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Sarasota Research

Vitamin E May Aid in Slowing down Alzheimer’s disease

A new study published in the January 1st online edition of the Journal of the American Medical Association discussed findings conducted at the Icahn School of Medicine at Mount Sinai. In this study, the school’s faculty worked with the Veterans Administration Medical Centers and found that alpha tocepherol, otherwise known as Vitamin E with antioxidants, could help slow functional decline of patients with mild-to-moderate Alzheimer’s disease. Problems of functional decline include issues with daily activities; shopping, preparing meals, planning, and traveling. This study could bring much welcomed aid from the estimated 5.4 million families and caregivers of 5.1 million patients suffering with mild to moderate Alzheimer’s disease.

Mary Sano, PhD, trial co-investigator, professor within the Icahn School of Medicine’s department of psychiatry, and director of research at the James J, Peters Veteran’s Administration Medical Center at the Bronx, New York headed up this study. She stated that since the days of cholesterase inhibitors, such as galantamine, donepezil, and rivastigmine, there were few options for patients with mild-to-moderate dementia. However, with the results of the current study run, the use of vitamin E could delay the progression of functional decline within mild-to-moderate Alzheimer’s disease patients by 19 percent per year, which would translate into 6.2 months benefit over the placebo. Vitamin E is nowadays easily purchasable and non-expensive, and it could be an effective treatment strategy for Alzheimer’s patients.

Team AD, the Veteran’s Administration Cooperative Randomized Trial of Vitamin E and mimantine in Alzheimer’s disease, examined the effects of vitamin E 2,000 IU/d, and 20 mg/d of memenatine, the placebo used. For the study, testing was conducted at 14 different Veteran’s Affairs Medical Centers, 613 patients with mild to moderate Alzheimer’s disease were followed from August 2007 until September 2012. Dr. Sano reported that in previous studies she conducted with moderately severe Alzheimer’s, vitamin E also slowed the disease’s progression.
References:
1) Maurice W. Dysken, Mary Sano, Sanjay Asthana, Julia E. Vertrees, Muralidhar Pallaki, Maria Llorente, Susan Love, Gerard D. Schellenberg, J. Riley McCarten, Julie Malphurs, Susana Prieto, Peijun Chen, David J. Loreck, George Trapp, Rajbir S. Bakshi, Jacobo E. Mintzer, Judith L. Heidebrink, Ana Vidal-Cardona, Lillian M. Arroyo, Angel R. Cruz, Sally Zachariah, Neil W. Kowall, Mohit P. Chopra, Suzanne Craft, Stephen Thielke, Carolyn L. Turvey, Catherine Woodman, Kimberly A. Monnell, Kimberly Gordon, Julie Tomaska, Yoav Segal, Peter N. Peduzzi, Peter D. Guarino. Effect of Vitamin E and Memantine on Functional Decline in Alzheimer Disease. JAMA, 2014; 311 (1): 33 DOI: 10.1001/jama.2013.282834
2) Mount Sinai Medical Center (2013, December 31). Vitamin E may delay decline in mild-to-moderate Alzheimer’s disease. ScienceDaily. Retrieved January 2, 2014, from http://www.sciencedaily.com¬ /releases/2013/12/131231163755.htm

By: Lauren Horne

The Roskamp Institute is a 501(c)3 research facility dedicated to translating the efforts of its qualified research staff into real-world results for those suffering from neurological diseases. To learn more about our programs and to get information about donating, visit www.rfdn.org.

Eleven new Alzheimer's Risk Gense

A study by the International Genomics Project, published in Nature Genetics, identified eleven previously unknown genes that increase risk of developing Alzheimer’s. The research, which brought together leading Alzheimer’s researchers, was comprised of four teams from one hundred and forty-five global academic centers working toward the common goal of determining new information surrounding the genetics of Alzheimer’s disease.

One of the most significant findings of the study, which involved the genome data of 74,076 people from fifteen different countries, relates to the HLA-DRB5/DRB1 major histocompatibility complex region of the brain. The research shows that this same region, associated with multiple sclerosis and Parkinson’s, is involved somehow in Alzheimer’s disease.

