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  • Thomas Drew, MD, Appointed to Rhode Island Hospital Board

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    Thomas Drew, MD, Appointed to Rhode Island Hospital Board

    (posted March 27, 2006)

    Thomas Drew

    Thomas Drew, MD, of Providence, RI, was recently named a member of the Rhode Island Hospital board of trustees. Chairman of the board, Edward Iannuccilli, MD, made the announcement.

    Drew has practiced as a cardiologist at Rhode Island Hospital since 1977, and has been an active leader in the University Cardiology Foundation. He has held physician leadership roles on various hospital committees, including president of the Staff Association, and served as a member of the Rhode Island Hospital board of trustees from 1977 to 2004.

    “We are very fortunate to have Dr. Drew return to the board of trustees,” Iannuccilli says. “His experience, long-standing support and dedication to the hospital will assist us as we continue to advance Rhode Island Hospital into the future.”

    Drew is a graduate of Wesleyan University and earned his medical degree from Columbia School of Physicians and Surgeons. He completed his internship and residency in medicine at Beth Israel Hospital in Boston. Following a tour of duty as an epidemiologist in the Public Health Service, Drew completed his fellowship in cardiology at the University of Pennsylvania.

    Rhode Island Hospital Recruiting Caregivers of Alzheimer's Patients for Unique Study

    (posted March 27, 2006)

    The Alzheimer's Disease and Memory Disorders Center at Rhode Island Hospital has started a unique research study focusing on the quality of life for caregivers of Alzheimer's patients. Providing care to patients with Alzheimer's can create stress that can impact a caregiver's health, mental well-being and the function of the family. The study will look for ways to help caregivers through telephone support, home or nursing home visits and education. They are currently recruiting caregivers who are placing their family members in a nursing home for long-term care after providing care at home.

    The Alzheimer's Disease and Memory Disorders Center at Rhode Island Hospital is the largest memory assessment program in Rhode Island and offers a full range of diagnostic and treatment services including cutting edge brain imaging, genetic tests and neuropsychological evaluations. For more information, please call 401-444-0368.

    Reduced Insulin in the Brain Triggers Alzheimer's Degeneration

    (posted March 23, 2006)

    Suzanne de la Monte, MD

    Read more about the study in the Journal of Alzheimer's Disease.

    Previous Research
    • November 2005
    • March 2005

    More about Alzheimer studies
    at Lifespan

    By depleting insulin and its related proteins in the brain, researchers at Rhode Island Hospital and Brown Medical School have replicated the progression of Alzheimer's disease - including plaque deposits, neurofibrillary tangles, impaired cognitive functioning, cell loss and overall brain deterioration—in an experimental animal model. The study demonstrates that Alzheimer's is a brain-specific neuroendocrine disorder, distinct from other types of diabetes.

    In the study, brain deterioration was not related to the pancreas, which regulates insulin for the body. When pancreatic insulin is deficient or the body fails to respond to it, the result is Type 1 or Type 2 diabetes. Previous work by the researchers with postmortem brain tissue of Alzheimer's patients showed a strong link between insulin depletion in the brain and Alzheimer's disease, raising the possibility that Alzheimer's is a neuroendocrine disorder, or a Type 3 diabetes.

    "We have demonstrated that a loss of insulin in the brain triggers the onset of Alzheimer's, probably because as the brain loses insulin, the cells that require insulin to function and survive also eventually die. The consequences are increased oxidative stress, brain deterioration, loss of cognitive function, and a buildup of plaques and tangles in the brain—all hallmarks of Alzheimer's, says senior author Suzanne de la Monte, MD, MPH, a neuropathologist at Rhode Island Hospital and a professor of pathology and clinical neuroscience at Brown Medical School in Providence, RI.

    "We now know that if you specifically target insulin and its actions in the brain, you could develop new treatments for this disease," de la Monte says.

    The study is published in the current issue (Volume 9, Issue 1) of the Journal of Alzheimer's Disease.

    Researchers injected the brains of rats with Streptozotocin (STZ), a compound that when metabolized, destroys beta cells in pancreatic islets and produces diabetes. When injected directly into the brain, the treatment caused neurodegeneration, while the pancreatic islet cells remained intact. That is because insulin depletion produced by STZ was confined to the brain, just like what occurs in most cases of Alzheimer's.

