrammed cells would be functional or stable when transplanted into living models is not yet known. For modified cells to be transplanted and become effective a system needs to be developed that will allow the transplanted cells to be monitored and modulated to serve the physiological environment into which they are introduced.

Previous studies have shown that only dopamine neurons from the mid brain region were successful in reversing motor function in lesioned rats.  This team developed an induced dopaminergic neuron (iDA) from fibroblast, so the challenge was to see if it could be as effective as mid brain dopamine neurons.  The grafted iDA neurons did improve the motor function of the animals, but not as well as native embryonic DA neurons.  Stereological cell counting showed that there were as many surviving iDA cells as there were native DA cells and this lead to the idea that iDA neurons were less functional intrinsically. The team believes that an improved method for generating better quality induced pluripotent stem cells from the fibroblasts will result in more uniformly expressing iDA neurons.

To measure the integration of the iDA neurons into the host environment, they used the DREADD technology.  This technology allows the addition of a uniquely designed receptor that permits a specific interaction with a pharmacological drug to manipulate the activity of the re-programmed neuron.  It thus enforces a sort of “remote control” over the transplanted neuron to enhance its effects in living animals. This method may offer a better approach to cell replacement therapy by combining an external, pharmacological agent with the transplanted re-programmed neurons to respond to the physiological needs and requirements of the recipient.

This research study was done by a large team of researchers under the direction of Vania Broccoli, Ph.D. who is a developmental neurologist at the Hospital San Rafaele in Milan, Italy.  It will be published in the Journal of Clinical Investigation on July 1, 2013.

Broccoli, V. et al; Remote control of induced dopaminergic neurons in parkinsonian rats; J Clin Invest. 2014;124(7):3215-3229. doi:10.1172/JCI74664

 Parkinson Research Foundation

Review by Marcia McCall

Picture Credits

http://www.stemcell.ucsb.edu/compliance/

http://www.salk.edu/news/pressrelease_details.php?press_id=580

http://www.ourprg.com/?p=8459

'Frenemy' in Parkinson's disease takes to crowdsourcing

Date:

September 29, 2014

Source:

University of California, San Diego Health Sciences

Summary:

A key neuronal protein called alpha-synuclein normally gathers in synapses, where aggregates of it help regulate neurotransmissions, researchers have found. In overabundance, though, a-synuclein can choke off communication altogether, leading to neuronal death and related diseases.

The protein alpha-synuclein is a well-known player in Parkinson's disease and other related neurological conditions, such as dementia with Lewy bodies. Its normal functions, however, have long remained unknown. An enticing mystery, say researchers, who contend that understanding the normal is critical in resolving the abnormal.

Alpha-synuclein typically resides at presynaptic terminals -- the communication hubs of neurons where neurotransmitters are released to other neurons. In previous studies, Subhojit Roy, MD, PhD, and colleagues at the University of California, San Diego School of Medicine had reported that alpha-synuclein diminishes neurotransmitter release, suppressing communication among neurons. The findings suggested that alpha-synuclein might be a kind of singular brake, helping to prevent unrestricted firing by neurons. Precisely how, though, was a mystery.

Then Harvard University researchers reported in a recent study that alpha-synuclein self-assembles multiple copies of itself inside neurons, upending an earlier notion that the protein worked alone. And in a new paper, published this month in Current Biology, Roy, a cell biologist and neuropathologist in the departments of Pathology and Neurosciences, and co-authors put two and two together, explaining how these aggregates of alpha-synuclein, known as multimers, might actually function normally inside neurons.

First, they confirmed that alpha-synuclein multimers do in fact congregate at synapses, where they help cluster synaptic vesicles and restrict their mobility. Synaptic vesicles are essentially tiny packages created by neurons and filled with neurotransmitters to be released. By clustering these vesicles at the synapse, alpha-synuclein fundamentally restricts neurotransmission. The effect is not unlike a traffic light -- slowing traffic down by bunching cars at street corners to regulate the overall flow.

"In normal doses, alpha-synuclein is not a mechanism to impair communication, but rather to manage it. However it's quite possible that in disease, abnormal elevations of alpha-synuclein levels lead to a heightened suppression of neurotransmission and synaptic toxicity," said Roy.

"Though this is obviously not the only event contributing to overall disease neuropathology, it might be one of the very first triggers, nudging the synapse to a point of no return. As such, it may be a neuronal event of critical therapeutic relevance."

Indeed, Roy noted that alpha-synuclein has become a major target for potential drug therapies attempting to reduce or modify its levels and activity.

end text

Story Source:

The above story is based on materials provided by University of California, San Diego Health Sciences. Note: Materials may be edited for content and length.

end story_source

Journal Reference:

•   Lina Wang, Utpal Das, David A. Scott, Yong Tang, Pamela J. McLean, Subhojit Roy. α-Synuclein Multimers Cluster Synaptic Vesicles and Attenuate Recycling. Current Biology, 2014; DOI: 10.1016/j.cub.2014.08.027

end journal_references

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University of California, San Diego Health Sciences. "'Frenemy' in Parkinson's disease takes to crowdsourcing." ScienceDaily. ScienceDaily, 29 September 2014. <www.sciencedaily.com/releases/2014/09/140929174413.htm>.

end citations

The Edmond J. Safra National Parkinson’s Wellness Initiative Launched by The National Parkinson Foundation, NYU Langone Medical Center, and The Jewish Community Center in Manhattan

Release date: 9/17/2014MIAMI—September 17, 2014—The National Parkinson Foundation (NPF) announced today a joint program with the NYU Langone Parkinson’s and Movement Disorders Center and The Jewish Community Center (JCC) in Manhattan to launch The Edmond J. Safra National Parkinson’s Wellness Initiative. With generous support from the Edmond J. Safra Philanthropic Foundation, this new initiative will launch in four U.S. cities across the country by 2016, and is designed to help improve the quality of life of thousands of individuals impacted by Parkinson’s disease through physical exercise, support, education, and socialization opportunities.