The discovered genes revolved mostly around late onset Alzheimer’s, the most common type of the disease. Professor Julie Williams, head of neurodegeneration at Cardiff School of Medicine’s Medical Research Council, says that the teams can now shift their focus to early on-set Alzheimer’s, the most severe form that usually begins around ages 40-50. The Professor says that indentified genetic architecture may make finding new genes easier, and that the genes yield clues for scientists to seek out during research.

These eleven genes bring the total of indentified risk genes to twenty-one, and scientists hope that such findings will help improve knowledge about the mechanisms behind the neurodegenerative disease. The four groups used genome-wide association analysis work that previously identified the first ten risk genes. Professor Williams cautions that although twenty-one of these genes are now uncovered, a large section of genetic risk for Alzheimer’s remains unknown. Williams ends by saying that the identification of more risk genes is imperative to the continued research and development of these findings.

Sources:
1) Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease; Jean-Charles Lambert, Carla A Ibrahim-Verbaas, Denise Harold, Adam C Naj, Rebecca Sims, Céline Bellenguez, Gyungah Jun, Anita L DeStefano, et al.; Nature Genetics Published online 27 October 2013; DOI:10.1038/ng.2802.
2) Medical News Today (Published 10/28/13). Scientists Discover Eleven New Alzheimer’s Risk Genes. Retrieved 10/30/13 from http://www.medicalnewstoday.com/articles/267998.php

By Emma Henson

The Roskamp Institute is a 501(c)3 research facility dedicated to translating the efforts of its qualified research staff into real-world results for those suffering from neurological diseases. To learn more about our programs and to get information about donating, visit www.rfdn.org.

ACE Inhibitors and Alzheimer’s Prevention

Cedars-Sinai scientists published a study in Journal of Clinical Investigation that suggests ACE inhibitors, in the right context and at the right time, can be a good thing.

Many people with high blood pressure take ACE inhibitors, medication meant to widen blood vessels by limiting activity of ACE (angiotensin-converting enzyme), a naturally occurring protein. However, in new research using a rodent model of Alzheimer's Disease, it is shown that genetically targeting certain immune blood cells to overproduce the ACE enzyme can systematically break down defective proteins in the brain associated with Alzheimer’s disease and cognitive decline. The results demonstrate that ACE, not known for central nervous system involvement, can actually induce a protective immune response in the brain to ultimately affect cognition. In addition, ACE could possibly have a novel role in the clearance of excessive beta-amyloid plaques from brain blood vessels.

Kenneth Bernstein, MD, designed a rodent model to study the effects of an over-expression of ACE in macrophages, microglia, and similar cells of the immune system. The study shows the value of a strategy that delivers an enzyme to attack and destroy beta-amyloid to eschew resultant inflammation. Scientists are yet to determine if the deposits result from overproduction of beta-amyloid or an inability of mechanisms, like the immune system, to clear the plaques. Either way, a common view supports any strategy that reduces the amount of beta-amyloid protein in the brain as a way to delay progression of Alzheimer's.

Ultimately, rodents in this model with Alzheimer’s-like symptoms and those engineered to over-express ACE in immune cells produced offspring with greatly reduced beta-amyloid protein levels, inflammation, and increased performance on learning and memory tests.

The research contemplates ACE as a natural enzyme that can be harmful or helpful, depending on how and where it is active. Though it contributes to angiotensin II production, a hormone that causes high blood pressure, it can also quickly and efficiently lead an immune system response to beta-amyloid protein.

Sources:
1) Kenneth E. Bernstein, Yosef Koronyo, Brenda C. Salumbides, Julia Sheyn, Lindsey Pelissier, Dahabada H.J. Lopes, Kandarp H. Shah, Ellen A. Bernstein, Dieu-Trang Fuchs, Jeff J.-Y. Yu, Michael Pham, Keith L. Black, Xiao Z. Shen, Sebastien Fuchs, Maya Koronyo-Hamaoui. Angiotensin-converting enzyme overexpression in myelomonocytes prevents Alzheimer’s-like cognitive decline. Journal of Clinical Investigation, 2014; DOI: 10.1172/JCI66541
2) Cedars-Sinai Medical Center. (2014, February 3). Can a protein controlling blood pressure enhance immune responses and prevent Alzheimer's?. ScienceDaily. Retrieved February 6, 2014 from www.sciencedaily.com/releases/2014/02/140203122541.htm

Written by Emma Henson
Edited by Patrizio Murdocca

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