    "This study provides definitive evidence that impairments in insulin/IGF signaling and deficiencies in the corresponding growth factors can occur in the central nervous system (CNS) independent of Type 1 or Type 2 diabetes," the authors write.

    As a result of the treatment, insulin and its IGF-I receptors were significantly reduced in the brain, triggering a cascade of neurodegeneration. Both insulin and IGF-I activate complex signaling pathways downstream, prompting energy metabolism and growth required for learning and memory, and inhibition of oxidative stress, which unchecked could trigger neurodegeneration. As insulin was depleted, neurons died and the brain dropped to half its size, a result of atrophy which is a prominent feature of Alzheimer's. At the same time, there was an increase in astrocytes and microglial cells, which are responsible for neuroinflammation, another critical and consistent feature of Alzheimer's and probably related to the increased amyloid deposition in the brain, the researchers say.

    Also, there was increased activation of a kinase called GSK-3 beta. This kinase is overactive in Alzheimer's and triggers tau phosphorylation, which is known to be at the core of neurofibrillary tangles. The researchers had previously shown that tau is regulated by insulin and insulin-like growth factor (IGF-I). In the current research, they found that as insulin and IGF-I were depleted in the brain, the expression of GSK-3 beta increased, leading to oxidative stress and cell death.

    While the link between insulin and tau had been established, researchers also looked at the connection between insulin and amyloid precursor protein gene expression, as increased levels could account for amyloid accumulation, or the buildup of plaques in the brain. They found that amyloid beta deposits in vessels and plaques did build up in the brain, and they suggest that these abnormalities occurred due to increased oxidative stress.

    Another feature of Alzheimer's affected by impaired insulin signaling, acetylcholine deficiency, is linked to dementia and has long recognized as an early abnormality in Alzheimer's. The enzyme that makes acetylcholine, choline acetyltransferase (ChAT), was previously found to be regulated by insulin and IGF-1. In brains with Alzheimer's, impairment of insulin and IGF-I signaling mechanisms correlate with deficits in acetylcholine production. In this study, ChAT was markedly reduced in the experimental Alzheimer's model.

    "Our previous work has shown that many of the important features of Alzheimer's—such as the accumulation of phosphorylated tau and the death of neurons—were somehow linked to insulin deficiency in the brain. This study shows that insulin is the controlling factor in all of these features of Alzheimer's disease," de la Monte says.

    "The evidence suggests that impaired insulin and IGF signaling must be addressed in order to make significant progress in the treatment and prevention of Alzheimer's disease," she says.

    This study was supported by grants from the National Institutes of Health.

    Miriam Hospital Celebrates 15th Annual Women's Wellness Day

    (posted March 21, 2006)

    Ladies, it's your turn to take a day off just for you. The Miriam Hospital is holding the 15th annual Women's Wellness Day on Saturday, May 6—a daylong event to empower women with the information they need to stay healthy.

    Keynote speaker Bonnie St. John, whom the NBC Nightly News has called, “one of the five most inspiring women in America,” will explain how she overcame the challenges of growing up poor and black and losing a leg to amputation at age five. In her presentation, St. John will describe how she went on to graduate from Harvard and Oxford, become a Rhodes Scholar, and win silver and bronze medals at the 1984 Innsbruck Paralympics.

    The remainder of the day will include workshops ranging from managing menopause to self-defense tips, a fashion show from Coldwater Creek during lunch, several health screenings, informational booths and much more. Take time to relax, take time to learn and take time for yourself!

    Coventry Credit Union Donates Devices to Soothe Patients at Hasbro Children's Hospital

    (posted March 21, 2006)

    Coventry Credit Union

    From left: Miriam Plitt, the director of marketing for Coventry Credit Union; Anne Marie Hecker, MS, RN; and Bruce Hecker, a member of the Coventry Credit Union board of trustees, stand with the devices the credit union donated to Hasbro Children's Hospital to help soothe the youngest, most critically ill patients at the hospital.

    Some of the most critically ill patients at Hasbro Children's Hospital will have a new way to be comforted during their hospital stay thanks to a recent donation from the Coventry Credit Union.

    Contributions from the credit union have allowed Hasbro Children's Hospital to purchase numerous toys and equipment that offers soothing sounds and vibrations, which research shows can help comfort irritable, distressed and neurologically impaired infants.

    The new devices will be used in the Pediatric Intensive Care Unit and can be used to soothe young children and their families.