This national initiative builds upon the Edmond J. Safra Parkinson’s Wellness Program-NYC, a ground-breaking, community-based partnership founded in 2007 by the NYU Langone Parkinson’s and Movement Disorders Center and The JCC in Manhattan.

Jewish Community Centers across the country will be invited to apply to participate in the initiative, and those chosen will be provided with a grant to develop a Parkinson’s wellness program in their cities.  Two sites will be selected for launch in 2015 with two more to follow in 2016.

"The National Parkinson Foundation has long shared the Edmond J. Safra Philanthropic Foundation’s belief in the importance of a holistic approach to fighting the disease," said Joyce Oberdorf, NPF’s President and CEO. "We are delighted to extend this innovative program that combines the benefits of expert care with wellness in a unique fashion."

In collaboration with Jewish Community Centers and NPF Centers of Excellence across the country, the mission of this national initiative will be to place wellness within reach of individuals and families affected by Parkinson’s. Unique among Parkinson's programs, it takes an evidence-based approach and connects the expert care of a NPF Center of Excellence with intentional wellness, through physical exercise, education, and support in community settings. The program’s low-cost services will be open to anyone with Parkinson’s.

"The goal of this new initiative will be to help build energetic, connected, and empowered local communities for individuals and families living with Parkinson’s nationwide," said Amy C. Lemen, Managing Director of The Edmond J. Safra National Parkinson’s Wellness Initiative, and Associate Director of Community Services at NYU Langone Parkinson’s and Movement Disorders Center. "The New York City program has become a welcoming hub for the Parkinson’s community. We’re excited to have the opportunity to help more and more people with a program that is redefining what it means to live well with Parkinson’s.”

"The JCC in Manhattan is proud to work with the NYU Langone Parkinson’s and Movement Disorders Center and we look forward to partnering with NPF to expand opportunities for wellness for individuals with Parkinson’s throughout the country and beyond,” said Rabbi Joy Levitt, Executive Director of the JCC in Manhattan.

“When he was sick with Parkinson’s, my husband Edmond would tell me, ‘Darling, please always protect my dignity.’ I am proud to support programs such as The Edmond J. Safra National Parkinson’s Wellness Initiative, which focus on enhancing quality of life and treating each patient as a human being with inherent dignity. I know my husband would have been deeply honored to have his name linked with such an important effort,” said Mrs. Lily Safra, Chairwoman of the Edmond J. Safra Philanthropic Foundation.

For more information about The Edmond J. Safra National Parkinson’s Wellness Initiative, call the NPF Helpline at 1-800-4PD-INFO (473-4636).

About Parkinson's Disease (PD)
Affecting an estimated one million Americans and four to six million worldwide, Parkinson’s is the second most common neurodegenerativedisease after Alzheimer's and is the 14th leading cause of death in the United States. It is associated with a progressive loss of motor control (e.g., shaking or tremor at rest and lack of facial expression) as well as non-motor symptoms (e.g., depression and anxiety). There is no cure for PD and 60,000 new cases are diagnosed each year in the United States alone.

About the Edmond J. Safra Philanthropic Foundation 
The Edmond J. Safra Foundation supports hundreds of projects related to science and medicine, education, religion, culture and humanitarian relief in over 40 countries. The Foundation has provided significant funding for Parkinson’s disease research  and patient care at dozens of hospitals and institutes in places as varied as Natal (Brazil), Toronto, New York, Grenoble, Paris, London, and Jerusalem. For more information, visit www.edmondjsafra.org.

About the National Parkinson Foundation (NPF)
Founded in 1957, the National Parkinson Foundation's mission is to improve the quality of care for people with Parkinson's disease through research, education, and outreach. NPF has funded more than $180 million in care, research and support services. NPF Centers of Excellence, at top medical institutes, includes 39 centers that deliver care to more than 50,000 Parkinson’s patients. For more information, visit www.parkinson.org, or call the NPF Helpline at 1-800-4PD-INFO (473-4636).

About the NYU Langone Parkinson’s and Movement Disorders Center
The Parkinson’s and Movement Disorders Center at NYU Langone Medical Center was established in 2007 with the generous support of the Edmond J. Safra Philanthropic Foundation to help individuals and families living with PD and other movement disorders to achieve the highest possible quality of life now. In only 7 years of existence, the Center has established itself as a leader in PD care, research, and outreach on the local, national and international levels, and it has quickly grown to be one of the largest movement disorders center in NYC. The Center was awarded the prestigious designation of NPF Center of Excellence in 2009. For more information, visit http://parkinson.med.nyu.edu/ or call 646-501-9241.

About the JCC in Manhattan 
Located on 76th Street and Amsterdam, the JCC is a vibrant non-profit community center on the Upper West Side. The cornerstone of progressive programming in Manhattan, the JCC serves over 55,000 people annually through 1,200 programs each season that educate, inspire, and transform participants' minds, bodies, and spirits.  The Marti Ann Meyerson Center for Health & Wellness is at the heart of the JCC's efforts to create a holistic environment that allows members to live their healthiest, most vibrant, and most complete life possible, serving people from every age and stage. For more information, visit www.jccmanhattan.org.