Alzheimer’s disease affects approximately 5.1 million Americans and is a characterized by a progressive debilitating disease that disrupts the tasks associated with daily living. There is still no treatment that cures Alzheimer’s disease and the prevailing research is aimed at treatments and methods to delay and alleviate the progression of the disease by addressing the symptoms. A new study, published online in the Journal of American Medical Association, from the Icahn School of Medicine at Mount Sinai in conjunction with the Veterans Administration Medical Center has found that alpha tocepherol, the fat-soluble Vitamin E and antioxidant, may slow functional decline (problems with daily activities such as shopping, preparing meals, planning, and traveling) in patients with mild-to-moderate Alzheimer’s disease and decrease caregiver burden. Vitamin E can be obtained at any drug store and is an inexpensive treatment remedy. This study involved 613 Alzheimer’s patients.
“Since the cholinesterase inhibitors [galantamine, donepezil, rivastigmine], we have had very little to offer patients with mild-to-moderate dementia,” said Mary Sano, PhD, trial co-investigator, and professor in the department of psychiatry, Icahn School of Medicine at Mount Sinai, and director of research at the James J. Peters Veteran’s Administration Medical Center, Bronx, New York.
“This trial showed that vitamin E delays progression of functional decline by 19% per year, which translates into 6.2 months benefit over placebo.”
A previous study investigated the ability of vitamin C to dissolve amyloid plagues found in the brains of people with Alzheimer’s disease. The amyloid plagues are formed by deposits of protein aggregates that accumulate in the brain and cause nerve cell death in the brain and the first nerves to be attacked are the ones in the brain’s memory center.
“When we treated brain tissue from mice suffering from Alzheimer’s disease with vitamin C, we could see that the toxic protein aggregates were dissolved. Our results show a previously unknown model for how vitamin C affects the amyloid plaques,” says Katrin Mani, reader in Molecular Medicine at Lund University.
“Another interesting finding is that the useful vitamin C does not need to come from fresh fruit. In our experiments, we show that the vitamin C can also be absorbed in larger quantities in the form of dehydroascorbic acid from juice that has been kept overnight in a refrigerator, for example.”
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.
F. Cheng, R. Cappai, G. D. Ciccotosto, G. Svensson, G. Multhaup, L.-A. Fransson, K. Mani. Suppression of Amyloid β A11 Antibody Immunoreactivity by Vitamin C: Possible Role Of Heparan Sulfate Oligosaccharides Derived From Glypican-1 By Ascorbate-induced, Nitric Oxide (NO)-catalyzed Degradation. Journal of Biological Chemistry, 2011; 286 (31): 27559 DOI: 10.1074/jbc.M111.243345